Oxidative stress and adipocyte biology: focus on the role of AGEs.
Florence BoyerJennifer Baraka VidotAlexis Guerin DubourgPhilippe RondeauM Faadiel EssopEmmanuel BourdonPublished in: Oxidative medicine and cellular longevity (2015)
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.
Keyphrases
- adipose tissue
- type diabetes
- insulin resistance
- oxidative stress
- diabetic rats
- cardiovascular disease
- glycemic control
- metabolic syndrome
- high fat diet
- high fat diet induced
- public health
- weight loss
- dna damage
- mental health
- fatty acid
- signaling pathway
- electronic health record
- induced apoptosis
- deep learning
- neoadjuvant chemotherapy
- body mass index
- drug induced
- big data
- high glucose
- heat stress
- heat shock protein
- locally advanced
- binding protein