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Pathologic role of dietary advanced glycation end products in cardiometabolic disorders, and therapeutic intervention.
Nutrition 2016; 32(2):157-65N

Abstract

Reactive derivatives from nonenzymatic glucose-protein condensation reactions, as well as lipids and nucleic acids exposed to reducing sugars, form a heterogeneous group of irreversible adducts called AGEs (advanced glycation end products). The glycation process begins with the conversion of reversible Schiff base adducts to more stable, covalently bound Amadori rearrangement products. Over the course of days to weeks, these Amadori products undergo further rearrangement and condensation reactions to form irreversibly cross-linked macroprotein derivatives known as AGEs. The formation and accumulation of AGEs have been known to progress in a physiological aging process and at an accelerated rate under hyperglycemic and oxidative stress conditions. There is growing evidence that AGEs play a pathologic role in numerous disorders. Indeed, glycation and/or cross-linking modification of circulating or organic matrix proteins by AGEs the senescence of moieties and deteriorate their physiological function and structural integrity in multiple organ systems. Moreover, AGEs elicit oxidative stress and inflammatory reactions through the interaction with the receptor for advanced glycation products in a variety of cells, thereby contributing to the development and progression of various aging- or diabetes-related disorders, such as cardiovascular disease, chronic kidney disease, insulin resistance, and Alzheimer's disease. Recently, diet has been recognized as a major environmental source of AGEs that could cause proinflammatory reactions and organ damage in vivo. Therefore, this review summarizes the pathophysiological role of dietary AGEs in health and disease, especially focusing on cardiometabolic disorders. We also discuss the potential utility in targeting exogenously derived AGEs for therapeutic intervention.

Authors+Show Affiliations

Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Japan. Electronic address: Shoichi@med.kurume-u.ac.jp.Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Japan.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

26602289

Citation

Yamagishi, Sho-Ichi, and Takanori Matsui. "Pathologic Role of Dietary Advanced Glycation End Products in Cardiometabolic Disorders, and Therapeutic Intervention." Nutrition (Burbank, Los Angeles County, Calif.), vol. 32, no. 2, 2016, pp. 157-65.
Yamagishi S, Matsui T. Pathologic role of dietary advanced glycation end products in cardiometabolic disorders, and therapeutic intervention. Nutrition. 2016;32(2):157-65.
Yamagishi, S., & Matsui, T. (2016). Pathologic role of dietary advanced glycation end products in cardiometabolic disorders, and therapeutic intervention. Nutrition (Burbank, Los Angeles County, Calif.), 32(2), pp. 157-65. doi:10.1016/j.nut.2015.08.001.
Yamagishi S, Matsui T. Pathologic Role of Dietary Advanced Glycation End Products in Cardiometabolic Disorders, and Therapeutic Intervention. Nutrition. 2016;32(2):157-65. PubMed PMID: 26602289.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathologic role of dietary advanced glycation end products in cardiometabolic disorders, and therapeutic intervention. AU - Yamagishi,Sho-Ichi, AU - Matsui,Takanori, Y1 - 2015/09/01/ PY - 2015/06/22/received PY - 2015/08/03/accepted PY - 2015/11/26/entrez PY - 2015/11/26/pubmed PY - 2016/12/16/medline KW - AGEs KW - Aging KW - Cardiometabolic disorder KW - Diet KW - Oxidative stress SP - 157 EP - 65 JF - Nutrition (Burbank, Los Angeles County, Calif.) JO - Nutrition VL - 32 IS - 2 N2 - Reactive derivatives from nonenzymatic glucose-protein condensation reactions, as well as lipids and nucleic acids exposed to reducing sugars, form a heterogeneous group of irreversible adducts called AGEs (advanced glycation end products). The glycation process begins with the conversion of reversible Schiff base adducts to more stable, covalently bound Amadori rearrangement products. Over the course of days to weeks, these Amadori products undergo further rearrangement and condensation reactions to form irreversibly cross-linked macroprotein derivatives known as AGEs. The formation and accumulation of AGEs have been known to progress in a physiological aging process and at an accelerated rate under hyperglycemic and oxidative stress conditions. There is growing evidence that AGEs play a pathologic role in numerous disorders. Indeed, glycation and/or cross-linking modification of circulating or organic matrix proteins by AGEs the senescence of moieties and deteriorate their physiological function and structural integrity in multiple organ systems. Moreover, AGEs elicit oxidative stress and inflammatory reactions through the interaction with the receptor for advanced glycation products in a variety of cells, thereby contributing to the development and progression of various aging- or diabetes-related disorders, such as cardiovascular disease, chronic kidney disease, insulin resistance, and Alzheimer's disease. Recently, diet has been recognized as a major environmental source of AGEs that could cause proinflammatory reactions and organ damage in vivo. Therefore, this review summarizes the pathophysiological role of dietary AGEs in health and disease, especially focusing on cardiometabolic disorders. We also discuss the potential utility in targeting exogenously derived AGEs for therapeutic intervention. SN - 1873-1244 UR - https://www.unboundmedicine.com/medline/citation/26602289/Pathologic_role_of_dietary_advanced_glycation_end_products_in_cardiometabolic_disorders_and_therapeutic_intervention_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0899-9007(15)00336-6 DB - PRIME DP - Unbound Medicine ER -