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Uncoupling protein 2 and islet function Chan CB; Saleh MC; Koshkin V; Wheeler MBDiabetes 2004[Feb]; 53 Suppl 1 (ä): S136-42Stressors 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.|Animals[MESH]|Diabetes Mellitus, Type 2/genetics/physiopathology[MESH]|Gene Expression Regulation/physiology[MESH]|Humans[MESH]|Insulin Secretion[MESH]|Insulin/genetics/metabolism[MESH]|Ion Channels[MESH]|Islets of Langerhans/*physiology[MESH]|Membrane Transport Proteins/*physiology[MESH]|Mitochondrial Proteins/*physiology[MESH]|Nutritional Physiological Phenomena[MESH]|Reactive Oxygen Species/metabolism[MESH]|Uncoupling Protein 2[MESH] |
