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Uncoupling protein 2 and islet function.

Catherine B Chan·Monique C Saleh·Vasilij Koshkin·Michael B Wheeler
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Abstract

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 posttranslational 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.

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AnimalsDiabetes Mellitus, Type 2Gene Expression RegulationHumansInsulinInsulin SecretionIon ChannelsIslets of LangerhansMembrane Transport ProteinsMitochondrial ProteinsNutritional Physiological PhenomenaReactive Oxygen SpeciesUncoupling Protein 2Journal ArticleResearch Support, Non-U.S. Gov'tReview

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Catherine B Chan, Monique C Saleh, Vasilij Koshkin, Michael B Wheeler. 2004. Uncoupling protein 2 and islet function.. https://doi.org/10.2337/diabetes.53.2007.s136

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