期刊
CELL
卷 105, 期 6, 页码 745-755出版社
CELL PRESS
DOI: 10.1016/S0092-8674(01)00378-6
关键词
-
资金
- NIDDK NIH HHS [DK57521, T32 DK07533, R01 DK040936, R01-DK53477, R37 DK053477, DK46200] Funding Source: Medline
B cells sense glucose through its metabolism and the resulting increase in ATP, which subsequently stimulates insulin secretion. Uncoupling protein-2 (UCP2) mediates mitochondrial proton leak, decreasing ATP production. In the present study, we assessed UCP2's role in regulating insulin secretion. UCP2-deficient mice had higher islet ATP levels and increased glucose-stimulated insulin secretion, establishing that UCP2 negatively regulates insulin secretion. Of pathophysiologic significance, UCP2 was markedly upregulated in islets of ob/ob mice, a model of obesity-induced diabetes. Importantly, ob/ob mice lacking UCP2 had restored first-phase insulin secretion, increased serum insulin levels, and greatly decreased levels of glycemia. These results establish UCP2 as a key component of beta cell glucose sensing, and as a critical link between obesity, B cell dysfunction, and type 2 diabetes.
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