Dietetics advanced glycation end-products and chronic complications of diabetes
Keywords:
Diabetes mellitus, Diet, Glycosylation end-products, advancedAbstract
The generation of advanced glycation end products is one of the principal mechanisms that lead to the pathologies associated with diabetes mellitus, which include cardiopathy, retinopathy, neuropathy and nephropathy. The objective of this revision is to analyse the role of the advanced glycation end products present in food as intermediaries of diabetic complications, presenting strategies to reduce their ingestion. For this purpose, research was carried out in databases of publications of the area, for the last 15 years, taking into account revision, experimental and clinical studies. Advanced glycation end products are a heterogenous group of molecules coming from non-enzymatic reactions between amino and carbonyl groups, examples being carboxymethyllisine and pentosidine found in food and in vivo. The advanced glycation end products ingested are absorbed and, along with endogenous advanced glycation end-products, promote the progression of the complications of diabetes. There is a direct correlation between advanced glycation end products consumption and blood concentration. Their restriction in food results in the suppression of serum levels of the markers of vascular disease and the intermediaries of inflammation directly involved in the development of diabetic degenerations. The current dietary orientations are concentrated on the proportion of nutrients and on energetic restriction. The risk of ingestion of advanced glycation end products formed during the processing of food should be taken in consideration. It is simply recommended that in the preparation of food, the use of low temperatures for short periods, in the presence of water, has important effects in the prevention of the complications of diabetes. The study of the mechanisms involved in the generation of advanced glycation end products and the antiglycation properties of compounds presented in foods can contribute to a therapeutic practice and an improvement in the quality of life of people with this disease.
References
Zimmet P, Alberti KGMM, Shaw J. Global and societal implications of the diabetes epidemic. Nature. 2001; 414(13):782-7.
Peppa M, Uribarri J, Vlassara H. Glucose, advanced glycation end products, and diabetes complications: what is new and what works. Clin Diabetes. 2003; 21(4):186-7.
Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001; 414(13):813-20.
Nishikawa T, Edelstein D, Brownlee M. The missing link: a single unifying mechanism for diabetic complications. Kidney Int Suppl. 2000; 58(77): 26-30.
Jakus V, Rietbrock N. Advanced glycation end products and the progress of diabetic vascular complications. Physiol Res. 2004; 53(2):131-42.
Baynes JW. The Maillard hypothesis on aging: time to focus on DNA. Ann NY Acad Sci. 2002; 959:3 60-7.
Monnier VM, Sell DR, Genuth S. Glycation products as markers and predictors of the progression of diabetic complications. Ann NY Acad Sci. 2005; 1043:567-81.
Martins SIFS, Jongen WMF, Boekel MAJSV. A review of Maillard reaction in food and implications to kinetic modelling. Trends Food Sci Technol. 2000; 11(9-10):364-73.
Nunes CS, Baptista AO. Implicações da reação de Maillard nos alimentos e nos sistemas biológicos. Rev Port Ciên Vet. 2001; 96(538):53-9.
Goldberg T, Cai W, Peppa M, Dardaine V, Baliga BS, Uribarri J, et al. Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc. 2004; 104(8):1287-91.
Vlassara H, Cai W, Crandall J, Goldberg T, Oberstein R, Dardaine V, et al. Inflamatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Proc Natl Acad Sci. 2002; 99(24):15596-601.
American Diabetes Association. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care. 2008; 31(Suppl 1): S61-78.
Ahmed N. Advanced glycation end-products-role in pathology of diabetic complications. Diabetes Res Clin Pract. 2005; 67(1):3-21.
Henle T. AGEs in food: do they play a role in uremia? Kidney Int Suppl. 2003; 63(84):145-7.
Monnier VM. Intervention against the Maillard reaction in vivo. Arch Biochem Biophys. 2003; 419(1):1-15.
Bierhaus A, Hofman MA, Ziegler R, Nauroth PP. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept. Cardiov Res. 1998; 37(3):586-600.
Huebschmann AG, Regensteiner JG, Vlassara H, Reusch JEB. Diabetes and advanced glycoxidation end products. Diabetes Care. 2006; 29(6):1420-32.
Meade SJ, Miller AG, Gerrard JA. The role of dicarbonyl compounds in non-enzimatic crosslinking: a structure-activity study. Bioorg Med Chem. 2003; 11(6):853-62.
Brownlee M. The pathobiology of diabetic complications: a unifying mecanism. Diabetes. 2005; 54(6):1615-25.
Leslie RDG, Beyan H, Sawtell P, Boehm BO, Spector TD, Snieder H. Level of an advanced glycated end product is genetically determined: a study of normal twins. Diabetes. 2003; 52(9):2441-4.
Kim W, Hudson BI, Moser B, Guo J, Rong LL, Qu W, et al. Receptor for advanced glycation end products and Its ligands: a journey from the complications of diabetes to its pathogenesis. Ann NY Acad Sci. 2005; 1043:553-61.
Lapolla A, Fedele D, Reitano R, Bonfante L, Pastori G, Segraglia R, et al. Advanced glycation end products/peptides. Ann NY Acad Sci. 2005; 1043: 1-9.
Vlassara H, Palace MR. Diabetes and advanced glycation end-products. J Intern Med. 2002; 251(2): 87-101.
Peppa M, Brem H, Ehrlich P, Zhang J, Cai W, Li Z, et al. Adverse effects of dietary glycotoxins on wound healing in genetically diabetic mice. Diabetes. 2003; 52(11):2805-13.
Bucala R, Makita Z, Vega G, Grundy S, Koschinsky T, Cerami A, et al. Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. Proc Natl Acad Sci. 1994; 91(9):9441-5.
Vlassara H. Advanced glycation in health and disease. Role of the modern environment. Ann NY Acad Sci. 2005; 1043:452-60.
Sandu O, Song K, Cai W, Zheng F, Uribarri J, Vlassara H. insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake. diabetes. 2005; 54(8):2314-19.
Hofmann S, Dong HJ, Li Z, Cai W, Altomonte J, Thung SN, et al. Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in db/db mouse. Diabetes. 2002; 51(7):2082-9.
Lin R, Choudhury RP, Cai W, Lu M, Fallon JT, Fisher EA, et al. Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice. Atherosclerosis. 2003;168(2):213-20.
Zheng F, He C, Cai W, Hattori M, Steffes M, Vlassara H. Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products. Diabetes Metab Res Rev. 2002; 18(3):224-37.
Lin R, Reis ED, Dore AT, Lu M, Ghodsi N, Fallon JT, et al. Lowering of dietary advanced glycation endproducts (AGE) reduces neointimal formation after arterial injury in genetically hypercholesterolemic mice. Atherosclerosis. 2002; 163(2):303-11.
Peppa M, He C, Hattori M, McEvoy R, Zheng F, Vlassara H. Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD mice. Diabetes. 2003; 52(6):1441-8.
Vlassara H, Palace MR. Glycoxidation: the menace of diabetes and aging. Mt Sinai J Med. 2003; 70(4): 232-41.
Uribarri J, Cai W, Sandu O, Peppa M, Goldberg T, Vlassara H. Diet-derived advanced glycation end products are major contributors to the body’s AGE pool and induce inflamation in health subjects. Ann NY Acad Sci. 2005; 1043:461-6.
Chappey O, Dosquet C, Wautier MP, Wautier JL. Advanced glycation end products, oxidant stress and vascular lesions. Eur J Clin Invest. 1997; 27(2):97-108.
Grunwald S, Krause R, Bruch M, Henle T, Brandsch M. Transepithelial flux of early and advanced glycation compounds across Caco-2 cell monolayers and their interaction with intestinal amino acid and peptide transport systems. Br J Nutr. 2006; 95(6):1221-8.
Koschinsky T, He C, Mitsuhashi T, Bucala R, Liu C, Buenting C, et al. Orally absorbed reactive glycation products (glicotoxins): an environmental risk factor in diabetic nephropathy. Proc Natl Acad Sci. 1997; 94(12):6476-9.
Schwenger V, Morath C, Schonfelder K, Klein W, Weigel K, Deppisch R, et al. An oral load of the early glycation compound lactuloselysine fails to accumulate in the serum of uraemic patients. Nephrol Dial Transplant. 2006; 21(2):383-8.
Cooper ME. Importance of advanced glycation end products in diabetes-associated cardiovascular and renal disease. Am J Hipertens. 2004; 17(12 Pt 2): 31-8.
Föster A, Kühne Y, Henle T. Studies on absorption and elimination of dietary Maillard reaction products. Ann NY Acad Sci. 2005; 1043:474-81.
Thorpe SR, Baynes JW. CML: a brief history. Int Congr Ser. 2002; 1245:91-9.
Uribarri J, Peppa M, Cai W, Goldberg T, Lu M, He C, et al. Restriction of dietary glicotoxins reduces excessive advanced glycation end products in renal failure patients. J Am Soc Nephrol. 2003; 14(3):728-31.
Cai W, He JC, Zhu L, Peppa M, Lu C, Uribarri J, et al. High levels of dietary advanced glycation end products transform low-dersity lipoprotein into a potent redox-sensitive mitogen-activated protein kinase stimulant in diabetic patients. Circulation. 2004; 110(3):285-91.
Stirban A, Negrean M, Stratmann B, Gawlowski T, Horstmann T, Gotting C, 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; 29(9):2064-71.
Reddy VP, Beyaz A. Inhibitors of the Maillard reaction and AGE breakers as therapeutics for multiple diseases. Drug Discov Today. 2006; 11(13/14):646-54.
Ahmad MS, Ahmed N. Antiglycation properties of aged garlic extract: possible role in prevention of diabetic complications. J Nutr. 2006; 136(3 Suppl): S796-9.
Osawa T, Kato Y. Protective role of antioxidative food factors in oxidative stress caused by hyperglycemia. Ann NY Acad Sci. 2005; 1043: 440-51.
Babu PVA, Sabitha KE, Shyamaladevi CS. Green tea impedes dyslipidemia, lipid peroxidation, protein glycation and ameliorates Ca2+-ATPase and Na+/K+-ATPase activity in the heart of streptozotocin-diabetic rats. Chem Biol Interact. 2006; 162(2):157-64.
Bousová I, Martin J, Jahodár R, Dusek J, Palicka V, Drsata J. Evaluation of in vitro effects of natural substances of plant origin using a model of protein glicoxidation. J Pharm Biomed Anal. 2005; 37(5): 957-62.
Higdon JV, Frei B. Tea catechins polyphenols: health effects, metabolism, and antioxidants functions. Crit Rev in Food Sci Nutr. 2003; 43(1):89-143.
Lunceford N, Gugliucci A. Ilex paraguaiensis extracts inhibit AGE formation more efficiently than green tea. Fitoterapia. 2005; 76(5):419-27.
Pari L, Venkateswaran S. Effect of an aqueous extract of phaseolus vulgaris on the properties of tail tendon collagen of rats with streptozotocininduced diabetes. Braz J Med Biol Res. 2003; 36(7):861-70.
Mustata GT, Rosca M, Biemel KM, Reihl O, Smith MA, Viswanathan A, et al. Paradoxical effects of green tea (Camellia sinensis) and antioxidant vitamins in diabetic rats. Diabetes. 2005; 54(2): 517-26.
Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, Thornalley PJ. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfothiamine. Diabetes. 2003; 52 (8):2110-20.
McCarty MF. The low-AGE content of low-fat vegan diets could benefit diabetics - though concurrent taurine supplementation may be needed to minimize endogenous AGE production. Med Hypotheses. 2005; 64(2):394-8.
Hobart LJ, Seibel I, Yeargans GS, Seidler NW. Anti-crosslinking properties of carnosine: significance of histidine. Life Sci. 2004; 75(11):1379-89.
Bauchart C, Rémond D, Chambon C, Mirand PP, Savary-Auzeloux I, Reynès C, et al. Small peptides (<5 kDa) found in ready-to-eat beef meat. Meat Sci. 2006; 74(4):658-66.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2023 Júnia Helena Porto BARBOSA, Suzana Lima de OLIVEIRA, Luci Tojal e SEARA
This work is licensed under a Creative Commons Attribution 4.0 International License.
