详细记录  
题名:The fractalkine/CX3CR1 system regulates beta cell function and insulin secretion.
作者:LEE YS; MORINAGA H; KIM JJ; LAGAKOS W; TAYLOR S; KESHWANI M; PERKINS G; DONG H; KAYALI AG; SWEET IR; OLEFSKY J;
来源:Cell. 2013 Apr 11;153(2):413-25. doi: 10.1016/j.cell.2013.03.001. [ IF= 32.40 ] ]
URL :10.1016/j.cell.2013.03.001
日期:20130430
摘要:Here, we demonstrate that the fractalkine (FKN)/CX3CR1 system represents a
regulatory mechanism for pancreatic islet beta cell function and insulin
secretion. CX3CR1 knockout (KO) mice exhibited a marked defect in glucose and
GLP1-stimulated insulin secretion, and this defect was also observed in vitro in
isolated islets from CX3CR1 KO mice. In vivo administration of FKN improved
glucose tolerance with an increase in insulin secretion. In vitro treatment of
islets with FKN increased intracellular Ca(2+) and potentiated insulin secretion
in both mouse and human islets. The KO islets exhibited reduced expression of a
set of genes necessary for the fully functional, differentiated beta cell state,
whereas treatment of wild-type (WT) islets with FKN led to increased expression
of these genes. Lastly, expression of FKN in islets was decreased by aging and
high-fat diet/obesity, suggesting that decreased FKN/CX3CR1 signaling could be a
mechanism underlying beta cell dysfunction in type 2 diabetes.

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