On the role of uncoupling protein-2 in pancreatic beta cells.

TitleOn the role of uncoupling protein-2 in pancreatic beta cells.
Publication TypeJournal Article
Year of Publication2008
AuthorsAffourtit, C, Brand, MD
JournalBiochim Biophys Acta
Volume1777
Issue7-8
Pagination973-9
Date Published2008 Jul-Aug
ISSN0006-3002
KeywordsBlood Glucose, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Secretion, Insulin-Secreting Cells, Ion Channels, Mitochondria, Mitochondrial Proteins, Models, Biological, Oxidative Phosphorylation, Oxygen Consumption, Uncoupling Protein 2
Abstract

Pancreatic beta cells secrete insulin when blood glucose levels are high. Dysfunction of this glucose-stimulated insulin secretion (GSIS) is partly responsible for the manifestation of type 2 diabetes, a metabolic disorder that is rapidly becoming a global pandemic. Mitochondria play a central role in GSIS by coupling glucose oxidation to production of ATP, a signal that triggers a series of events that ultimately leads to insulin release. Beta cells express a mitochondrial uncoupling protein, UCP2, which is rather surprising as activity of such a protein is anticipated to lower the efficiency of oxidative phosphorylation, and hence to impair GSIS. The mounting evidence demonstrating that insulin secretion is indeed blunted by UCP2 agrees with this prediction, and has provoked the idea that UCP2 activity contributes to beta cell pathogenesis and development of type 2 diabetes. Although this notion may be correct, the evolved function of UCP2 remains unclear. With this paper we aim to provide a brief account of the present state of affairs in this field, suggest a physiological role for UCP2, and highlight some of our own recent results.

DOI10.1016/j.bbabio.2008.03.022
Alternate JournalBiochim. Biophys. Acta
Citation Key10.1016/j.bbabio.2008.03.022
PubMed ID18433713
Grant ListMC_U105663137 / / Medical Research Council / United Kingdom