Pyridoxal-5’-phosphate (Vitamin B6): What is known as ‘Vitamin B6’ has three vitamers (chemically individual related compounds): pyridoxine, pyridoxamine, and pyridoxal. Some sources incorrectly state pyridoxamine to be the strongest anti-glycation agent, but the most effective form of vitamin B6 is the metabolically active form that the vitamers convert to – pyridoxal-5’-phosphate (P5P). Against pyridoxamine, P5P more efficiently reduced the accumulation of major advanced protein glycation products CML and imidazolone in vivo. (222) Moreover, the same study revealed P5P to be an anti-DNA glycation agent based on its inhibition of N2-(1-carboxyethyl)-2′-deoxyguanosine (CEdG), unlike pyridoxamine which offered no protection at all against this particular AGE adduct. (223) P5P has additionally proven to be a potent retarder of lipid glycation and compared very favorably in this ability against both formidable pharmaceutical and natural protein glycation inhibitors including aminoguadinine, carnosine, ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), quercetin and rutin (flavonoids), and amino acids lysine and cysteine. (224) It was briefly discussed in Glycation: Part I (See here) how DNA glycation is an underrated threat in diabetes and its complications, though lipid glycation also has a substantial impact in the development of diabetes and related complications. (225-228)
Other than preventing the accumulation of lipid-AGEs, an ability that most other potent anti-AGE compounds do not share, P5P is a renowned anti-AGE nutrient for its unusual but effective mechanism of trapping intermediate carbonyl products (pre-AGEs) to directly block AGE formation. Although the main theme of this article series was to focus on existing AGEs formed in food that are exogenously absorbed, some food products such as honey (229) are high in intermediate AGE products and form AGEs inside the body rapidly with the glycation process already set in motion. In this instance, P5P can loosely prevent dietary sourced AGEs if they are currently in the intermediate phase of glycation such as in processed or cooked carbohydrate foods where necessary amino acids will not be present for the formation of irreversible late-term AGE products.
By inhibiting all forms of glycation and outcompeting other powerful natural AGE inhibitors and pharmaceuticals, P5P demonstrates protection against a host of diabetic complications in vivo. (222)(230)
Riboflavin: There is presently a limited amount of data on riboflavin as an anti-glycation agent, but early research suggests it does have AGE-inhibiting potential based on in vitro results against methylglyoxal-induced glycation of bovine serum albumin. (89) It is also observed that a deficiency in the B2 vitamin, which is seen in much greater frequency in diabetics, causes even more lipid peroxidation … sharply increasing the potential for glycation. (90-91) Therefore, repletion in this vitamin should also be a goal in limiting AGE formation.
Selenium Yeast: Selenium in the organic form, such as yeast-bound selenium has been shown to strongly inhibit glycation and AGEs at physiological concentrations more impressively than other formidable anti-glycation agents including ascorbic acid (vitamin C), tocopherol (vitamin E), niacinamide, carnosine, and pyridoxal (active vitamin B6) at similar concentrations. (102) Sodium selenite as inorganic selenium was also included but did not significantly prevent glycation, especially compared to yeast-bound selenium. (I03) Selenium itself has decreased glucose, glyclated hemoglobin, lipid peroxidation products, and downregulated RAGE (receptors for AGEs) and AGE-induced activation of NFkB in vivo (104), but the added yeast component is theorized to further contribute to glycation-limiting abilities by addition of lysine – also a glycation limiter, at least in vitro. (105) Additionally, organic selenium has greater bioavailability and appears to possess better radical-scavenging abilities, which translates to better AGE inhibition. (106-108)
As far back as the early 1980s, it was discovered that high doses of selenium (500mcg w/ co-supplementation of vitamin E, C, and A) worked to reverse the beginnings of diabetic retinopathy and halt the process in advanced cases. (109) Diabetic retinopathy is majorly associated with glycation damage, notably by inducing VEGF expression (110) Therefore, selenium’s pivotal role in diabetic eye damage would be explainable.
One caveat with recommending a similar dose for potent anti-glycation effects is selenium’s status as a trace element. As such, the therapeutic window is narrow, meaning negative side effects and toxicity can result from high dosages. There is also some concern about selenium’s relationship to diabetes. In diabetes there is an increased concentration of plasma selenium (111), which does not exactly mean that diabetics have more selenium storage or consume more selenium-containing foods but rather that there is a higher demand of selenium usage and in a broader sense, a greater strain on antioxidant response to combat the increased lipid peroxidation and AGE generation in the disease. Defense of selenium as a reactant and not as a causal agent in this disease in discussed in greater detail in “Selenium”. In short, the verdict suggests a helpful role rather than a harmful one, but nevertheless those already with diabetes should take precautions before adding supplementary selenium to their regime.
Silymarin/Milk Thistle: Found in milk thistle, this flavonoid is rich in health-enhancing properties, two of which pertinent to glycation are anti-inflammation activity and carbonyl trapping ability. Using diabetic rats, silymarin prompted a decrease in inflammatory markers (255), and when compared with other polyphenols, silymarin was one out of the three of five tested to exhibit an inhibitory effect on the inflammatory marker TNF-alpha and the inflammatory mediator nitric oxide induced by glycation. (256)With an interdependent existence between inflammation and AGEs, silymarin could both prevent endogenously formed AGEs and lessen the inflammation produced from existing AGEs.
As for a more direct anti-AGE action, silymarin displays blockage of late stage glycation by trapping reactive carbonyls and subsequent cross-linking as well as mitigating glycated albumin concentrations … equaling less AGE accumulation and resulting in protection from diabetic complications in diabetic rodents. (255) This leaves potential to obviate AGE intake from food with reversible, mid-term glycation products.
Silymarin in a dosage of 200mg daily used as an adjunct to gliberclamide in a double-blinded placebo-controlled study demonstrated mass improvement in glycated hemoglobin values on top of lowering fasting glucose levels and BMI in type II diabetes who responded poorly to glibenclamide therapy alone. (257)
Taurine: In diabetes, greater excretion rates of the sulfur-containing amino acid occur. (241) The increased AGE accumulation seen in diabetes occurs partially due to the loss of taurine as taurine was confirmed as an anti-(protein)glycation nutrient in human RBC (red blood cells)(242), which explains the accompaniment of increased Hlabc with the diminished plasma taurine concentrations. (243) In vivo, taurine markedly decreased the accumulation of CML, a protein-based AGE, in red blood cells. (244) Compared to the supplementation of vitamin E and selenium, diabetes-associated mortality (the most popular being vascular-related ) in diabetic rats was lower in those supplemented with taurine.( 245) Taurine’s opposing effect on diabetic vascular complications can be understood by its capability to significantly block glycation of red blood cells. The alteration of RBC adhesion as affected by glycation correlates with the severity of vascular complications in diabetes. (246) Additionally, there is a well-recognized association between glycated hemoglobin and microvascular disease and a stronger predictive capacity of glycated hemoglobin for cardiovascular disease than fasting glucose.(247-248) In a very short-term human study involving young type I diabetics, 500mg of daily taurine reversed measures of endothelial dysfunction including arterial stiffness and flow-mediated dilatation to normal levels seen in non-diabetic before any effect could be observed on glycation activity represented by glycated hemoglobin and fructosamine levels. (249) As AGEs are notable contributors of endothelial dysfunction (250-251), this could mean taurine can immediately reduce AGE activity (eg. communication with AGE receptors, AGE-mediated oxidative stress and inflammation) without lowering AGE concentrations.
Second to its protective power over erythrocytes, it has an indirect anti-AGE mechanism as a chief inhibitor of lipid peroxidation. (252) Due to its strength in suppressing lipid peroxidation, taurine by itself was superior to vitamin E combined with selenium for better control of diabetic retinopathy. (253) By extension, uncooked or treated dietary fats lacking the sufficient protein to generate AGE formation will be protected by taurine from glycating endogenously and forming AGEs through lipid peroxidation.
Despite promising findings, taurine’s anti-glycation benefits may be tissue-selective, or at least much stronger for the health of the retina and the nerves. It may even slightly negatively affect the kidney when supplemented alone judging by an increase in the glomeruler volume and an increase in glomerular cell loss of diabetic rats. Moreover, a non-effect on AGE reduction was observed in the kidney. However, when taurine was supplemented alongside NAC (N-acetylcysteine), adverse glomeruler changes were completely reversed and the synergic relationship of the nutrients became a strong target for allaying kidney- residing AGE accumulatio, moreso than when either was used alone. (254)
Repletion of taurine status is the norm in the generally healthy as acquired by diet, so further supplementation is rarely indicated. Taurine supplementation will be of most use primarily to diabetics where taurine clearance is amplified and in vegetarians where taurine is deficient in the diet. For optimal effect of glycation reduction and glycaton-related symptoms, taurine replenishment should accompany NAC supplementation.
Thiamine: Thiamine, otherwise known as vitamin B1, is vital to energy metabolism and glucose metabolism. (56) A mild deficiency in the vitamin is enough to adversely affect glucose metabolism and enhance glycation activity. (57) A significant thiamine deficiency exists in type I and type II diabetes from the disease-mediated dysregulation of thiamine transport and resultant thiamine excretion that not even twice the consumption of the recommended daily value can account for. (58-59)
As yet another mechanism by which AGE levels increase in diabetes, a thiamine deficiency indirectly creates a bigger AGE burden since enzymes that require thiamine as a cofactor to inhibit glycation formation pathways cannot perform their function.(60-61) On top of inhibiting biochemical pathways that facilitate the accumulation of AGEs, thiamine is helpful with anti-glycation as a protector of oxidative stress and as a possible metal chelator. (63-65) It is an even stronger AGE-inhibitor than aminoguanidine in vitro, which only weakly inhibited late stages of glycation (62), and furthermore, thiamine in vitro outperformed carnosine by completely inhibiting the formation of AGE cross-linking.
Given that the disease process fuels the loss of available thiamine and renders cells more susceptible to glycation (66), thiamine should have a designated role over conventional AGE-inhibitors like aminoguaidine for diabetes control. Replenishment of thiamine by means of high-dose therapy in diabetic rats normalizes CML as well as CEL (N-carboxyethyl-lysine) – another AGE product – in plasma, and it does so by preventing the formation of AGE precursors, namely glyoxal and methylglyoxal, that form in excess in lipid peroxidation and in a hyperglycemic environment. (67-69) Other than the demonstrating blockage of DNA damage by glycated protein (70), thiamine inhibits DNA glycation (71), possibly implicating it in post-diabetic carcinogenesis prevention. In a human trial where diabetic patients with nephropathy were divided into two groups receiving either vitamin B6 treatment with thiamine and vitamin B6 treatment alone, only the group given thiamine reduced DNA-AGEs in leukocytes (white blood cells). (72) Other human data presents compelling evidence for a prominent role of thiamine in preventing (and perhaps reversing) the development of diabetic nephropathy. Thiamine administered in three 100mg capsules daily to type II diabetics with microalbuminuria (urinary albumin leakage) prompted a regression in UAE (urinary albumin excretion) from baseline scores, resulting in significantly lowered UAE compared that of the placebo group. (75) In another study with patients already experiencing early diabetic nephropathy, 250mg of thiamine combined with 250mg of pyridoxine (vitamin B6) therapy led to a halt in serum AGEs whereas the untreated placebo group revealed an increase in serum AGEs after the 5-month course of the study. (73) . In another double-blind placebo-controlled trial., high doses of thiamine (300mg) for three months prevented the progression of glycation, kidney dysfunction, and microangioplasty in type II diabetics based on the thiamine-induced reduction of glycated hemoglobin, microalbuminuria, and PKC (protein kinase C) respectively. (74) Although thiamine was not used as therapy in humans for diabetes-related vascular disease, a strong association with found between thiamine loss and sVCAM-1 (soluble vascular adhesion molecule 1), a marker and risk factor for vascular (micro and macro) dysfunction and disease. (76) Another study with type II diabetics has found a significant correlation between dietary thiamine and EPC/endothelial progenitor cells, which underlie healthy endothelial function (77). Two human trials have detected improvement in pain symptoms with thiamine, including from its synthetic derivative – benfotiamine, in a specific microvascular diabetic complication, neuropathy. (81-82) Taken altogether, the multiple and growing findings strengthen the indication that supplemental thiamine in human trials will protect against other macro and microvascular complications in diabetics, extending to diabetic retinopathy and cardiomyopathy, and this would corroborate with its success in rodent diabetic models. (78-80) The closest confirmation of this is a human study that, as an exception, used benfotiamine against dietary AGE exposure in the form of a heat-processed meal. It was shown that exogenous AGE consumption dramatically reduced blood flow responsiveness to stimuli and impaired FMD ( flow-mediated vasodilatation) – both features of atherosclerosis and future heart complications and stroke (84-87) – whereas supplementation with 1500mg of benfotiamine completely thwarted these effects in type II diabetics. (83)
Thiamine is water-soluble while its synthetic derivative benfotiamine is lipid-soluble. It is suggested that benfotiamine might be a better alternative since the fat-soluble variant leads to higher blood and tissue levels compared to equal amounts of thiamine. (88) Both are safely ingested in large amounts, so ~30-50mg of thiamine in B-complex formulas is patently safe and more than adequate for preventative purposes. However, diabetics often require 100-1000mg to overcome deficiency and achieve high enough concentrations to offset hyperglycemia and glycation-induced damage. Alcohol consumption will decrease thiamine absorption and is not recommended especially in thiamine stores are in need of replenishment.
Vitamin C&E (plus bioflavonoids): Ascorbic acid acts as an antagonist to glycation by competing with the bonding of protein to glucose, including vital proteins hemoglobin and albumin. (39-40) The same research that validated GSE’s (grape seed extract) ability to lower AGE-induced 8-isoprostane formation identified vitamin C’s efficacy in this domain as well due to a secondary indirect anti-glycation mechanism as an antioxidant. Vitamin C administered in tablet form totaling 1.2 g (or 1200mg) reduced 8-isoprostane levels to a greater extent than GSE did in an amount of 530mg. (41) In vivo evidence for protection from the glycation of hemoglobin is captured human studies. One gram of vitamin C (divided in two doses) significantly decreased HbA1c – a measure of glycated hemoglobin in diabetic patients after twelve months, which corresponded to when serum vitamin C levels became markedly elevated. Granted, these patients were concurrently treated with metformin at equal dosages (500mg x 2), although this trial was placebo-controlled and double-blinded. Patients on metformin alone did not experience equally impressive declines. Rather, declines in HbA1c did not reach statistical significance. (42) Supplementation with as much as 20 grams of oral vitamin C has been studied with more pronounced effects. Each increase of 30 30 micromol/L of ascorbic in plasma correlated with an approximate 0.1 decrease in HbA1c/glycated hemoglobin. (43) Supplementation <1g does not produce auspicious changes in this measure or in fasting glucose in diabetic subjects. (44) It is recommended that at least one gram of ascorbic acid is taken to produce auspicious changes in terms of glycation in diabetes. Complimentary intake of vitamin C with diet is likely to help as well, including for preventative purposes. Vitamin C intake is negatively associated with HbA1c in nondiabetic subjects. (45) In this group, a high dietary intake and/or ~200-500mg of extra supplementation is all that would be required.
Vitamin C with bioflavonoids might offer even more betterment in an AGE-rich milieu. One gram of vitamin C plus bioflavonoids decreased serum protein glycation by an average of 46.8% by four weeks in normal college-aged and middle-aged study participants. (46) Rutin, a flavonoid found in citrus food and naturally consumed alongside ascorbic acid, is also a natural aldose reductase inhibitor, which will prevent the conversion of glucose to fructose, and in turn, inhibit further glycation due to the enhanced reactivity of fructose to autooxidation. (47-48) In diabetic rats it was shown to have comparable effects to aminoguanidine on preventing collagen-linked AGE fluorescence. (49) Rutin and its metabolites were found to inhibit both fluorescent (e.g., pentosidine) and nonfluorescent (e.g., CML) AGEs in a later in vitro study (50), which corroborates with the results in vivo from aldose reductase inhibitors. While rutin was not tested specifically, an aldose reductase inhibitor reduced AGEs and their intermediates such as CML and 3-DG (3-deoxyglucosone) in diabetic patients. (51)
Other citrus flavonoids such as hesperidin and naringin possess strong activity against AGE formation. (52-53) The rutin and hesperidin in lemon juice probably had a potentiating effect on the dramatic reduction of AGEs during the cooking of beef mentioned in Glycation I. (54) It is fair to assume that the synergic intake numerous bioflavonoids and vitamin C naturally found together in food accounts for the negative correlation between dietary vitamin C and HbA1c.
Moreover, co-supplementation of vitamin C and E is a popular method of antioxidant supplementation for good reason. As expected, the established antioxidant synergy between vitamin C and vitamin E extends to anti-glycation. A combination of vitamin C and vitamin E inhibits glycation better than either used alone, probably owing to their synergistic effect on inhibiting lipid peroxidation, one of the known causes of AGE formation. (46) (55)
Whole Spices and Herbs: Popular culinary spices such as cloves, Jamaican allspice, and cinnamon are among the most potent household spices in terms of in vitro anti-glycation activity. (197) Among herbs, rosemary, sage, tarragon, and marjoram were shown to also contain strong AGE inhibitory potential in vitro. (198) Limited in vivo studies of the several herbs and spices appear to suggest promising anti-preglycation and anti-glycation activity as well. (199-200) Inhibitory strength correlated with phenolic content (197), so it may be more convenient to include a plentiful selection of these herbs and spices into daily meals as opposed to supplementing with single phenolic compounds.
Zinc: Zinc levels decline in the face of AGE exposure. (123) Nearly 25% of diabetic patients have lowered serum zinc concentrations, and all diabetics suffer from hyperzincuria, or high zinc loss through urine. (124) If zinc stores are not so deprived as to reflect a deficiency in serum, it is almost certain that tissue is lacking in zinc considering the increased rate of zinc loss. Faulty zinc metabolism is not restricted to type II diabetes; depressed zinc levels is also a feature in type I diabetes. (125) With diabetes (type I and type II) being ‘AGE-ing’ diseases, the untrammeled rate of glycation most likely is to blame.
Correcting a zinc deficiency will not be limited to restoring zinc concentrations and avoiding consequences of deficiency (e.g., impaired immune function, defective wound healing, poor bone growth, anemia, hypogonadism, diarrhea, skin lesions, etc. (126)) but zinc also restrains the effect of glycation on endothelial cells and tubular epithelial cells that manifest as vascular and renal complications by upregulation intracellular NO (nitric oxide) production, which is otherwise disrupted by AGEs. (123)(127-128) Additionally, zinc interferes with AGEs activation of the NF-kappaB signaling pathway and RAGE expression (receptor for advanced glycation end products) to limit late-term AGE-induced inflammation and deleterious AGE-related signaling mechanisms. (123) Zinc confers benefits to a multifarious range of diabetic conditions that are known to stem from and/or worsen with glycation including fasting blood glucose, postprandial blood glucose, insulin secretion, glycated hemoglobin/ HbA1c, lipid peroxidation, systolic and diastolic blood pressures, neuropathy symptoms, cardiovascular risk markers (e.g., homocysteine, microalbuminuria), and glomerular dysfunction. (129) Very general mechanisms have been proposed such as an ‘antioxidant effect’, though it is known that beyond oxidative stress, inflammation and AGE-RAGE interaction causes the aforementioned disturbances.
For diabetes purposes, doses normally ranging from 20 to 30mg are used to correct deficiency and improve disease symptoms. Zinc supplementation containing as much as 660mg of zinc sulphate (i.e. 150mg of elemental zinc) was used to significantly lower HbA1c, triglycerides, cholesterol, and systolic blood pressure by 12 weeks in type II diabetic subjects (130), but such high doses are not advised in self-treatment without follow-ups.
Serious but reversible potential side effects from zinc overload due to long-term excess zinc consumption include zinc-induced copper deficiency symptoms (e.g., anemia, neutropenia, leucopenia, myelodysplastic syndrome, nephrotic syndrome, immune suppression, and thrombogenesis. (131-132) A large decline in HDL cholesterol is also reported in healthy individuals given exceedingly high amounts of zinc, and this trend has repeated itself in later studies in amounts over 50mg daily. (133)
Milder and more common side effects from zinc supplementation (e.g., abdominal pain, nausea, loss of appetite and vomiting) are less common in the amounts recommended especially when taken with a meal. (134-135) For prevention in the healthy, ~15mg is ideal.
As is seen, the amount of safe, natural substances that perform against the glycation reaction is vast. Furthermore, differing mechanisms disallow the possibility for much of these substances to substitute for each other. Instead, they should act as complimentary allies. An intensive and costly supplementary regimedoes not necessarily follow despite the implication; rather, at least some of these sources should be sourced from the diet while others can be supplemented together as certain extracts that contain a number of anti-glycation compounds. In the catechin section, some extracts and food sources were mentioned. Another perfect example would be tomato paste. As a whole, it is a potent inhibitor of glycation (surpassing aminoguanidine in efficacy (323)) since it is made up of lycopene, rutin, naringin, quercetin, luteolin and chlorogenic acid (324-325) to name a few, leaving multiple avenues for glycation suppression. If the taste is displeasing, tomato-based supplements and powders are available. Other examples include red grape seed extract, which contains a number of flavonoids and cinnamic acids (e.g., catechin, epicatechin, chlorogenic acid, ferulic acid, etc. (326-327); Chrysanthemum morifolium, comprised of apigenin, chlorogenic acid, hesperidin, luteolin, and other healthful polyphenols that are responsible for imparting the ability the flower (extract or powder) to block both nonfluorescent and fluorescent AGE formation (328); ginkgo biloba, which not only is neuroprotective but with the flavonoids quercetin, kaempferol, and isorhamnetin (not previously mentioned), is efficiently AGE-preventing (including intermediate products and post-AGE biological dysfunction) (330-333); and milk thistle that is made up of silymarin and also apigenin, naringin, chrysoeriol (not previously mentioned), eriodictyol (not previously mentioned), etc. that is more effective than silymarin alone in preventing the development of diabetic complications (e.g. nephropathy) fueled by glycation. (334) Mulberry leaf extract, which already serves as a nontoxic herbal type II diabetes treatment in Asia, is composed of many single anti-glycation aids including but not limited to chlorogenic acid, rutin, quercetin, kaempferol derivative, gallic acid (not previous mentioned), luteolin, morin (not previously mentioned), umbelliferone (not previously mentioned), etc. (335-337) With multiple anti-diabetic and anti-glycative components, in vivo results reveal hypoglycemic effects (decreased endogenous glycation), lowered lipid hydroperoxide concentrations (pre-AGE markers), decreased MDA (intermediate AGE), reduced HbA1c levels and equally promising results (e.g., ) in human trials. (335)(338-340)
Overall a diverse and minimally cooked diet replete with healthful foods will automatically provide hearty servings of the amino acids, vitamins, minerals, herbs and spices, and polyphenols presented here, and at the same time, replace highly-processed harmful choices that would have otherwise been consumed.
*Choosing to supplement any compound here in high amounts would require medical guidance, especially if taking other forms of medication.
1. Thornalley PJ. Use of aminoguanidine (Pimagedine) to prevent the formation of advanced glycation endproducts. Arch Biochem Biophys. 2003 Nov 1;419(1):31-40.
2. Aronson D. Hyperglycemia and the pathobiology of diabetic complications. Adv Cardiol. 2008;45:1-16. doi: 10.1159/0000115118.
3. Miyata T, Wada Y, Cai Z, et al. Implication of an increased oxidative stress in the formation of advanced glycation end products in patients withend-stage renal failure. Kidney Int. 1997 Apr;51(4):1170-81.
4. Tsukahara H, Sekine K, Uchiyama M, et al. Formation of advanced glycosylation end products and oxidative stress in young patients with type 1 diabetes. Pediatr Res. 2003 Sep;54(3):419-24. Epub 2003 May 21.
5. Mahajan N, Bahl A, Dhawan V. C-reactive protein (CRP) up-regulates expression of receptor for advanced glycation end products (RAGE) and its inflammatory ligand EN-RAGE in THP-1 cells: inhibitory effects of atorvastatin. Int J Cardiol. 2010 Jul 23;142(3):273-8. doi: 10.1016/j.ijcard.2009.01.008. Epub 2009 Feb 6.
6. Anderson MM, Heinecke JW. Production of N(epsilon)-(carboxymethyl)lysine is impaired in mice deficient in NADPH oxidase: a role forphagocyte-derived oxidants in the formation of advanced glycation end products during inflammation. Diabetes. 2003 Aug;52(8):2137-43.
7. Yan H, Guo Y, Zhang J, et al. Effect of carnosine, aminoguanidine, and aspirin drops on the prevention of cataracts in diabetic rats. Mol Vis. 2008;14:2282-91. Epub 2008 Dec 11.
8. Barski OA, Xie Z, Baba SP et al. Dietary carnosine prevents early atherosclerotic lesion formation in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol. 2013 Jun;33(6):1162-70. doi: 10.1161/ATVBAHA.112.300572. Epub 2013 Apr 4.
9. Janssen B, Hohenadel D, Brinkkoetter P, et al. Carnosine as a protective factor in diabetic nephropathy: association with a leucine repeat of the carnosinasegene CNDP1. Diabetes. 2005 Aug;54(8):2320-7.
10. Peters V, Schmitt CP, Zschocke J, et al. Carnosine treatment largely prevents alterations of renal carnosine metabolism in diabetic mice. Amino Acids. 2012 Jun;42(6):2411-6. doi: 10.1007/s00726-011-1046-4. Epub 2011 Aug 11.
11. Boldyrev A, Bulygina E, Leinsoo T, et al. Protection of neuronal cells against reactive oxygen species by carnosine and related compounds. Comp Biochem Physiol137 :81 –88,2004
12. Forbes JM, Cooper ME, Thallas V, et al. Reduction of the accumulation of advanced glycation end products by ACE inhibition in experimental diabetic nephropathy. Diabetes. 2002 Nov;51(11):3274-82.
13. Price DL, Rhett PM, Thorpe SR et al. Chelating activity of advanced glycation end-product inhibitors. J Biol Chem. 2001 Dec 28;276(52):48967-72. Epub 2001 Oct 24.
14 . Hipkiss, A. R., Worthington, V. C., Himsworth, et al. (1997) Biochim. Biophys. Acta, 1380, 46-54.
15. Hipkiss AR. Carnosine and protein carbonyl groups: a possible relationship. Biochemistry (Mosc). 2000 Jul;65(7):771-8.
16. Hipkiss AR, Brownson C, Bertani MF, et al. Reaction of carnosine with aged proteins: another protective process? Ann N Y Acad Sci. 2002 Apr;959:285-94.
17. Sebeková K, Krajcoviová-Kudlácková M, Schinzel R, et al. Plasma levels of advanced glycation end products in healthy, long-term vegetarians and subjects on a westernmixed diet. Eur J Nutr. 2001 Dec;40(6):275-81.
18. Nagai K, Niijima A, Yamano T, et al. Possible role of L-carnosine in the regulation of blood glucose through controlling autonomic nerves. Exp Biol Med (Maywood). 2003 Nov;228(10):1138-45.
19. Gayova, E., Kron, I., Suchozova, K., Pavlisak, V., Fedurco, M., Novakova,
I., 1999. Carnosine in patients with type 1 diabetes mellitus. Bratisl.
Lek. Listy 100, 500–502.
20. Bolton WK, Cattran DC, Williams ME, et al. Randomized trial of an inhibitor of formation of advanced glycation end products in diabetic nephropathy. Am J Nephrol. 2004 Jan-Feb;24(1):32-40. Epub 2003 Dec 17.
21. Stefanska B. Curcumin ameliorates hepatic fibrosis in type 2 diabetes mellitus – insights into its mechanisms of action. Br J Pharmacol. 2012 Aug;166(8):2209-11. doi: 10.1111/j.1476-5381.2012.01959.x.
22. Sajithlal GB, Chithra P, Chandrakasan G. Effect of curcumin on the advanced glycation and cross-linking of collagen in diabetic rats. Biochem Pharmacol. 1998 Dec 15;56(12):1607-14.
23. Ulrich P, Cerami A. Protein glycation, diabetes, and aging. Recent Prog Horm Res. 2001;56:1-21.
24. Wautier JL, Guillausseau PJ. Advanced glycation end products, their receptors and diabetic angiopathy. Diabetes Metab. 2001 Nov;27(5 Pt 1):535-42.
25. Hu TY, Liu CL, Chyau CC, et al. Trapping of methylglyoxal by curcumin in cell-free systems and in human umbilical vein endothelial cells. J Agric Food Chem. 2012 Aug 22;60(33):8190-6. doi: 10.1021/jf302188a. Epub 2012 Aug 14.
26. Padhye S, Chavan D, Pandey S, et al. Perspectives on chemopreventive and therapeutic potential of curcumin analogs in medicinal chemistry. Mini Rev Med Chem. 2010 May;10(5):372-87.
27. Arun N, Nalini N. Efficacy of turmeric on blood sugar and polyol pathway in diabetic albino rats. Plant Foods Hum Nutr. 2002 Winter;57(1):41-52.
28. Lekshmi PC, Arimboor R, Raghu KG, et al. Turmerin, the antioxidant protein from turmeric (Curcuma longa) exhibits antihyperglycaemic effects. Nat Prod Res. 2012;26(17):1654-8. doi: 10.1080/14786419.2011.589386. Epub 2011 Oct 6.
29. Bischoff H. The mechanism of alpha-glucosidase inhibition in the management of diabetes. Clin Invest Med. 1995 Aug;18(4):303-11.
30. Sales PM, Souza PM, Simeoni LA, et al. α-Amylase inhibitors: a review of raw material and isolated compounds from plant source. J Pharm Pharm Sci. 2012;15(1):141-83.
31. Aggarwal BB, Yuan W, Li S, et al.Curcumin-free turmeric exhibits anti-inflammatory and anticancer activities: Identification of novel componentsof turmeric. Mol Nutr Food Res. 2013 Sep;57(9):1529-42. doi: 10.1002/mnfr.201200838. Epub 2013 Jul 12.
32. Taylor RA, Leonard MC. Curcumin for inflammatory bowel disease: a review of human studies. Altern Med Rev. 2011 Jun;16(2):152-6.
33. Jariyapamornkoon N, Yibchok-anun S, Adisakwattana S. Inhibition of advanced glycation end products by red grape skin extract and its antioxidant activity. BMC Complement Altern Med. 2013 Jul 12;13:171. doi: 10.1186/1472-6882-13-171.
34. Cui XP, Li BY, Gao HQ, et al. Effects of grape seed proanthocyanidin extracts on peripheral nerves in streptozocin-induced diabetic rats. J Nutr Sci Vitaminol (Tokyo). 2008 Aug;54(4):321-8.
35. Li X, Xu L, Gao H, et al. Effects of grape seed proanthocyanidins extracts on AGEs and expression of bone morphogenetic protein-7 in diabetic rats. J Nephrol. 2008 Sep-Oct;21(5):722-33.
36. Rabovsky A, Cuomo J, Eich N. Measurement of plasma antioxidant reserve after supplementation with various antioxidants in healthy subjects. Clin Chim Acta. 2006 Sep;371(1-2):55-60. Epub 2006 Mar 6.
37. Zhang FL, Gao HQ, Shen L. Inhibitory effect of GSPE on RAGE expression induced by advanced glycation end products in endothelial cells. J Cardiovasc Pharmacol. 2007 Oct;50(4):434-40.
38. Cheng M, Gao HQ, Xu L, et al. Cardioprotective effects of grape seed proanthocyanidins extracts in streptozocin induced diabetic rats. J Cardiovasc Pharmacol. 2007 Nov;50(5):503-9.
39. Davie SJ, Gould BJ, Yudkin JS. Effect of vitamin C on glycosylation of proteins. Diabetes. 1992 Feb;41(2):167-73.
40. Safari MR., N. Sheikh, and K. Mani Kashani. Study on the Effect of Vitamin C on the In Vitro Albumin Glycation Reaction.” Iranian Journal of Pharmaceutical Research 5.4 (2010): 275-279.
41. Rabovsky A, Cuomo J, Eich N. Measurement of plasma antioxidant reserve after supplementation with various antioxidants in healthy subjects. Clin Chim Acta. 2006 Sep;371(1-2):55-60. Epub 2006 Mar 6.
42. Dakhale GN, Chaudhari HV, Shrivastava M. Supplementation of vitamin C reduces blood glucose and improves glycosylated hemoglobin in type 2 diabetesmellitus: a randomized, double-blind study. Adv Pharmacol Sci. 2011;2011:195271. doi: 10.1155/2011/195271. Epub 2011 Dec 28.
43. Krone CA, Ely JT. Ascorbic acid, glycation, glycohemoglobin and aging. Med Hypotheses. 2004;62(2):275-9.
45. Shoff SM, Mares-Perlman JA, Cruickshanks KJ, et al. Glycosylated hemoglobin concentrations and vitamin E, vitamin C, and beta-carotene intake in diabetic andnondiabetic older adults. Am J Clin Nutr. 1993 Sep;58(3):412-6.
46. Vinson, Joe A., and Thomas B. Howard III. Inhibition of protein glycation and advanced glycation end products by ascorbic acid and other vitamins and nutrients.The Journal of Nutritional Biochemistry 7.12 (1996): 659-663.
47. Soulis-Liparota T, Cooper ME, Dunlop M, et al. The relative roles of advanced glycation, oxidation and aldose reductase inhibition in the development ofexperimental diabetic nephropathy in the Sprague-Dawley rat. Diabetologia. 1995 Apr;38(4):387-94.
48. Lawrence GD, Mavi A, Meral K. Promotion by phosphate of Fe(III)- and Cu(II)-catalyzed autoxidation of fructose. Carbohydr Res. 2008 Mar 17;343(4):626-35. doi: 10.1016/j.carres.2007.12.016. Epub 2007 Dec 25.
49. Odetti PR, Borgoglio A, De Pascale A, et al. Prevention of diabetes-increased aging effect on rat collagen-linked fluorescence by aminoguanidine and rutin. Diabetes. 1990 Jul;39(7):796-801.
50. Cervantes-Laurean D, Schramm DD, Jacobson EL, et al. Inhibition of advanced glycation end product formation on collagen by rutin and its metabolites. J Nutr Biochem. 2006 Aug;17(8):531-40. Epub 2005 Oct 28.
51. Hamada Y, Nakamura J, Naruse K, et al. Epalrestat, an aldose reductase ihibitor, reduces the levels of Nepsilon-(carboxymethyl)lysine protein adductsand their precursors in erythrocytes from diabetic patients. Diabetes Care. 2000 Oct;23(10):1539-44.
52. Li D, Mitsuhashi S, Ubukata M. Protective effects of hesperidin derivatives and their stereoisomers against advanced glycation end-productsformation. Pharm Biol. 2012 Dec;50(12):1531-5. doi: 10.3109/13880209.2012.694106. Epub 2012 Sep 11.
53. Sadowska-Bartosz I, Galiniak S, Bartosz G. Kinetics of glycoxidation of bovine serum albumin by methylglyoxal and glyoxal and its prevention by various compounds. Molecules. 2014 Apr 17;19(4):4880-96. doi: 10.3390/molecules19044880.
54. Uribarri J, Woodruff S, Goodman S, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010 Jun;110(6):911-16.e12. doi: 10.1016/j.jada.2010.03.018.
55. Sato K Niki E, Shimasaki H. Free radical-mediated chain oxidation of low density lipoprotein and its synergistic inhibition by vitamin E andvitamin C. Arch Biochem Biophys. 1990 Jun;279(2):402-5.
56. Lonsdale D.A review of the biochemistry, metabolism and clinical benefits of thiamin(e) and its derivatives. Evid Based Complement Alternat Med. 2006 Mar;3(1):49-59.
57. Thornalley PJ. The potential role of thiamine (vitamin B1) in diabetic complications. Curr Diabetes Rev. 2005 Aug;1(3):287-98.
58. Thornalley PJ, Babaei-Jadidi R, Al Ali H, et al. High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia. 2007 Oct;50(10):2164-70. Epub 2007 Aug 4.
59. Vindedzis SA, Stanton KG, Sherriff JL, et al. Thiamine deficiency in diabetes – is diet relevant? Diab Vasc Dis Res. 2008 Sep;5(3):215. doi: 10.3132/dvdr.2008.035.
60. Hamada Y, Araki N, Koh N, et al. Rapid formation of advanced glycation end products by intermediate metabolites of glycolytic pathway andpolyol pathway. Biochem Biophys Res Commun. 1996 Nov 12;228(2):539-43.
61. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabeticretinopathy. Nat Med. 2003 Mar;9(3):294-9. Epub 2003 Feb 18.
62. Booth AA, Khalifah RG, Hudson BG. Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation end-products:comparison with aminoguanidine. Biochem Biophys Res Commun. 1996 Mar 7;220(1):113-9.
63. Lukienko, PI., Mel’nichenko, NG., Zverinskii, IV., et al. “Antioxidant properties of thiamine.” Bulletin of experimental biology and medicine 130.3 (2000): 874-876.
64. Tunc-Ozdemir M1, Miller G, Song L, et al. Thiamin confers enhanced tolerance to oxidative stress in Arabidopsis. Plant Physiol. 2009 Sep;151(1):421-32. doi: 10.1104/pp.109.140046. Epub 2009 Jul 29.
65. Nagai R, Murray DB, Metz TO, et al. Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications. Diabetes. 2012 Mar;61(3):549-59. doi: 10.2337/db11-1120.
66. Shangari N, Mehta R, O’brien PJ. Hepatocyte susceptibility to glyoxal is dependent on cell thiamin content. Chem Biol Interact. 2007 Jan 30;165(2):146-54.
67. Karachalias N, Babaei-Jadidi R, Kupich C, et al. High-dose thiamine therapy counters dyslipidemia and advanced glycation of plasma protein in streptozotocin-induced diabetic rats. Ann N Y Acad Sci. 2005 Jun;1043:777-83.
68. Thornalley PJ, Jahan I, Ng R. Suppression of the accumulation of triosephosphates and increased formation of methylglyoxal in human red blood cells during hyperglycaemia by thiamine in vitro. J Biochem. 2001 Apr;129(4):543-9.
69. Fu MX, Requena JR, Jenkins AJ, et al. The advanced glycation end product, Nepsilon-(carboxymethyl)lysine, is a product of both lipid peroxidation and glycoxidation reactions. J Biol Chem. 1996 Apr 26;271(17):9982-6.
70. Suji G, Sivakami S. DNA damage during glycation of lysine by methylglyoxal: assessment of vitamins in preventing damage. Amino Acids. 2007 Nov;33(4):615-21. Epub 2007 Feb 16.
71. Mironova R, Niwa T, Handzhiyski Y, et al. Evidence for non-enzymatic glycosylation of Escherichia coli chromosomal DNA. Mol Microbiol. 2005 Mar;55(6):1801-11.
72. Polizzi FC, Andican G, Çetin E, et al. Increased DNA-glycation in type 2 diabetic patients: the effect of thiamine and pyridoxine therapy. Exp Clin Endocrinol Diabetes. 2012 Jun;120(6):329-34. doi: 10.1055/s-0031-1298016. Epub 2012 Jan 9.
73. Cetin E, Civelek S, Andican G, et al. Plasma AGE-peptides and C-peptide in early-stage diabetic nephropathy patients on thiamine and pyridoxine therapy. Minerva Med. 2013 Feb;104(1):93-101.
74. Alam, Saadia Shahzad, Samreen Riaz, and M. Waheed Akhtar. Effect of High Dose Thiamine Therapy on Risk Factors in Type 2 Diabetics. Journal of Diabetes & Metabolism (2012).
75. Rabbani N, Alam SS, Riaz S, et al.High-dose thiamine therapy for patients with type 2 diabetes and microalbuminuria: a randomised, double-blind placebo-controlled pilot study. Diabetologia. 2009 Feb;52(2):208-12. doi: 10.1007/s00125-008-1224-4. Epub 2008 Dec 5.
76. Thornalley PJ, Babaei-Jadidi R, Al Ali H, et al. High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Diabetologia. 2007 Oct;50(10):2164-70. Epub 2007 Aug 4.
77. Wong CY, Qiuwaxi J, Chen H, et al. Daily intake of thiamine correlates with the circulating level of endothelial progenitor cells and the endothelial function in patients with type II diabetes. Mol Nutr Food Res. 2008 Dec;52(12):1421-7. doi: 10.1002/mnfr.200800056.
78. Yun JS, Ko SH, Kim JH, et al. Diabetic retinopathy and endothelial dysfunction in patients with type 2 diabetes mellitus. Diabetes Metab J. 2013;37:262–269.
79. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9. Epub 2003 Feb 18.
80. Kohda Y, Shirakawa H, Yamane K, et al. Prevention of incipient diabetic cardiomyopathy by high-dose thiamine. J Toxicol Sci. 2008 Oct;33(4):459-72.
81. Abbas ZG, Swai AB. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy. East Afr Med J. 1997 Dec;74(12):803-8.
82. Stracke H, Gaus W, Achenbach U, et al. Benfotiamine in diabetic polyneuropathy (BENDIP): results of a randomised, double blind, placebo-controlled clinical study. Exp Clin Endocrinol Diabetes. 2008 Nov;116(10):600-5. doi: 10.1055/s-2008-1065351. Epub 2008 May 13.
83. Stirban A, Negrean M, Stratmann B, et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care. 2006 Sep;29(9):2064-71.
84. Bonetti PO, Pumper GM, Higano ST, et al. Noninvasive identification of patients with early coronary atherosclerosis by assessment of digital reactive hyperemia. J Am Coll Cardiol. 2004 Dec 7;44(11):2137-41.
85. Santos-García D, Blanco M, Serena J, et al. Brachial arterial flow mediated dilation in acute ischemic stroke. Eur J Neurol. 2009 Jun;16(6):684-90. doi: 10.1111/j.1468-1331.2009.02564.x. Epub 2009 Feb 19.
86. Shechter M, Shechter A, Koren-Morag N, et al. Usefulness of brachial artery flow-mediated dilation to predict long-term cardiovascular events in subjects without heart disease. Am J Cardiol. 2014 Jan 1;113(1):162-7. doi: 10.1016/j.amjcard.2013.08.051. Epub 2013 Oct 5.
87. Silber HA, Lima JA, Bluemke DA, et al. Arterial reactivity in lower extremities is progressively reduced as cardiovascular risk factors increase:comparison with upper extremities using magnetic resonance imaging. J Am Coll Cardiol. 2007 Mar 6;49(9):939-45. Epub 2007 Feb 16.
88. Bitsch R, Wolf M, Möller J, et al. Bioavailability assessment of the lipophilic benfotiamine as compared to a water-soluble thiamin derivative. Ann Nutr Metab. 1991;35(5):292-6.
89. Tarwadi KV, Agte VV. Effect of micronutrients on methylglyoxal-mediated in vitro glycation of albumin. Biol Trace Elem Res. 2011 Nov;143(2):717-25. doi: 10.1007/s12011-010-8915-7. Epub 2010 Dec 17.
90. Das BS, Thurnham DI, Patnaik JK, et al. Increased plasma lipid peroxidation in riboflavin-deficient, malaria-infected children. Am J Clin Nutr. 1990 May;51(5):859-63.
91. Das BS, Thurnham DI, Patnaik JK, et al. Increased plasma lipid peroxidation in riboflavin-deficient, malaria-infected children. Am J Clin Nutr. 1990 May;51(5):859-63.
92. Mamoulakis D, Galanakis E, Dionyssopoulou E, et al. Carnitine deficiency in children and adolescents with type 1 diabetes. J Diabetes Complications. 2004 Sep-Oct;18(5):271-4.
93. Tamamoğullari N, Siliğ Y, Içağasioğlu S, et al. Carnitine deficiency in diabetes mellitus complications. J Diabetes Complications. 1999 Sep-Dec;13(5-6):251-3.
94. Rajasekar P, Anuradha CV. L-Carnitine inhibits protein glycation in vitro and in vivo: evidence for a role in diabetic management. Acta Diabetol. 2007 Jun;44(2):83-90. Epub 2007 May 27.
95. Adachi T, Fukami K, Yamagishi S, et al. Decreased serum carnitine is independently correlated with increased tissue accumulation levels of advancedglycation end products in haemodialysis patients. Nephrology (Carlton). 2012 Nov;17(8):689-94. doi: 10.1111/j.1440-1797.2012.01642.x.
96. Fukami K, Yamagishi S, Sakai K, et al. Potential inhibitory effects of L-carnitine supplementation on tissue advanced glycation end products in patientswith hemodialysis. Rejuvenation Res. 2013 Dec;16(6):460-6. doi: 10.1089/rej.2013.1459.
97. Rajasekar P, Anuradha CV. L-Carnitine inhibits protein glycation in vitro and in vivo: evidence for a role in diabetic management. Acta Diabetol. 2007 Jun;44(2):83-90. Epub 2007 May 27.
98. Broquist HP, Borum PR. Carnitine biosynthesis: nutritional implications. Adv Nutr Res. 1982;4:181-204.
99. Noland RC, Koves TR, Seiler SE, et al. Carnitine insufficiency caused by aging and overnutrition compromiss mitochondrial performance and metabolic control. J Biol Chem. 2009 Aug 21;284(34):22840-52. doi: 10.1074/jbc.M109.032888. Epub 2009 Jun 24.
100. Eder K, Felgner J, Becker K, et al. Free and total carnitine concentrations in pig plasma after oral ingestion of various L-carnitine compounds. Int J Vitam Nutr Res. 2005 Jan;75(1):3-9.
101. van Es A, Henny FC, Kooistra MP, et al. Amelioration of cardiac function by L-carnitine administration in patients on haemodialysis. Contrib Nephrol. 1992;98:28-35.
102. Vinson, Joe A., and Thomas B. Howard III. Inhibition of protein glycation and advanced glycation end products by ascorbic acid and other vitamins and nutrients. The Journal of Nutritional Biochemistry 7.12 .1996: 659-663.
104. Pillai SS, Sugathan JK, Indira M. Selenium downregulates RAGE and NFκB expression in diabetic rats. Biol Trace Elem Res. 2012 Oct;149(1):71-7. doi: 10.1007/s12011-012-9401-1. Epub 2012 Apr 5.
105. Sensi M, Pricci F, De Rossi MG, et al. D-lysine effectively decreases the non-enzymic glycation of proteins in vitro. Clin Chem. 1989 Mar;35(3):384-7.
106. Shen Q, Zhang B, Xu R, et al. Antioxidant activity in vitro of the selenium-contained protein from the Se-enriched Bifidobacterium animalis 01. Anaerobe. 2010 Aug;16(4):380-6. doi: 10.1016/j.anaerobe.2010.06.006. Epub 2010 Jun 23.
107. Bansal MP, Kaur T. Growth characteristics and selenium status changes of yeast cells with inorganic and organic seleniumsupplementation: selenium, a chemopreventive agent. J Med Food. 2002 Summer;5(2):85-90.
108. Malbe M, Klaassen M, Fang W, et al. Comparisons of selenite and selenium yeast feed supplements on Se-incorporation, mastitis and leucocytefunction in Se-deficient dairy cows. Zentralbl Veterinarmed A. 1995 Apr;42(2):111-21.
109. Crary EJ, McCarty MF. Potential clinical applications for high-dose nutritional antioxidants. Med Hypotheses. 1984 Jan;13(1):77-98.
110. Miyajima H, Osanai M, Chiba H, et al. Glyceraldehyde-derived advanced glycation end-products preferentially induce VEGF expression and reduceGDNF expression in human astrocytes. Biochem Biophys Res Commun. 2005 May 6;330(2):361-6.
111. Gebre-Medhin M, Kylberg E, Ewald U, et al. Dietary intake, trace elements and serum protein status in young diabetics. Acta Paediatr Scand Suppl. 1985;320:38-43.
112. Ahmad MS, Ahmed N. Antiglycation properties of aged garlic extract: possible role in prevention of diabetic complications. J Nutr. 2006 Mar;136(3 Suppl):796S-799S.
113. Ou CC, Tsao SM, Lin MC, et al. Protective action on human LDL against oxidation and glycation by four organosulfur compounds derived from garlic. Lipids. 2003 Mar;38(3):219-24.
114. Ahmad MS, Pischetsrieder M, Ahmed N. Aged garlic extract and S-allyl cysteine prevent formation of advanced glycation endproducts. Eur J Pharmacol. 2007 Apr 30;561(1-3):32-8. Epub 2007 Feb 1.
115. Colín-González AL, Santana RA, Silva-Islas CA, et al. The antioxidant mechanisms underlying the aged garlic extract- and S-allylcysteine-induced protection. Oxid Med Cell Longev. 2012;2012:907162. doi: 10.1155/2012/907162. Epub 2012 May 17.
116. Tsai SJ, Chiu CP, Yang HT, et al. s-Allyl cysteine, s-ethyl cysteine, and s-propyl cysteine alleviate β-amyloid, glycative, and oxidative injury inbrain of mice treated by D-galactose. J Agric Food Chem. 2011 Jun 8;59(11):6319-26. doi: 10.1021/jf201160a. Epub 2011 May 12.
117. Thomson M, Al-Qattan K, Divya JS, et al. Dose response of aged garlic extract in streptozotocin-induced diabetic rats (829.9). The FASEB Journal 28.1 Supplement .2014: 829-9.
118. Lal MA, Brismar H, Eklöf AC, et al. Role of oxidative stress in advanced glycation end product-induced mesangial cell activation. Kidney Int. 2002 Jun;61(6):2006-14.
119. Ahmed N, Balamash K, Albar O, et al. Effect of Kyolic® aged garlic extract on glycaemia, lipidaemia and oxidative stress in patients with type 2 diabetes mellitus. Journal of Diabetes Research and Clinical Metabolism 1.1 (2012): 18.
120. Durak I, Kavutcu M, Aytaç B, et al. Effects of garlic extract consumption on blood lipid and oxidant/antioxidant parameters in humans with highblood cholesterol. J Nutr Biochem. 2004 Jun;15(6):373-7.
121. Macan H, Uykimpang R, Alconcel M, et al Aged garlic extract may be safe for patients on warfarin therapy.. J Nutr. 2006 Mar;136(3 Suppl):793S-795S.
122. Steiner M, Khan AH, Holbert D, et al. A double-blind crossover study in moderately hypercholesterolemic men that compared the effect of aged garlic extract and placebo administration on blood lipids. Am J Clin Nutr. 1996 Dec;64(6):866-70.
123. Zhuang X, Pang X, Zhang W, et al. Effects of zinc and manganese on advanced glycation end products (AGEs) formation and AGEs-mediated endothelial cell dysfunction. Life Sci. 2012 Jan 16;90(3-4):131-9. doi: 10.1016/j.lfs.2011.10.025. Epub 2011 Nov 9.
124. Fitzharris JW. Abnormal zinc metabolism in type II diabetes mellitus. Am J Med. 1984 Jun;76(6):A60, A75.
125. Isbir T, Tamer L, Taylor A, et al. Zinc, copper and magnesium status in insulin-dependent diabetes. Diabetes Res. 1994;26(1):41-5.
126. Haase H, Rink L.The immune system and the impact of zinc during aging. Immun Ageing. 2009 Jun 12;6:9. doi: 10.1186/1742-4933-6-9.
127. Hogan M, Cerami A, Bucala R. Advanced glycosylation endproducts block the antiproliferative effect of nitric oxide. Role in the vascular andrenal complications of diabetes mellitus. J Clin Invest. 1992 Sep;90(3):1110-5.
128. Verbeke P, Perichon M, Friguet B, et al. Inhibition of nitric oxide synthase activity by early and advanced glycation end products in cultured rabbitproximal tubular epithelial cells. Biochim Biophys Acta. 2000 Nov 15;1502(3):481-94.
129. Jayawardena R, Ranasinghe P, Galappatthy P, et al. Effects of zinc supplementation on diabetes mellitus: a systematic review and meta-analysis. Diabetol Metab Syndr. 2012 Apr 19;4(1):13. doi: 10.1186/1758-5996-4-13.
131. Willis MS, Monaghan SA, Miller ML, et al. Zinc-induced copper deficiency: a report of three cases initially recognized on bone marrow examination. Am J Clin Pathol. 2005 Jan;123(1):125-31.
132. Hughes S, Samman S. The effect of zinc supplementation in humans on plasma lipids, antioxidant status and thrombogenesis. J Am Coll Nutr. 2006 Aug;25(4):285-91.
133. Black MR, Medeiros DM, Brunett E, et al. Zinc supplements and serum lipids in young adult white males. Am J Clin Nutr. 1988 Jun;47(6):970-5.
134. Samman S, Roberts DC. The effect of zinc supplements on plasma zinc and copper levels and the reported symptoms in healthy volunteers. Med J Aust. 1987 Mar 2;146(5):246-9.
135. Ghavami-Maibodi SZ, Collipp PJ, Castro-Magana M, et al. Effect of oral zinc supplements on growth, hormonal levels, and zinc in healthy short children. Ann Nutr Metab. 1983;27(3):214-9.
136. Luk E, Carroll M, Baker M, et al. Manganese activation of superoxide dismutase 2 in Saccharomyces cerevisiae requires MTM1, a member of the mitochondrial carrier family. Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10353-7. Epub 2003 Jul 30.
137. Breyer V, Weigel I, Huang TT, et al. Endogenous mitochondrial oxidative stress in MnSOD-deficient mouse embryonic fibroblasts promotesmitochondrial DNA glycation. Free Radic Biol Med. 2012 May 1;52(9):1744-9. doi: 10.1016/j.freeradbiomed.2012.02.021. Epub 2012 Feb 25.
138. Koh ES, Kim SJ, Yoon HE, et al. Association of blood manganese level with diabetes and renal dysfunction: a cross-sectional study of the Korean general population. BMC Endocr Disord. 2014 Mar 8;14:24. doi: 10.1186/1472-6823-14-24.
139. Tuvemo T, Gebre-Medhin M. The role of trace elements in juvenile diabetes mellitus. Pediatrician. 1983-1985;12(4):213-9.
140. el-Yazigi A, Hannan N, Raines DA. Urinary excretion of chromium, copper, and manganese in diabetes mellitus and associated disorders. Diabetes Res. 1991 Nov;18(3):129-34.
141. Nasli-Esfahani E, Faridbod F., Larijani B, et al. Trace element analysis of hair, nail, serum and urine of diabetes mellitus patients by inductively coupled plasma atomic emission spectroscopy.” Iranian Journal of Diabetes and Lipid Disorders 10. 2011: 1-9.
142. Kazi TG1, Afridi HI, Kazi N, et al. Copper, chromium, manganese, iron, nickel, and zinc levels in biological samples of diabetes mellitus patients. Biol Trace Elem Res. 2008 Apr;122(1):1-18. doi: 10.1007/s12011-007-8062-y. Epub 2008 Jan 11.
143. Murley JS, Kataoka Y, Hallahan DE, et al. Activation of NFkappaB and MnSOD gene expression by free radical scavengers in human microvascular endothelial cells. Free Radic Biol Med. 2001 Jun 15;30(12):1426-39.
144. Wegner M, Rawłuszko-Wieczorek AA, Araszkiewicz A, et al. Expression of mitochondrial superoxide dismutase in polymorphonuclear leukocytes from patients with type 1diabetes with and without microvascular complications. Pol Arch Med Wewn. 2014;124(5):239-46. Epub 2014 Apr 15.
145. Shen X, Zheng S, Metreveli NS, et al. Protection of cardiac mitochondria by overexpression of MnSOD reduces diabetic cardiomyopathy. Diabetes. 2006 Mar;55(3):798-805.
146. Challem, Jack, ed. User’s Guide to Nutritional Supplements. Basic Health Publications, Inc., 2003.
147. Lim M, Park L, Shin G, et al. Induction of apoptosis of Beta cells of the pancreas by advanced glycation end-products, important mediators ofchronic complications of diabetes mellitus. Ann N Y Acad Sci. 2008 Dec;1150:311-5. doi: 10.1196/annals.1447.011.
148. O’Dell, Boyd L., and Roger A. Sunde, eds. Handbook of nutritionally essential mineral elements. CRC Press, 1997.
149. Leonhardt W, Hanefeld M, Müller G, et al. Impact of concentrations of glycated hemoglobin, alpha-tocopherol, copper, and manganese on oxidation of low-density lipoproteins in patients with type I diabetes, type II diabetes and control subjects. Clin Chim Acta. 1996 Oct 29;254(2):173-86.
150. Gottlieb MG, Schwanke CH, Santos AF, et al. Association among oxidized LDL levels, MnSOD, apolipoprotein E polymorphisms, and cardiovascular riskfactors in a south Brazilian region population. Genet Mol Res. 2005 Dec 30;4(4):691-703.
151. Bucala R, Makita Z, Koschinsky T, et al. Lipid advanced glycosylation: pathway for lipid oxidation in vivo. Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6434-8.
152. Schube U, Nowicki M, Jogschies P, et al. Resveratrol and desferoxamine protect human OxLDL-treated granulosa cell subtypes from degeneration. J Clin Endocrinol Metab. 2014 Jan;99(1):229-39. doi: 10.1210/jc.2013-2692. Epub 2013 Dec 20.
153. Menzel EJ, Sobal G, Staudinger A. The role of oxidative stress in the long-term glycation of LDL. Biofactors. 1997;6(2):111-24.
154. Napoli C, Lerman LO, de Nigris F, et al. Glycoxidized low-density lipoprotein downregulates endothelial nitricoxide synthase in human coronary cells. J Am Coll Cardiol. 2002 Oct 16;40(8):1515-22.
155. Lamharzi N, Renard CB, Kramer F, et al. Hyperlipidemia in concert with hyperglycemia stimulates the proliferation of macrophages in atheroscleroticlesions: potential role of glucose-oxidized LDL. Diabetes. 2004 Dec;53(12):3217-25.
156. Chen M, Masaki T, Sawamura T. LOX-1, the receptor for oxidized low-density lipoprotein identified from endothelial cells: implications inendothelial dysfunction and atherosclerosis. Pharmacol Ther. 2002 Jul;95(1):89-100.
157. Shiu SW, Tan KC, Wong Y, et al. Glycoxidized LDL increases lectin-like oxidized low density lipoprotein receptor-1 in diabetes mellitus. Atherosclerosis. 2009 Apr;203(2):522-7. doi: 10.1016/j.atherosclerosis.2008.07.012. Epub 2008 Jul 23.
158. Yan M, Mehta JL, Zhang W, et al. LOX-1, oxidative stress and inflammation: a novel mechanism for diabetic cardiovascular complications. Cardiovasc Drugs Ther. 2011 Oct;25(5):451-9. doi: 10.1007/s10557-011-6342-4.
159. Fukui M, Tanaka M, Senmaru T, et al. LOX-1 is a novel marker for peripheral artery disease in patients with type 2 diabetes. Metabolism. 2013 Jul;62(7):935-8. doi: 10.1016/j.metabol.2013.01.018. Epub 2013 Feb 19.
160. Yamamoto N, Toyoda M, Abe M, et al. Lectin-like oxidized LDL receptor-1 (LOX-1) expression in the tubulointerstitial area likely plays an important rolein human diabetic nephropathy. Intern Med. 2009;48(4):189-94. Epub 2009 Feb 16.
161. Vincent AM1, Hayes JM, McLean LL, et al. Dyslipidemia-induced neuropathy in mice: the role of oxLDL/LOX-1. Diabetes. 2009 Oct;58(10):2376-85. doi: 10.2337/db09-0047. Epub 2009 Jul 10.
162. D’Archivio M, Scazzocchio B, Filesi C, et al. Oxidised LDL up-regulate CD36 expression by the Nrf2 pathway in 3T3-L1 preadipocytes. FEBS Lett. 2008 Jun 25;582(15):2291-8. doi: 10.1016/j.febslet.2008.05.029. Epub 2008 Jun 2.
163. Kuniyasu A, Ohgami N, Hayashi S, et al. CD36-mediated endocytic uptake of advanced glycation end products (AGE) in mouse 3T3-L1 and humansubcutaneous adipocytes. FEBS Lett. 2003 Feb 27;537(1-3):85-90.
164. Kennedy DJ, Kuchibhotla S, Westfall KM, et al. A CD36-dependent pathway enhances macrophage and adipose tissue inflammation and impairs insulinsignalling. Cardiovasc Res. 2011 Feb 15;89(3):604-13. doi: 10.1093/cvr/cvq360. Epub 2010 Nov 18.
165. Lue LF, Andrade C, Sabbagh M, et al. Is There Inflammatory Synergy in Type II Diabetes Mellitus and Alzheimer’s Disease? Int J Alzheimers Dis. 2012;2012:918680. doi: 10.1155/2012/918680. Epub 2012 Jun 21.
166. Institute of Medicine (US). Panel on Micronutrients, Institute of Medicine (US). Food, and Nutrition Board. DRI, Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc: A Report of the Panel on Micronutrients…[et Al.], Food and Nutrition Board, Institute of Medicine. National Academies Press, 2001.
167. Davidsson L, Almgren A, Juillerat MA, et al. Manganese absorption in humans: the effect of phytic acid and ascorbic acid in soy formula. Am J Clin Nutr. 1995 Nov;62(5):984-7.
168. Wapnir, Raul A. Protein nutrition and mineral absorption. CRC Press, 1990.
169. Klimis-Tavantzis D, ed. Manganese in health and disease. Boca Raton, FL: CRC Press,
170. Davis CD, Greger JL. Longitudinal changes of manganese-dependent superoxide dismutase and other indexes of manganese and ironstatus in women. Am J Clin Nutr. 1992 Mar;55(3):747-52.
171. Finley JW, Penland JG, Pettit RE, et al. Dietary manganese intake and type of lipid do not affect clinical or neuropsychological measures in healthy young women. J Nutr. 2003 Sep;133(9):2849-56.
172. Greger JL. Nutrition versus toxicology of manganese in humans: evaluation of potential biomarkers. Neurotoxicology. 1999 Apr-Jun;20(2-3):205-12.
173. Miller KB, Newman SM Jr, Caton JS, et al. Manganese alters mitochodrial integrity in the hearts of swine marginally deficient in magnesium. Biofactors. 2004;20(2):85-96.
174. Adisakwattana S, Sompong W, Meeprom A, et al. Cinnamic acid and its derivatives inhibit fructose-mediated protein glycation. Int J Mol Sci. 2012;13(2):1778-89. doi: 10.3390/ijms13021778. Epub 2012 Feb 8.
175. Akilen R, Tsiami A, Robinson N. Efficacy and safety of ‘true’ cinnamon (Cinnamomum zeylanicum) as a pharmaceutical agent in diabetes: a systematic review and meta-analysis. Diabet Med. 2013 Apr;30(4):505-6. doi: 10.1111/dme.12068.
176. Jin S, Cho KH. Water extracts of cinnamon and clove exhibits potent inhibition of protein glycation and anti-atheroscleroticactivity in vitro and in vivo hypolipidemic activity in zebrafish. Food Chem Toxicol. 2011 Jul;49(7):1521-9. doi: 10.1016/j.fct.2011.03.043. Epub 2011 Apr 5.
177. Lungarini S, Aureli F, Coni E. Coumarin and cinnamaldehyde in cinnamon marketed in Italy: a natural chemical hazard? Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Nov;25(11):1297-305. doi: 10.1080/02652030802105274.
178. Wickenberg J, Lindstedt S, Berntorp K, et al. Ceylon cinnamon does not affect postprandial plasma glucose or insulin in subjects with impaired glucose tolerance. Br J Nutr. 2012 Jun;107(12):1845-9. doi: 10.1017/S0007114511005113. Epub 2011 Sep 20.
179. Kikuzaki H, Hisamoto M, Hirose K, et al. Antioxidant properties of ferulic acid and its related compounds. J Agric Food Chem. 2002 Mar 27;50(7):2161-8.
180. Silván JM, Assar SH, Srey C, et al. Control of the Maillard reaction by ferulic acid. Food Chem. 2011 Sep 1;128(1):208-13. doi: 10.1016/j.foodchem.2011.03.047. Epub 2011 Mar 12.
181. Kang J, Liu Y, Xie MX, et al. Interactions of human serum albumin with chlorogenic acid and ferulic acid. Biochim Biophys Acta. 2004 Sep 24;1674(2):205-14.
182. Sompong W, Meeprom A, Cheng H, et al. A comparative study of ferulic acid on different monosaccharide-mediated protein glycation and oxidativedamage in bovine serum albumin. Molecules. 2013 Nov 11;18(11):13886-903. doi: 10.3390/molecules181113886.
183. Choi R1, Kim BH, Naowaboot J, et al. Effects of ferulic acid on diabetic nephropathy in a rat model of type 2 diabetes. Exp Mol Med. 2011 Dec 31;43(12):676-83. doi: 10.3858/emm.2011.43.12.078.
184. Ghaisas MM, Kshirsagar SB, Sahane RS. Evaluation of wound healing activity of ferulic acid in diabetic rats. Int Wound J. 2014 Oct;11(5):523-32. doi: 10.1111/j.1742-481X.2012.01119.x. Epub 2012 Dec 12.
185. Xu X, Xiao H, Zhao J, et al. Cardioprotective effect of sodium ferulate in diabetic rats. Int J Med Sci. 2012;9(4):291-300. doi: 10.7150/ijms.4298. Epub 2012 Jun 5.
186. Srey C, Hull GL, Connolly L, et al. Effect of inhibitor compounds on Nε-(carboxymethyl)lysine (CML) and Nε-(carboxyethyl)lysine (CEL) formation inmodel foods. J Agric Food Chem. 2010 Nov 24;58(22):12036-41. doi: 10.1021/jf103353e. Epub 2010 Nov 2.
187. Kim J, Jeong IH, Kim CS, et al. Chlorogenic acid inhibits the formation of advanced glycation end products and associated protein cross-linking. Arch Pharm Res. 2011 Mar;34(3):495-500. doi: 10.1007/s12272-011-0319-5. Epub 2011 May 6.
188. Kim YS, Kim NH, Lee YM, et al. Preventive effect of chlorogenic acid on lens opacity and cytotoxicity in human lens epithelial cells. Biol Pharm Bull. 2011;34(6):925-8.
189. Lee CW, Kim HR., and Hwang KW. Protective effect of chlorogenic acid against Aβ-induced neurotoxicity. Biomolecules & Therapeutics), 19(2),181-186.
190. Li XH, Du LL, Cheng XS, et al. Glycation exacerbates the neuronal toxicity of β-amyloid. Cell Death Dis. 2013 Jun 13;4:e673. doi: 10.1038/cddis.2013.180.
191. Moon JK, Yoo HS, Shibamoto T. Role of roasting conditions in the level of chlorogenic acid content in coffee beans: correlation with coffee acidity. J Agric Food Chem. 2009 Jun 24;57(12):5365-9. doi: 10.1021/jf900012b.
192. Monteiro M, Farah A, Perrone D, et al. Chlorogenic acid compounds from coffee are differentially absorbed and metabolized in humans. J Nutr. 2007 Oct;137(10):2196-201.
193. Arribas-Lorenzo G, Morales FJ. Estimation of dietary intake of 5-hydroxymethylfurfural and related substances from coffee to Spanishpopulation. Food Chem Toxicol. 2010 Feb;48(2):644-9. doi: 10.1016/j.fct.2009.11.046. Epub 2009 Dec 24.
194. Loaëc G, Jacolot P, Helou C, et al. Acrylamide, 5-hydroxymethylfurfural and N(ε)-carboxymethyl-lysine in coffee substitutes and instant coffees. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2014 Apr;31(4):593-604. doi: 10.1080/19440049.2014.885661. Epub 2014 Mar 28.
195. Zill H, Bek S, Hofmann T, et al. RAGE-mediated MAPK activation by food-derived AGE and non-AGE products. Biochem Biophys Res Commun. 2003 Jan 10;300(2):311-5.
196. Seiquer I, Ruiz‐Roca B, Mesías M, et al. The antioxidant effect of a diet rich in Maillard reaction products is attenuated after consumption by healthy male adolescents. In vitro and in vivo comparative study. Journal of the Science of Food and Agriculture88.7 (2008): 1245-1252.
197. Dearlove RP, Greenspan P, Hartle DK, et al. Inhibition of protein glycation by extracts of culinary herbs and spices. J Med Food. 2008 Jun;11(2):275-81. doi: 10.1089/jmf.2007.536.
199. Jin S, Cho KH. Water extracts of cinnamon and clove exhibits potent inhibition of protein glycation and anti-atherosclerotic activity in vitro and in vivo hypolipidemic activity in zebrafish. Food Chem Toxicol. 2011 Jul;49(7):1521-9. doi: 10.1016/j.fct.2011.03.043. Epub 2011 Apr 5.
200. Bakirel T, Bakirel U, Keleş OU, et al. In vivo assessment of antidiabetic and antioxidant activities of rosmary (Rosmarinus officinalis) in alloxan – diabetic rabbits. J Ethnopharmacol . 2008;116:64–73
201. Seshiah, V., ed. Microvascular Complications of Diabetes-ECAB. Elsevier Health Sciences, 2009.
202. Reddi AS, Jyothirmayi GN, DeAngelis B, et al. Effect of short- and long-term diabetes on carnitine and myo-inositol in rats. Comp Biochem Physiol A Comp Physiol. 1991;98(1):39-42.
203. Ramakrishnan S, Sulochana KN, Punitham R. Two new functions of inositol in the eye lens: antioxidation and antiglycation and possible mechanisms. Indian J Biochem Biophys. 1999 Apr;36(2):129-33.
204. Sulochana KN, Ramprasad S, Coral K, et al. Glycation and glycoxidation studies in vitro on isolated human vitreous collagen. Med Sci Monit. 2003 Jun;9(6):BR220-4.
205. YAO Y, CHENG XZ, and REN, GX. Application of Near-Infrared Reflectance Spectroscopy to the Evaluation of D- chiro-lnositol, Vitexin, and Isovitexin Contents in Mung Bean. Agricultural Sciences in China10.12 .2011;1986-1991.
206. Ostlund RE, McGill JB, Herskowitz I, et al. D-chiro-inositol metabolism in diabetes mellitus.Proceedings of the National Academy of Sciences 90.2.1993;9988-9992
208. Clements RS Jr, Reynertson R. Myoinositol metabolism in diabetes mellitus. Effect of insulin treatment. Diabetes. 1977 Mar;26(3):215-21.
209. Kedikova S, Sirakov M, Boyadzhieva M. Myoinositol–alternative treatment of insulin resistance in adolescents. Akush Ginekol (Sofiia). 2011;50(7):16-9.
210. Gallicchio MA, Bach LA. Advanced glycation end products inhibit Na+ K+ ATPase in proximal tubule epithelial cells: role of cytosolicphospholipase A2alpha and phosphatidylinositol 4-phosphate 5-kinase gamma. Biochim Biophys Acta. 2010 Aug;1803(8):919-30. doi: 10.1016/j.bbamcr.2010.04.009. Epub 2010 May 5.
211. Corrado F, D’Anna R, Di Vieste G, et al. The effect of myoinositol supplementation on insulin resistance in patients with gestational diabetes. Diabet Med. 2011 Aug;28(8):972-5. doi: 10.1111/j.1464-5491.2011.03284.x.
212. Sima AA, Dunlap JA, Davidson EP, et al. Supplemental myo-inositol prevents L-fucose-induced diabetic neuropathy. Diabetes. 1997 Feb;46(2):301-6.
213. Farias VX, Macêdo FH, Oquendo MB, et al. Chronic treatment with D-chiro-inositol prevents autonomic and somatic neuropathy in STZ-induced diabeticmice. Diabetes Obes Metab. 2011 Mar;13(3):243-50. doi: 10.1111/j.1463-1326.2010.01344.x.
214. Li WY. The biochemical mechanism in vitro of pericyte drop-out in diabetic retinopathy. Zhonghua Yan Ke Za Zhi. 1989 Jul;25(4):222-6.
215. MacGregor LC, Matschinsky FM. Experimental diabetes mellitus impairs the function of the retinal pigmented epithelium. Metabolism. 1986 Apr;35(4 Suppl 1):28-34.
216. Nascimento NR, Lessa LM, Kerntopf MR, et al. Inositols prevent and reverse endothelial dysfunction in diabetic rat and rabbit vasculature metabolically and by scavenging superoxide. Proc Natl Acad Sci U S A. 2006 Jan 3;103(1):218-23. Epub 2005 Dec 22.
217. Salway JG, Whitehead L, Finnegan JA, et al. Effect of myo-inositol on peripheral-nerve function in diabetes. Lancet. 1978 Dec 16;2(8103):1282-4.
218. Gunn R, and Allan G. Compositions comprising D-chiro inositol and lipid lowering compounds and methods of treatment thereof. U.S. Patent No. 6,486,127. 26 Nov. 2002.
219. Larner J, Brautigan DL, Thorner MO. D-chiro-inositol glycans in insulin signaling and insulin resistance. Mol Med. 2010 Nov-Dec;16(11-12):543-52. doi: 10.2119/molmed.2010.00107. Epub 2010 Aug 27.
220. Corrado F, D’Anna R, Di Vieste G, et al. The effect of myoinositol supplementation on insulin resistance in patients with gestational diabetes. Diabet Med. 2011 Aug;28(8):972-5. doi: 10.1111/j.1464-5491.2011.03284.x.
222. Nakamura S, Li H, Adijiang A, et al. Pyridoxal phosphate prevents progression of diabetic nephropathy. Nephrol Dial Transplant. 2007 Aug;22(8):2165-74. Epub 2007 Apr 20.
224. Higuchi O, Nakagawa K, Tsuzuki T, et al. Aminophospholipid glycation and its inhibitor screening system: a new role of pyridoxal 5′-phosphate as theinhibitor. J Lipid Res. 2006 May;47(5):964-74. Epub 2006 Feb 9.
225. Negre-Salvayre A, Coatrieux C, Ingueneau C, et al. Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases andtherapeutic prospects for the inhibitors. Br J Pharmacol. 2008 Jan;153(1):6-20. Epub 2007 Jul 23.
226. Suzuki K, Nakagawa K, Miyazawa T. Augmentation of blood lipid glycation and lipid oxidation in diabetic patients. Clin Chem Lab Med. 2014 Jan 1;52(1):47-52. doi: 10.1515/cclm-2012-0886.
227. Škrha, J. Pathogenesis of angiopathy in diabetes. Acta diabetologica 40.2 (2003): s324-s329.
228. Miyata T, Sugiyama S, Suzuki D, et al. Increased carbonyl modification by lipids and carbohydrates in diabetic nephropathy. Kidney Int Suppl. 1999 Jul;71:S54-6.
229. Degen J, Beyer H, Heymann B, et al. Dietary influence on urinary excretion of 3-deoxyglucosone and its metabolite 3-deoxyfructose. J Agric Food Chem. 2014 Mar 19;62(11):2449-56. doi: 10.1021/jf405546q. Epub 2014 Mar 10.
230.Kiran SG, Dorisetty RK, Umrani MR,et al. Pyridoxal 5′ phosphate protects islets against streptozotocin-induced beta-cell dysfunction–in vitro and in vivo. Exp Biol Med (Maywood). 2011 Apr 1;236(4):456-65. doi: 10.1258/ebm.2011.010361. Epub 2011 Apr 4.
231. Pazdro R, Burgess JR. Differential effects of α-tocopherol and N-acetyl-cysteine on advanced glycation end product-induced oxidativedamage and neurite degeneration in SH-SY5Y cells. Biochim Biophys Acta. 2012 Apr;1822(4):550-6. doi: 10.1016/j.bbadis.2012.01.003. Epub 2012 Jan 10.
232. Sagara M, Satoh J, Wada R, et al. Inhibition of development of peripheral neuropathy in streptozotocin-induced diabetic rats with N-acetylcysteine. Diabetologia. 1996 Mar;39(3):263-9.
233. Guo Q, Mori T, Jiang Y, et al. Methylglyoxal contributes to the development of insulin resistance and salt sensitivity in Sprague-Dawley rats. J Hypertens. 2009 Aug;27(8):1664-71. doi: 10.1097/HJH.0b013e32832c419a.
234. Odetti P, Pesce C, Traverso N, et al. Comparative trial of N-acetyl-cysteine, taurine, and oxerutin on skin and kidney damage in long-termexperimental diabetes. Diabetes. 2003 Feb;52(2):499-505.
235. Cai W, Gao QD, Zhu L, et al. Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction. Mol Med. 2002 Jul;8(7):337-46.
236. Pacher P, Obrosova IG, Mabley JG, et al. Role of nitrosative stress and peroxynitrite in the pathogenesis of diabetic complications. Emerging newtherapeutical strategies. Curr Med Chem. 2005;12(3):267-75.
237. Nagai R, Unno Y, Hayashi MC, et al. Peroxynitrite induces formation of N( epsilon )-(carboxymethyl) lysine by the cleavage of Amadori product andgeneration of glucosone and glyoxal from glucose: novel pathways for protein modification by peroxynitrite. Diabetes. 2002 Sep;51(9):2833-9.
238. Koppal T, Drake J, Butterfield DA. In vivo modulation of rodent glutathione and its role in peroxynitrite-induced neocortical synaptosomalmembrane protein damage. Biochim Biophys Acta. 1999 Mar 30;1453(3):407-11.
239. Cabassi A, Dumont EC, Girouard H, et al. Effects of chronic N-acetylcysteine treatment on the actions of peroxynitrite on aortic vascular reactivity inhypertensive rats. J Hypertens. 2001 Jul;19(7):1233-44.
240. Liu Y, Ma Y, Wang R, et al. Advanced glycation end products accelerate ischemia/reperfusion injury through receptor of advanced endproduct/nitrative thioredoxin inactivation in cardiac microvascular endothelial cells. Antioxid Redox Signal. 2011 Oct 1;15(7):1769-78. doi: 10.1089/ars.2010.3764. Epub 2011 Apr 26.
241. Hansen, SH. The role of taurine in diabetes mellitus and development of diabetic complications. Diabetes Metab Res Rev. 2001 Sep-Oct;17(5):330-46.
242. Nandhini TA, Anuradha CV. Inhibition of lipid peroxidation, protein glycation and elevation of membrane ion pump activity by taurine in RBCexposed to high glucose. Clin Chim Acta. 2003 Oct;336(1-2):129-35.
243. Franconi F, Bennardini F, Mattana A, et al. Plasma and platelet taurine are reduced in subjects with insulin-dependent diabetes mellitus: effects of taurinesupplementation. Am J Clin Nutr. 1995 May;61(5):1115-9.
244. Odetti P, Pesce C, Traverso N, et al. Comparative trial of N-acetyl-cysteine, taurine, and oxerutin on skin and kidney damage in long-termexperimental diabetes. Diabetes. 2003 Feb;52(2):499-505.
245. Franconi F, Di Leo MA S., Santini SA, Gentiloni Silveri N, Caputo S, Giardina B, and Ghirlanda G. Taurine supplementation prolongs the survival and reduces glycemia in streptozotocin-induced diabetic rats. Taurine in the 21st century, September 20–23 2002, Radisson Kauai Beach Resort, Hawaii.
246. Wautier JL, Wautier MP. Molecular basis of erythrocyte adhesion to endothelial cells in diseases. Clin Hemorheol Microcirc. 2013;53(1-2):11-21. doi: 10.3233/CH-2012-1572.
247. American Diabetes Association. “Diagnosis and classification of diabetes mellitus.” Diabetes care 31.Supplement 1.2008;S55-S60.
248. Selvin E, Steffes MW, Zhu H, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med. 2010 Mar 4;362(9):800-11. doi: 10.1056/NEJMoa0908359.
249. Moloney MA, Casey RG, O’Donnell DH, et al. Two weeks taurine supplementation reverses endothelial dysfunction in young male type 1 diabetics. Diab Vasc Dis Res. 2010 Oct;7(4):300-10. doi: 10.1177/1479164110375971. Epub 2010 Jul 28.
250. Moloney MA, Casey RG, O’Donnell DH, et al. Two weeks taurine supplementation reverses endothelial dysfunction in young male type 1 diabetics. Diab Vasc Dis Res. 2010 Oct;7(4):300-10. doi: 10.1177/1479164110375971. Epub 2010 Jul 28.
251. Syngle A, Vohra K, Garg N, et al. Advanced glycation end-products inhibition improves endothelial dysfunction in rheumatoid arthritis. Int J Rheum Dis. 2012 Feb;15(1):45-55. doi: 10.1111/j.1756-185X.2011.01679.x. Epub 2011 Oct 10.
252. You JS, Chang KJ. Effects of taurine supplementation on lipid peroxidation, blood glucose and blood lipid metabolism instreptozotocin-induced diabetic rats. Adv Exp Med Biol. 1998;442:163-8.
253. Di Leo MA, Ghirlanda G, Gentiloni Silveri N, et al. Potential therapeutic effect of antioxidants in experimental diabetic retina: a comparison between chronic taurineand vitamin E plus selenium supplementations. Free Radic Res. 2003 Mar;37(3):323-30.
254. Odetti P, Pesce C, Traverso N, et al. Comparative trial of N-acetyl-cysteine, taurine, and oxerutin on skin and kidney damage in long-termexperimental diabetes. Diabetes. 2003 Feb;52(2):499-505.
255. Wu CH, Huang SM, Yen GC. Silymarin: a novel antioxidant with antiglycation and antiinflammatory properties in vitro and in vivo. Antioxid Redox Signal. 2011 Feb 1;14(3):353-66. doi: 10.1089/ars.2010.3134. Epub 2010 Sep 29.
256. Chandler D, Woldu A, Rahmadi A, et al. Effects of plant-derived polyphenols on TNF-alpha and nitric oxide production induced by advanced glycationendproducts. Mol Nutr Food Res. 2010 Jul;54 Suppl 2:S141-50. doi: 10.1002/mnfr.200900504.
257. Hussain SA. Silymarin as an adjunct to glibenclamide therapy improves long-term and postprandial glycemic control andbody mass index in type 2 diabetes. J Med Food. 2007 Sep;10(3):543-7.
258. Wu Q, Li S, Li X, et al. A significant inhibitory effect on advanced glycation end product formation by catechin as the major metaboliteof lotus seedpod oligomeric procyanidins. Nutrients. 2014 Aug 13;6(8):3230-44. doi: 10.3390/nu6083230.
259. Kim J, Kim CS, Moon MK, et al. Epicatechin breaks preformed glycated serum albumin and reverses the retinal accumulation of advancedglycation end products. Eur J Pharmacol. 2014 Dec 19;748C:108-114. doi: 10.1016/j.ejphar.2014.12.010. [Epub ahead of print]
260. Lo CY, Li S, Tan D, et al. Trapping reactions of reactive carbonyl species with tea polyphenols in simulated physiological conditions. Mol Nutr Food Res. 2006 Dec;50(12):1118-28.
261. Lo CY, Li S, Tan D, et al. Trapping reactions of reactive carbonyl species with tea polyphenols in simulated physiological conditions. Molecular nutrition & food research 50.12. 2006;1118-1128.
262. Terao J, Piskula M, Yao Q. Protective effect of epicatechin, epicatechin gallate, and quercetin on lipid peroxidation in phospholipid bilayers. Arch Biochem Biophys. 1994 Jan;308(1):278-84.
263. Sahin K, Orhan C, Tuzcu M, et al. Epigallocatechin-3-gallate prevents lipid peroxidation and enhances antioxidant defense system via modulatinghepatic nuclear transcription factors in heat-stressed quails. Poult Sci. 2010 Oct;89(10):2251-8. doi: 10.3382/ps.2010-00749.
264. Sang S, Shao X, Bai N, et al. Tea polyphenol (-)-epigallocatechin-3-gallate: a new trapping agent of reactive dicarbonyl species. Chem Res Toxicol. 2007 Dec;20(12):1862-70. Epub 2007 Nov 15.
265. Babu PV, Sabitha KE, Shyamaladevi CS. Effect of green tea extract on advanced glycation and cross-linking of tail tendon collagen in streptozotocininduced diabetic rats. Food Chem Toxicol. 2008 Jan;46(1):280-5. Epub 2007 Aug 15.
267. Babu PV, Sabitha KE, Shyamaladevi CS. Therapeutic effect of green tea extract on advanced glycation and cross-linking of collagen in the aorta ofstreptozotocin diabetic rats. Clin Exp Pharmacol Physiol. 2006 Apr;33(4):351-7.
268. Gu L, House SE, Wu X, et al. Procyanidin and catechin contents and antioxidant capacity of cocoa and chocolate products. J Agric Food Chem. 2006 May 31;54(11):4057-61.
269. Rothwell, J; Phenol-Explorer 3.5; 2014
271. Bhagwat S, Haytowitz DB, and Holden JM. USDA Database for the Flavonoid Content of Selected Foods Release 3. US Deparment of Agriculture, ARS. Available online: http://www. nal. usda. gov/fnic/foodcomp/Data/Flav/flav. pdf (accessed on 5 October 2012) 2011.
272. Ambati RR, Phang SM, Ravi S, et al. Astaxanthin: sources, extraction, stability, biological activities and its commercial applications–a review. Mar Drugs. 2014 Jan 7;12(1):128-52. doi: 10.3390/md12010128.
273. Sun Z, Liu J, Zeng X, et al. Protective actions of microalgae against endogenous and exogenous advanced glycation endproducts (AGEs) inhuman retinal pigment epithelial cells. Food Funct. 2011 May;2(5):251-8. doi: 10.1039/c1fo10021a. Epub 2011 Apr 21.
276. Vlassara H, Striker LJ, Teichberg S, et al. Advanced glycation end products induce glomerular sclerosis and albuminuria in normal rats. Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11704-8.
277. Naito Y, Uchiyama K, Aoi W, et al. Prevention of diabetic nephropathy by treatment with astaxanthin in diabetic db/db mice. Biofactors. 2004;20(1):49-59.
278. Park CH, Xu FH, Roh SS, et al. Astaxanthin and Corni Fructus Protect Against Diabetes-Induced Oxidative Stress, Inflammation, and AdvancedGlycation End Product in Livers of Streptozotocin-Induced Diabetic Rats. J Med Food. 2015 Jan 8. [Epub ahead of print]
279. Brown KM, Morrice PC, Duthie GG. Erythrocyte vitamin E and plasma ascorbate concentrations in relation to erythrocyte peroxidation in smokersand nonsmokers: dose response to vitamin E supplementation. Am J Clin Nutr. 1997 Feb;65(2):496-502.
280. Coral-Hinostroza GN, Ytrestøyl T, Ruyter B, et al. Plasma appearance of unesterified astaxanthin geometrical E/Z and optical R/S isomers in men given singledoses of a mixture of optical 3 and 3’R/S isomers of astaxanthin fatty acyl diesters. Comp Biochem Physiol C Toxicol Pharmacol. 2004 Oct;139(1-3):99-110.
281. Park JS, Chyun JH, Kim YK, et al. Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. Nutr Metab (Lond). 2010 Mar 5;7:18. doi: 10.1186/1743-7075-7-18.
282. Mercke Odeberg J, Lignell A, Pettersson A, et al. Oral bioavailability of the antioxidant astaxanthin in humans is enhanced by incorporation of lipid based formulations. Eur J Pharm Sci. 2003 Jul;19(4):299-304.
283. Østerlie M, Bjerkeng B, Liaaen-Jensen S. Plasma appearance and distribution of astaxanthin E/Z and R/S isomers in plasma lipoproteins of men aftersingle dose administration of astaxanthin. J Nutr Biochem. 2000 Oct;11(10):482-90.
284. Iwamoto T, Hosoda K, Hirano R, et al. Inhibition of low-density lipoprotein oxidation by astaxanthin. J Atheroscler Thromb. 2000;7(4):216-22.
285. Coral-Hinostroza GN, Ytrestøyl T, Ruyter B, et al. Plasma appearance of unesterified astaxanthin geometrical E/Z and optical R/S isomers in men given singledoses of a mixture of optical 3 and 3’R/S isomers of astaxanthin fatty acyl diesters. Comp Biochem Physiol C Toxicol Pharmacol. 2004 Oct;139(1-3):99-110.
286. Naguib YM. Antioxidant activities of astaxanthin and related carotenoids. J Agric Food Chem. 2000 Apr;48(4):1150-4.
287. Li W, Wang G, Lu X, Lycopene ameliorates renal function in rats with streptozotocin-induced diabetes. Int J Clin Exp Pathol. 2014 Jul 15;7(8):5008-15. eCollection 2014.
288. Sarkar PD, Sahu A, & Gupta T. Lycopene-tomato’s secret weapon against oxidative stress. Bangladesh Journal of Medical Science 10.4.2011; 275-279.
289. Shanmugam N, Figarola JL, Li Y, et al. Proinflammatory effects of advanced lipoxidation end products in monocytes. Diabetes. 2008 Apr;57(4):879-88. Epub 2007 Nov 14.
290. Metz TO, Alderson NL, Chachich ME, et al. Pyridoxamine traps intermediates in lipid peroxidation reactions in vivo: evidence on the role of lipids inchemical modification of protein and development of diabetic complications. J Biol Chem. 2003 Oct 24;278(43):42012-9. Epub 2003 Aug 15.
291. Milne R and Brownstein S. Advanced glycation end products and diabetic retinopathy.” Amino acids 44.6.2013;1397-1407.
292. Brazionis L, Rowley K, Itsiopoulos C, et al. Plasma carotenoids and diabetic retinopathy.” British journal of nutrition 101.02.2009;270-277.
293. Ghaffari, MA and Mojab S. In Vitro Effect of?-Tocopherol, Ascorbic Acid and Lycopene on Low Density Lipoprotein Glycation. Iranian Journal of Pharmaceutical Research.2010;265-271.
294. Bayramoglu A, Bayramoglu G, Senturk H. Lycopene partially reverses symptoms of diabetes in rats with streptozotocin-induced diabetes. J Med Food. 2013 Feb;16(2):128-32. doi: 10.1089/jmf.2012.2277. Epub 2013 Jan 24.
295. Suzuki K, Ito Y, Nakamura S, Relationship between serum carotenoids and hyperglycemia: a population-based cross-sectional study. J Epidemiol. 2002 Sep;12(5):357-66.
296. Pierine DT, Navarro ME, Minatel IO, et al. Lycopene supplementation reduces TNF-α via RAGE in the kidney of obese rats. Nutr Diabetes. 2014 Nov 10;4:e142. doi: 10.1038/nutd.2014.39.
297. Lee W, Ku SK, Bae JW, et al. Inhibitory effects of lycopene on HMGB1-mediated pro-inflammatory responses in both cellular and animal models. Food Chem Toxicol. 2012 Jun;50(6):1826-33. doi: 10.1016/j.fct.2012.03.003. Epub 2012 Mar 10.
298. Wu CH, Yen GC. Inhibitory effect of naturally occurring flavonoids on the formation of advanced glycation endproducts. J Agric Food Chem. 2005 Apr 20;53(8):3167-73.
300. Liu L, Xie Y, Song Z, et al. Influence of dietary flavonoids on the glycation of plasma proteins. Mol Biosyst. 2012 Aug;8(8):2183-7. doi: 10.1039/c2mb25038a. Epub 2012 Jun 18.
301. Lv L, Shao X, Chen H, et al. Genistein inhibits advanced glycation end product formation by trapping methylglyoxal. Chem Res Toxicol. 2011 Apr 18;24(4):579-86. doi: 10.1021/tx100457h. Epub 2011 Feb 23.
303. Tong M, Wang Y, Wang Y, et al. Genistein attenuates advanced glycation end product-induced expression of fibronectin and connective tissuegrowth factor. Am J Nephrol. 2012;36(1):34-40. doi: 10.1159/000339168. Epub 2012 Jun 13.
304. Zhou G, Li C, Cai L. Advanced glycation end-products induce connective tissue growth factor-mediated renal fibrosis predominantlythrough transforming growth factor beta-independent pathway. Am J Pathol. 2004 Dec;165(6):2033-43.
305. Kota SK, Meher LK, Jammula S, et al. Aberrant angiogenesis: The gateway to diabetic complications. Indian J Endocrinol Metab. 2012 Nov;16(6):918-30. doi: 10.4103/2230-8210.102992.
306. Li D, Mitsuhashi S, Ubukata M. Protective effects of hesperidin derivatives and their stereoisomers against advanced glycation end-productsformation. Pharm Biol. 2012 Dec;50(12):1531-5. doi: 10.3109/13880209.2012.694106. Epub 2012 Sep 11.
307. Manuel y Keenoy B, Vertommen J, De Leeuw I. The effect of flavonoid treatment on the glycation and antioxidant status in Type 1 diabetic patients. Diabetes Nutr Metab. 1999 Aug;12(4):256-63.
308. Maher P, Dargusch R, Ehren JL, et al. Fisetin lowers methylglyoxal dependent protein glycation and limits the complications of diabetes. LoS One. 2011;6(6):e21226. doi: 10.1371/journal.pone.0021226. Epub 2011 Jun 27.
309. Sengupta B, Swenson J. Properties of normal and glycated human hemoglobin in presence and absence of antioxidant. Biochem Biophys Res Commun. 2005 Sep 2;334(3):954-9.
310. Battino M, Ferreiro MS, Bompadre S, et al. Elevated hydroperoxide levels and antioxidant patterns in Papillon-Lefèvre syndrome. Periodontol. 2001 Dec;72(12):1760-6.
311. Lim SC, Tan HH, Goh SK, et al. Oxidative burden in prediabetic and diabetic individuals: evidence from plasma coenzyme Q(10). Diabet Med. 2006 Dec;23(12):1344-9.
312. Battino M, Bullon P, Wilson M, et al. Oxidative injury and inflammatory periodontal diseases: the challenge of anti-oxidants to free radicals andreactive oxygen species. Crit Rev Oral Biol Med. 1999;10(4):458-76.
313. Amin MM, Asaad GF, Abdel Salam RM, et al. Novel CoQ10 antidiabetic mechanisms underlie its positive effect: modulation of insulin and adiponectinereceptors, Tyrosine kinase, PI3K, glucose transporters, sRAGE and visfatin in insulin resistant/diabetic rats. PLoS One. 2014 Feb 20;9(2):e89169. doi: 10.1371/journal.pone.0089169. eCollection 2014.
314. Sena CM1, Nunes E, Gomes A, et al. Supplementation of coenzyme Q10 and alpha-tocopherol lowers glycated hemoglobin level and lipidperoxidation in pancreas of diabetic rats. Nutr Res. 2008 Feb;28(2):113-21. doi: 10.1016/j.nutres.2007.12.005.
315. Mohamed AK, Bierhaus A, Schiekofer S, et al. The role of oxidative stress and NF-kappaB activation in late diabetic complications. Biofactors. 1999;10(2-3):157-67.
316. Zahedi ., Eghtesadi S, Seifirad S, et al. Effects of CoQ10 Supplementation on Lipid Profiles and Glycemic Control in Patients with Type 2 Diabetes: a randomized, double blind, placebo-controlled trial. Journal of Diabetes & Metabolic Disorders 13.1.2014;1-8.
318. Huntington Study Group Pre2CARE Investigators, Hyson HC, Kieburtz K, et al. Safety and tolerability of high-dosage coenzyme Q10 in Huntington’s disease and healthy subjects. Mov Disord. 2010 Sep 15;25(12):1924-8. doi: 10.1002/mds.22408.
319. Saini, R. Coenzyme Q10: The essential nutrient. Journal of Pharmacy And Bioallied Sciences 3.3 (2011): 466.
320. Alf D, Schmidt ME, Siebrecht SC. Ubiquinol supplementation enhances peak power production in trained athletes: a double-blind, placebo controlled study. J Int Soc Sports Nutr. 2013 Apr 29;10:24. doi: 10.1186/1550-2783-10-24. eCollection 2013.
321. Hosoe K, Kitano M, Kishida H, et al. Study on safety and bioavailability of ubiquinol (Increased bioavailability of ubiquinol compared to that of ubiquinone is due to more efficient micellarization during digestion and greater GSH-dependent uptake and basolateral secretion by Caco-2 cells.
322. Hosoe K, Kitano M, Kishida H, et al. Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers. Regul Toxicol Pharmacol. 2007 Feb;47(1):19-28. Epub 2006 Aug 21.
323. Kiho T, Usui S, Hirano K, et al. Tomato paste fraction inhibiting the formation of advanced glycation end-products. Biosci Biotechnol Biochem. 2004 Jan;68(1):200-5.
324. Simonetti P, Gardana C, Riso, P, et al. Glycosylated flavonoids from tomato puree are bioavailable in humans. Nutrition research 25.8. 2005; 717-726.
325. Bugianesi R, Salucci M, Leonardi C, et al. Effect of domestic cooking on human bioavailability of naringenin, chlorogenic acid, lycopene and beta-carotenein cherry tomatoes. Eur J Nutr. 2004 Dec;43(6):360-6. Epub 2004 Apr 5.
326. Budak HN, Guzel-Seydim ZB. Antioxidant activity and phenolic content of wine vinegars produced by two different techniques. J Sci Food Agric. 2010 Sep;90(12):2021-6. doi: 10.1002/jsfa.4047.
327. Yilmaz Y, Toledo RT. Major flavonoids in grape seeds and skins: antioxidant capacity of catechin, epicatechin, and gallic acid. J Agric Food Chem. 2004 Jan 28;52(2):255-60.
328. Wang YJ, Yang XW, Guo QS. Studies on chemical constituents in Huangjuhua (flowers of Chrysanthemum morifolium). Zhongguo Zhong Yao Za Zhi. 2008 Mar;33(5):526-30.
329. Tsuji-Naito K, Saeki H, and Hamano M. Inhibitory effects of Chrysanthemum species extracts on formation of advanced glycation end products. Food Chemistry 116.4. 2009; 854-859.
330. Wei T, Xiong FF, Wang SD, et al. Flavonoid ingredients of Ginkgo biloba leaf extract regulate lipid metabolism through Sp1-mediated carnitine palmitoyltranferase 1A up-regulation. Journal of biomedical science 21.1. 2014;87.
331. Li XX, Chen SX, Ye QS, Protective effects of extract of Ginkgo biloba on vascular endothelial dysfunction induced by AGEs-BSA in vivo. Zhong Yao Cai. 2007 Sep;30(9):1109-13.
332. Ye C, Lu C, Zhuang L, et al. Study on the effect of Ginkgo biloba extract on the tension of diabetic rat artery. Zhong Yao Cai. 2005 Aug;28(8):690-3.
333. Li XZ, Yan HD, Wang J. Extract of Ginkgo biloba and alpha-lipoic acid attenuate advanced glycation end products accumulation andRAGE expression in diabetic nephropathy rats. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2011 Apr;31(4):525-31.
334. Vessal G, Akmali M, Najafi P, et al. Silymarin and milk thistle extract may prevent the progression of diabetic nephropathy in streptozotocin-induceddiabetic rats. Ren Fail. 2010 Jul;32(6):733-9. doi: 10.3109/0886022X.2010.486488.
335. Hunyadi A, Martins A, Hsieh TJ, et al. Chlorogenic acid and rutin play a major role in the in vivo anti-diabetic activity of Morus alba leaf extract on type II diabetic rats. PLoS One. 2012;7(11):e50619. doi: 10.1371/journal.pone.0050619. Epub 2012 Nov 21.
336. Kim DS, Kang YM, Jin WY, et al. Antioxidant activities and polyphenol content of Morus alba leaf extracts collected from varying regions. Biomed Rep. 2014 Sep;2(5):675-680. Epub 2014 Jun 6.
337. Chu Q, Lin M, Tian X, et al. Study on capillary electrophoresis-amperometric detection profiles of different parts of Morus alba L. J. Chromatogr. A 2006, 1116, 286–290.
338. Naowaboot J, Pannangpetch P, Kukongviriyapan V, et al. Antihyperglycemic, antioxidant and antiglycation activities of mulberry leaf extract in streptozotocin-induced chronic diabetic rats. Plant Foods Hum Nutr. 2009 Jun;64(2):116-21. doi: 10.1007/s11130-009-0112-5.
339. Murata K, Yatsunami K, Mizukami O, et al. Effects of propolis and mulberry leaf extract on type 2 diabetes. Focus Alternat Complement Ther 8:4524–525, 2003
340. Andallu B, Suryakantham V, Srikanthi BL, et al. Effect of mulberry (Morus indica L.) therapy on plasma and erythrocyte membrane lipids in patients with type 2 diabetes. Clin Chim Acta 314:47–53, 2001