Oxidative Stress and Adipocyte Biology: Focus on the Role of AGEs

Abstract

Diabetes is a major health problem that is usually associated with obesity, together with hyperglycemia and increased advanced glycation endproducts (AGEs) formation. Elevated AGEs elicit severe downstream consequences via their binding to receptors of AGEs (RAGE). This includes oxidative stress and oxidative modifications of biological compounds together with heightened inflammation. For example, albumin (major circulating protein) undergoes increased glycoxidation with diabetes and may represent an important biomarker for monitoring diabetic pathophysiology. Despite the central role of adipose tissue in many physiologic/pathologic processes, recognition of the effects of greater AGEs formation in this tissue is quite recent within the obesity/diabetes context. This review provides a brief background of AGEs formation and adipose tissue biology and thereafter discusses the impact of AGEs-adipocyte interactions in pathology progression. Novel data are included showing how AGEs (especially glycated albumin) may be involved in hyperglycemia-induced oxidative damage in adipocytes and its potential links to diabetes progression.

A method for the measurement of lactate, glycerol and fatty acid production from14C-glucose in primary cultures of rat epididymal adipocytes

“…In our opinion, there is yet much to learn from WAT from the "basic" biochemical-metabolic point of view. We know much about its metabolic modulation by cytokines 71 and hormones [72][73][74][75] , and even its responses to oxidative stress 76 and hypoxia 77,78 , however, we know very little on the quantitative importance of Randall's glucose-fatty acid cycle, the classical Cori cycle and the interchange of glutamine and ornithine-arginine with the splanchnic bed. Consequently, we developed a tool, which can be used for that purpose, adapted, modified, and, we hope, improved to fulfill its function.…”

Inflammation and Oxidative Stress: Critical Role for Metabolic Syndrome

“…Hyperglycemia-induced oxidative damage in adipocytes and its potential links to diabetes progression when advanced glycation endproducts (AGEs) -especially glycated albumin formation is increased [29]. Elevated AGEs elicit severe downstream consequences via their binding to receptors of AGEs (RAGE), this includes oxidative stress and oxidative modifications of biological compounds together with heightened inflammation [30].…”

Advanced Glycation End Products (Ages) in Food: Focusing on Mediterranean Pasta

“…RAGE, a single trans-membrane multi-ligand receptor, belongs to the immunoglobulin superfamily, whose members include AGE-R, SR-A (macrophage scavenger receptor types I and II), and SR-B (SR-B type I and CD36) [3,37].…”

“…RAGE receptors are physiologically mainly expressed on vascular, endothelial and smooth muscle cells and on monocyte/macrophage membranes [36,37]. The ligands of RAGE a part from AGEs and CML include also amyloid-β peptide, members of the S100 protein family, proteins of the high mobility group box-1 (HMGB1) and prions [38].…”