The Fractalkine/CX3CR1 System Regulates beta Cell Function and Insulin Secretion

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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 Ca2+ 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 b 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 b cell dysfunction in type 2 diabetes.
Publisher
CELL PRESS
Issue Date
2013-04
Language
English
Article Type
Article
Keywords

NECROSIS-FACTOR-ALPHA; PANCREATIC-ISLETS; CHEMOKINE FRACTALKINE; GENE-EXPRESSION; IN-VITRO; MICE; INFLAMMATION; RESISTANCE; ADHESION; GLUCOSE

Citation

CELL, v.153, no.2, pp.413 - 425

ISSN
0092-8674
DOI
10.1016/j.cell.2013.03.001
URI
http://hdl.handle.net/10203/198366
Appears in Collection
MSE-Journal Papers(저널논문)
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