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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Clin+Med 2014 ; 3 (2): 646-62 Nephropedia Template TP
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Roles of Sphingolipid Metabolism in Pancreatic ? Cell Dysfunction Induced by Lipotoxicity #MMPMID26237395
Véret J; Bellini L; Giussani P; Ng C; Magnan C; Le Stunff H
J Clin Med 2014[Jun]; 3 (2): 646-62 PMID26237395show ga
Pancreatic ? cells secrete insulin in order to maintain glucose homeostasis. However, various environmental stresses such as obesity have been shown to induce loss of secretory responsiveness in pancreatic ? cells and pancreatic ? cell apoptosis which can favor the development of type 2 diabetes (T2D). Indeed, elevated levels of free fatty acids (FFAs) have been shown to induce ? cell apoptosis. Importantly, the chronic adverse effects of FFAs on ? cell function and viability are potentiated in the presence of hyperglycaemia, a phenomenon that has been termed gluco-lipotoxicity. The molecular mechanisms underlying the pathogenesis of gluco-lipotoxicity in pancreatic ? cells are not completely understood. Recent studies have shown that sphingolipid metabolism plays a key role in gluco-lipotoxicity induced apoptosis and loss of function of pancreatic ? cells. The present review focuses on how the two main sphingolipid mediators, ceramides and sphingoid base-1-phosphates, regulate the deleterious effects of gluco-lipotoxicity on pancreatic ? cells. The review highlights the role of a sphingolipid biostat on the dysregulation of ? cell fate and function induced by gluco-lipotoxicity, offering the possibility of new therapeutic targets to prevent the onset of T2D.