Advanced glycation end products (AGEs) - Revision history

Dmitry Dzhagarov: /* AGEs inhibitors */

2024-07-14T20:27:41Z

AGEs inhibitors

← Older revision		Revision as of 20:27, 14 July 2024
Line 24:		Line 24:

	Newer types of drugs based on anti-glucosepane antibodies aim to remove the most abundant form of AGE in the body and appeared to be successful in detecting glucosepane in the retina.<ref>M. D. Streeter ''et al.'', “Generation and Characterization of Anti-Glucosepane Antibodies Enabling Direct Detection of Glucosepane in Retinal Tissue,” ''ACS Chem. Biol.'', vol. 15, no. 10, pp. 2655–2661, 2020</ref> However, no AGE inhibitors are currently approved for humans by the FDA.		Newer types of drugs based on anti-glucosepane antibodies aim to remove the most abundant form of AGE in the body and appeared to be successful in detecting glucosepane in the retina.<ref>M. D. Streeter ''et al.'', “Generation and Characterization of Anti-Glucosepane Antibodies Enabling Direct Detection of Glucosepane in Retinal Tissue,” ''ACS Chem. Biol.'', vol. 15, no. 10, pp. 2655–2661, 2020</ref> However, no AGE inhibitors are currently approved for humans by the FDA.

			Low-molecular-weight natural compounds in traditional medicines inhibit the generation of intracellular methylglyoxal-derived AGEs (MGO-AGEs) and GO-AGEs (MG-H1, argpyrimidine, CML, CEL, and G-H1) through the carbonyl trap system and/or GLO-1 activation. '''Quercetin, chrysin, genistein, epigallocatechin-3-gallate, p-hydroxy cinnamic acid, (+)-catechin, (-)-epicatechin, aspalathin, and hesperidin''' inhibited AGE generation based on the carbonyl trap system.<ref>Takata, T., Inoue, S., Masauji, T., Miyazawa, K., & Motoo, Y. (2024). Generation and Accumulation of Various Advanced Glycation End-Products in Cardiomyocytes May Induce Cardiovascular Disease. International Journal of Molecular Sciences, 25(13), 7319. https://doi.org/10.3390/ijms25137319</ref>

	=== AGEs in aging ===		=== AGEs in aging ===

Dmitry Dzhagarov: /* AGEs in aging */

2023-09-16T12:50:34Z

AGEs in aging

← Older revision		Revision as of 12:50, 16 September 2023
Line 29:		Line 29:

	Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction\|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>		Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction\|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>

			See also: [[Extracellular matrix]]
			== References ==
	<references />		<references />
	[[Category:Main list]]		[[Category:Main list]]
	[[Category:Aging pathways and hallmarks]]		[[Category:Aging pathways and hallmarks]]

Andrea: Update with recent literature

2023-03-04T20:43:17Z

Update with recent literature

← Older revision		Revision as of 20:43, 4 March 2023
Line 26:		Line 26:

	=== AGEs in aging ===		=== AGEs in aging ===
	AGEs accumulate during normal aging and have been proposed as a [[Hallmarks of aging\|hallmark of aging]].<ref>A. Fedintsev and A. Moskalev, “Stochastic non-enzymatic modification of long-lived macromolecules – a missing hallmark of aging” ''Aging Research Reviews''” 2020</ref> They are believed to accelerate all other hallmarks of aging by, for instance, increasing [[cellular senescence]], inflammation, oxidative stress, [[Telomeres\|telomere]] attrition and [[mitochondrial dysfunction]], as well as altering intracellular communication.<ref name=":6" /><ref>C. Correia-Melo, G. Hewitt, and J. F. Passos, “Telomeres, oxidative stress and inflammatory factors: partners in cellular senescence?,” ''Longev. Heal.'', vol. 3, no. 1, p. 1, 2014</ref><ref>J. Zhao, “Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart,” ''World J. Diabetes'', vol. 5, no. 6, p. 860, 2014</ref>		AGEs accumulate during normal aging and have been proposed as a [[Hallmarks of aging\|hallmark of aging]].<ref>A. Fedintsev and A. Moskalev, “Stochastic non-enzymatic modification of long-lived macromolecules – a missing hallmark of aging” ''Aging Research Reviews''” 2020</ref> They are believed to accelerate all other hallmarks of aging by, for instance, increasing [[cellular senescence]], inflammation, oxidative stress, [[Telomeres\|telomere]] attrition and [[mitochondrial dysfunction]], as well as altering intracellular communication.<ref name=":6" /><ref>C. Correia-Melo, G. Hewitt, and J. F. Passos, “Telomeres, oxidative stress and inflammatory factors: partners in cellular senescence?,” ''Longev. Heal.'', vol. 3, no. 1, p. 1, 2014</ref><ref>J. Zhao, “Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart,” ''World J. Diabetes'', vol. 5, no. 6, p. 860, 2014</ref> Additionally, AGEs can increase the occurrence of DNA damage and lead to transcriptional stress, a hallmark of wild-type aging and accelerated aging models.<ref>Tamae, D., Lim, P., Wuenschell, G. E. & Termini, J. Mutagenesis and repair induced by the DNA advanced glycation end product N2-1-(carboxyethyl)-2′-deoxyguanosine in human cells. ''Biochemistry'' 50, 2321–2329 (2011).</ref><ref>Gyenis, A., Chang, J., Demmers, J.J.P.G. ''et al.'' Genome-wide RNA polymerase stalling shapes the transcriptome during aging. ''Nat Genet'' 55, 268–279 (2023). <nowiki>https://doi.org/10.1038/s41588-022-01279-6</nowiki></ref>

	Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction\|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>		Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction\|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>

Andrea: /* categories */

2023-02-16T17:34:38Z

Andrea: Added entry

2023-02-16T17:28:03Z

Added entry

New page

Advanced glycation end products (AGEs), sometimes referred to as glycotoxins, are harmful oxidant compounds that result from glycation reactions during the metabolism of macromolecules in the bloodstream. Glycation (also known as the Maillard reaction or advanced glycation) is a non-enzymatic reaction that attaches a sugar (glucose or fructose) to proteins or lipids. The end-products of these reactions are implicated in diseases such as diabetes type-2,<ref name=":0">Yan, S. F.; D'Agati, V.; Schmidt, A. M.; Ramasamy, R. (2007). "Receptor for Advanced Glycation Endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & aging". ''Current Molecular Medicine''. '''7''' (8): 699–710. doi: 10.2174/156652407783220732</ref> cardiovascular diseases,<ref name=":1">Semba, R. D.; Ferrucci, L.; Sun, K.; Beck, J.; Dalal, M.; Varadhan, R.; Walston, J.; Guralnik, J. M.; Fried, L. P. (2009). "Advanced glycation end products and their circulating receptors predict cardiovascular disease mortality in older community-dwelling women". ''Aging Clinical and Experimental Research''. '''21''' (2): 182–190. doi: 10.1007/BF03325227</ref> [[Aging and eye disease|retinal disease]]<ref name=":2">Glenn, J.; Stitt, A. (2009). "The role of advanced glycation end products in retinal ageing and disease". ''Biochimica et Biophysica Acta (BBA) - General Subjects''. '''1790''' (10): 1109–1116. doi: 10.1016/j.bbagen.2009.04.016</ref> or [[Aging and neurodegeneration|neurodegenerative diseases]].<ref name=":3">Munch, G; Deuther-Conrad W; Gasic-Milenkovic J. (2002). "Glycoxidative stress creates a vicious cycle of neurodegeneration in Alzheimer's disease--a target for neuroprotective treatment strategies?". ''J Neural Transm Suppl''. '''62''' (62): 303–307. doi: 10.1007/978-3-7091-6139-5_28</ref><ref name=":4">Münch, Gerald; et al. (27 February 1997). "Influence of advanced glycation end-products and AGE-inhibitors on nucleation-dependent polymerization of β-amyloid peptide". ''Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease''. '''1360''' (1): 17–29. doi: 10.1016/S0925-4439(96)00062-2</ref> They are also believed to play a causative role in normal aging.<ref name=":0" />

=== Dietary AGEs (dAGEs) ===
Highly processed foods found abundantly in western diets are rich in AGEs, which is worrisome given that dietary AGEs (dAGEs) have been shown to contribute to increased inflammation and oxidative stress, both precursor states for disease.<ref name=":5">Uribarri, J., Woodruff, S., Goodman, S., Cai, W., Chen, X. U. E., Pyzik, R., ... & Vlassara, H. (2010). Advanced glycation end products in foods and a practical guide to their reduction in the diet. ''Journal of the American Dietetic Association'', ''110''(6), 911-916.</ref> The cooking method also has a high impact in the formation of AGEs from the diet: '''dry heat was found to increase AGE formation''' by 10 to 100 fold more than uncooked food, '''especially in animal-derived food'''.<ref name=":5" /> Vegetarian, carbohydrate-rich diets based on vegetables, milk and fruits lead to very few AGE formation even after being heat-processed.

Due to the impact of diet, conditions such as obesity or post-menopausal changes in body weight also lead to an increase in AGEs formation and therefore increased risk of cardiovascular disease.<ref>Pertynska-Marczewska, M., & Merhi, Z. (2015). Relationship of advanced glycation end products with cardiovascular disease in menopausal women. ''Reproductive Sciences'', ''22'', 774-782.</ref>

=== AGEs in disease ===
The formation of AGEs occurs during normal metabolism, however high levels might lead to disease due to '''protein-protein crosslinking''' in the bloodstream.<ref name=":6">Ulrich P, Cerami A. Protein glycation, diabetes, and aging. Recent Prog Horm Res. 2001;56:1–21.</ref> AGE processes particularly affect long-lived proteins with high turnover rates, such as structural collagen or other '''components of the extracellular matrix, which usually become pathogenic targets'''. When crosslinking of collagen occurs in the walls of the vasculature, this can be extremely deleterious. Damage to the micro- or macro-vasculature can lead to the formation of plaques, impair vascular elasticity and increase the risk for atherosclerosis and cardiovascular disease.<ref name=":1" />

One of the most common types of AGEs is '''glucosepane''', which forms an irreversible, covalent cross-link molecule in collagen that might last decades before the body is able to fully remove it. It is also believed that glucosepane has a causal effect in the wrinkling of the skin over time and in the thickening of basement membranes in the vasculature.<ref>Sell, D. R., Biemel, K. M., Reihl, O., Lederer, M. O., Strauch, C. M., & Monnier, V. M. (2005). "Glucosepane is a major protein cross-link of the senescent human extracellular matrix: Relationship with diabetes". ''Journal of Biological Chemistry''. '''280''' (13): 12310–12315. doi: 10.1074/jbc.M500733200</ref> It is also found in high levels in conditions of diabetes type-2.<ref>Monnier, V. M., Mustata, G. T., Biemel, K. L., Reihl, O., Lederer, M. O., Zhenyu, D.; et al. (2005). "Cross-linking of the extracellular matrix by the maillard reaction in aging and diabetes: An update on "a puzzle nearing resolution"". ''Annals of the New York Academy of Sciences''. '''1043''': 533–544.</ref>

There is extensive evidence that AGEs develops more quickly in patients with diabetes, which negatively contributes to the state of their vascular system.<ref>Singh, V. P., Bali, A., Singh, N., & Jaggi, A. S. (2014). Advanced glycation end products and diabetic complications. ''The Korean journal of physiology & pharmacology: official journal of the Korean Physiological Society and the Korean Society of Pharmacology'', ''18''(1), 1.</ref> AGEs also build over time in the heart muscle and might lead to a decreased respiratory capacity.<ref>Zieman, S. J., & Kass, D. A. (2004). Advanced glycation end product cross‐linking: pathophysiologic role and therapeutic target in cardiovascular disease. ''Congestive Heart Failure'', ''10''(3), 144-151.</ref> Other diseases that might be highly impacted by AGEs formation are [[Aging and eye disease|retinal disease]] or [[Aging and neurodegeneration|neurodegenerative diseases]] such as Alzheimer's.<ref name=":2" /><ref name=":3" /><ref name=":4" />

=== AGE receptors ===
AGEs contribute to disease by engaging with the '''receptor for advanced glycation endproducts (RAGE)''', which is believed to result in pro-inflammatory gene activation.<ref>Gasparotto, J; Ribeiro, CT; da Rosa-Silva, HT; Bortolin, RC; Rabelo, TK; Peixoto, DO; Moreira, JCF; Gelain, DP (May 2019). "Systemic Inflammation Changes the Site of RAGE Expression from Endothelial Cells to Neurons in Different Brain Areas". ''Mol Neurobiol''. '''56''' (5): 3079–3089. doi: 10.1007/s12035-018-1291-6</ref> RAGE is found up-regulated in diabetes and Alzheimer's disease, and in turn activates NF-κB signalling which might mediate the inflammatory components of these diseases.<ref>Gasparotto, J; Girardi, CS; Somensi, N; Ribeiro, CT; Moreira, JCF; Michels, M; Sonai, B; Rocha, M; Steckert, AV; Barichello, T; Quevedo, J; Dal-Pizzol, F; Gelain, DP (Nov 2017). "Receptor for advanced glycation end products mediates sepsis-triggered amyloid-β accumulation, Tau phosphorylation, and cognitive impairment". ''J Biol Chem''. '''293''' (1): 226–244. doi: 10.1074/jbc.M117.786756</ref><ref>Bierhaus A, Schiekofer S, Schwaninger M, Andrassy M, Humpert PM, Chen J, Hong M, Luther T, Henle T, Klöting I, Morcos M, Hofmann M, Tritschler H, Weigle B, Kasper M, Smith M, Perry G, Schmidt AM, Stern DM, Häring HU, Schleicher E, Nawroth PP (December 2001). "Diabetes-associated sustained activation of the transcription factor nuclear factor-kappaB". ''Diabetes''. '''50''' (12): 2792–808. doi: 10.2337/diabetes.50.12.2792</ref> Interestingly, RAGE is down-regulated in pulmonary fibrosis and other conditions such as lung cancer.<ref>Oczypok, EA; Perkins, TN; Oury, TD (June 2017). "All the "RAGE" in lung disease: The receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses". ''Paediatric Respiratory Reviews''. '''23''': 40–49. doi: 10.1016/j.prrv.2017.03.012</ref> However, expression of RAGE in the lungs differs significantly from the rest of the body, and is normally highly expressed in lung cells in the absence of disease.<ref>Queisser MA, Kouri FM, Königshoff M, Wygrecka M, Schubert U, Eickelberg O, Preissner KT (September 2008). "Loss of RAGE in pulmonary fibrosis: molecular relations to functional changes in pulmonary cell types". ''American Journal of Respiratory Cell and Molecular Biology''. '''39''' (3): 337–45. doi: 10.1165/rcmb.2007-0244OC</ref>

Other receptors exist, such as AGE-R1/3 which are able to recognise and bind to AGE molecules, however they don't appear to transduce cellular signals and might instead play a role in the removal and detoxification of AGE from the bloodstream.<ref>Bucciarelli LG, Wendt T, Rong L, Lalla E, Hofmann MA, Goova MT, Taguchi A, Yan SF, Yan SD, Stern DM, Schmidt AM. RAGE is a multiligand receptor of the immunoglobulin superfamily: implications for homeostasis and chronic disease. '''Cell Mol Life Sci'''. 2002; 59: 1117–1128.</ref>

=== AGEs inhibitors ===
Several AGEs inhibitors have been developed to remove these harmful compounds from the body. One approach is the carbonyl reagent aminoguanidine hydrochloride, which targets the reactive carbonyl groups believed to be required for AGEs formation.<ref>Hou, F. F., Boyce, J., Chertow, G. M., Kay, J., & Owen Jr, W. F. (1998). Aminoguanidine inhibits advanced glycation end products formation on beta2-microglobulin. ''Journal of the American Society of Nephrology'', ''9''(2), 277-283.</ref> Studies have shown that aminoguanidine (Pimagedine) is able to improve the symptoms and progression of AGEs-related diseases such as diabetes type-2 and aging.<ref>Thornalley, P. J. (2003). Use of aminoguanidine (Pimagedine) to prevent the formation of advanced glycation endproducts. ''Archives of biochemistry and biophysics'', ''419''(1), 31-40.</ref>

Another class of agents, 4,5-dimethyl-3-phenacylthiazolium chloride (DPTC) showed able to break down the protein-protein crosslinks formed by AGEs and was proposed to revert the vascular damage in animals.<ref>Asif, M., Egan,J.,Vasan,S.,Jyothirmayi,G.N., Masurekar,M.R., Lopez,S.,Williams, C.,Torres,R.L., Wagle, D., Ulrich, P., Cerami, A., Brines, M., and Regan,T.J. (2000). Proc. Nat/. Acad. Sci. U.S.A.97,2809-2813.</ref><ref>Wolffenbuttel, B.H., Boulanger, C.M., Crijns, F.R., Huijberts, M.S., Poitevin, P., Swennen, G.N., Vasan, S., Egan, J.J., Ulrich, P., Cerami, A , and Levy, B.I. (1998). Proc. Nat!. Acad. Sci. U.S.A. 95,4630-4634</ref>

Newer types of drugs based on anti-glucosepane antibodies aim to remove the most abundant form of AGE in the body and appeared to be successful in detecting glucosepane in the retina.<ref>M. D. Streeter ''et al.'', “Generation and Characterization of Anti-Glucosepane Antibodies Enabling Direct Detection of Glucosepane in Retinal Tissue,” ''ACS Chem. Biol.'', vol. 15, no. 10, pp. 2655–2661, 2020</ref> However, no AGE inhibitors are currently approved for humans by the FDA.

=== AGEs in aging ===
AGEs accumulate during normal aging and have been proposed as a [[Hallmarks of aging|hallmark of aging]].<ref>A. Fedintsev and A. Moskalev, “Stochastic non-enzymatic modification of long-lived macromolecules – a missing hallmark of aging” ''Aging Research Reviews''” 2020</ref> They are believed to accelerate all other hallmarks of aging by, for instance, increasing [[cellular senescence]], inflammation, oxidative stress, [[Telomeres|telomere]] attrition and [[mitochondrial dysfunction]], as well as altering intracellular communication.<ref name=":6" /><ref>C. Correia-Melo, G. Hewitt, and J. F. Passos, “Telomeres, oxidative stress and inflammatory factors: partners in cellular senescence?,” ''Longev. Heal.'', vol. 3, no. 1, p. 1, 2014</ref><ref>J. Zhao, “Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart,” ''World J. Diabetes'', vol. 5, no. 6, p. 860, 2014</ref>

Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>

← Older revision		Revision as of 17:34, 16 February 2023
Line 29:		Line 29:

	Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction\|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>		Diets low in animal-derived fat and high in carbohydrates, such as vegetarian diets, are thought to decrease the rate of AGEs accumulation.<ref name=":5" /> Raw, boiled or steamed food also decreases the formation of AGEs when carbohydrate-rich diets are not possible.<ref name=":5" /> Studies in rats have shown that [[Calorie restriction\|caloric restriction]] benefits the rate of serum AGE accumulation.<ref>W. T. Cefalu ''et al.'', “Caloric Restriction Decreases Age-Dependent Accumulation of the Glycoxidation Products, N?-(Carboxymethyl)lysine and Pentosidine, in Rat Skin Collagen,” ''Journals Gerontol. Ser. A'', vol. 50A, no. 6, pp. B337–B341, 1995</ref> Exercise is also able to decrease the levels of AGE formation in both healthy and diabetic patients.<ref>M. H. Macías-Cervantes, J. M. D. Rodríguez-Soto, J. Uribarri, F. J. Díaz-Cisneros, W. Cai, and M. E. Garay-Sevilla, “Effect of an advanced glycation end product-restricted diet and exercise on metabolic parameters in adult overweight men,” ''Nutrition'', vol. 31, no. 3, pp. 446–451, 2015</ref><ref>P. M. Magalhães, H. J. Appell, and J. A. Duarte, “Involvement of advanced glycation end products in the pathogenesis of diabetic complications: the protective role of regular physical activity,” ''Eur. Rev. Aging Phys. Act.'', vol. 5, no. 1, pp. 17–29, 2008</ref>
			<references />
			[[Category:Main list]]
			[[Category:Aging pathways and hallmarks]]