アルコール依存症と薬物依存のジャーナル
オープンアクセス

概要

Association of Advanced Glycation End Products (AGEs) with Diabetic Nephropathy and Alcohol Consumption

Kirti Parwani, Palash Mandal

The occurrence of diabetes is accelerating worldwide, with consequent increase in the secondary complication like diabetic nephropathy (DN). Diabetic nephropathy refers to a set of structural and functional abnormalities of kidney in patients with diabetes. Detrimental changes like glomerular hypertrophy, glomerulosclerosis, hyperfiltration, proteinuria, etc. occur in DN. One of the major pathways suggested for the pathogenesis is formation of Advanced Glycation End Products (AGEs) via non enzymatic glycation (NEG). NEG is the process in which reducing sugars irreversibly modify free amino groups of proteins, by various events leading to the formation of a Schiff base resulting in Amadori products, culminating into AGEs. AGEs activate several cascades of intracellular signaling via interaction with Receptor for AGEs (RAGE) that results in responses like release of pro-inflammatory cytokines resulting in inflammation, autophagy and programmed cell death. AGEs can also come into circulation from baked food and processed food items. AGEs can also be formed through various oxidative reactions, including the chronic use of alcohol. Alcohol in excess could result in accumulation of acetaldehyde that would lead to insulin resistance. Many risk factors like race, genetic susceptibility, hypertension, hyperglycemia, hyper filtration, smoking, advanced age, male sex, and high-protein diet account for development of DN. Therapeutic interventions include glycemic control, control of blood pressure. This review focuses on the formation of AGEs via non enzymatic glycation, its implications in pathogenesis of DN and therapies designed to break AGEs so as to prevent the development of DN.