Abstract
There is increasing evidence for the role of intestinal permeability as a contributing factor in the pathogenesis of diabetes; however, the molecular mechanisms are poorly understood. Advanced glycation endproducts, of both exogenous and endogenous origin, have been shown to play a role in diabetes pathophysiology, in part by their ligation to the receptor for advanced glycation endproducts (RAGE), leading to a proinflammatory signalling cascade. RAGE signalling has been demonstrated to play a role in the development of intestinal inflammation and permeability in Crohn’s disease and ulcerative colitis. In this review, we explore the role of AGE-RAGE signalling and intestinal permeability and explore whether activation of RAGE on the intestinal epithelium may be a downstream event contributing to the pathogenesis of diabetes complications.
Highlights
Diabetes mellitus has become one of the most problematic health concerns of the 21st century as the number of cases continues to multiply in both young and aged populations
There are two main forms of diabetes; type 1 diabetes (T1D) is characterised by an absolute insulin deficiency resulting from autoimmune destruction of pancreatic β-cells, whereas type 2 diabetes (T2D) is defined by a resistance to the actions of insulin, resulting in the reduction of glucose uptake and storage [3,4]
EsRAGE expression reduced the expression of proinflammatory and profibrotic genes when transfected into wild-type (WT) mesangial cells in vitro, whereas the opposite effect was apparent when fulllength receptor for advanced glycation endproducts (RAGE) was overexpressed in these cells [49]
Summary
Diabetes mellitus has become one of the most problematic health concerns of the 21st century as the number of cases continues to multiply in both young and aged populations. There are two main forms of diabetes; type 1 diabetes (T1D) is characterised by an absolute insulin deficiency resulting from autoimmune destruction of pancreatic β-cells, whereas type 2 diabetes (T2D) is defined by a resistance to the actions of insulin, resulting in the reduction of glucose uptake and storage [3,4] In both cases, hyperglycaemia is a defining feature and is the basis for the development of many diabetic complications [3]. Advanced glycation endproducts (AGEs) are a group of sugar-derived compounds commonly found in processed foods treated with dry heat Their excess consumption is strongly associated with the pathophysiology of T2D [6]. Some AGEs that have been well characterised include Nε-carboxymethyllysine (CML), carboxyethyllysine, pentosidine and pyrraline, which are used extensively to examine the physiological repercussions of AGEs, as is discussed later [17]
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