Uncoupling protein 2 and islet function
Uncoupling protein 2 and islet function
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DOI：
10.2337/diabetes.53.2007.s136
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发表时间：
2004-02-01
期刊：
影响因子：
7.7
通讯作者：
Wheeler, MB
中科院分区：
文献类型：
--
作者：
Chan, CB;Saleh, MC;Wheeler, MB
Stressors such as chronic hyperglycemia or hyperlipidemia may lead to insufficient insulin secretion in susceptible individuals, contributing to type 2 diabetes; The molecules mediating this effect are just beginning to be identified. Uncoupling protein (UCP)-2 may be one such negative modulator of insulin secretion. Accumulating evidence shows that beta-cell UCP2 expression is upregulated by glucolipotoxic conditions and that increased activity of UCP2 decreases insulin secretion. Mitochondrial superoxide has been identified as a post-translational regulator of UCP2 activity in islets; thus, UCP2 may provide protection to beta-cells at one level while simultaneously having detrimental effects on insulin secretion. Interestingly, the latter appears to be the dominant outcome, because UCP2 knockout mice display an increased beta-cell mass and retained insulin secretion capacity in the face of glucolipotoxicity.
