| pubmed-article:17824844 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C0021670 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C0536847 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C0033727 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C1256369 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:17824844 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:17824844 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17824844 | pubmed:dateCreated | 2007-12-7 | lld:pubmed |
| pubmed-article:17824844 | pubmed:abstractText | Proton leak exerts stronger control over ATP/ADP in mitochondria from clonal pancreatic beta-cells (INS-1E) than in those from rat skeletal muscle, due to the higher proton conductance of INS-1E mitochondria [Affourtit and Brand (2006) Biochem. J. 393, 151-159]. In the present study, we demonstrate that high proton leak manifests itself at the cellular level too: the leak rate (measured as myxothiazol-sensitive, oligomycin-resistant respiration) was nearly four times higher in INS-1E cells than in myoblasts. This relatively high leak activity was decreased more than 30% upon knock-down of UCP2 (uncoupling protein-2) by RNAi (RNA interference). The high contribution of UCP2 to leak suggests that proton conductance through UCP2 accounts for approx. 20% of INS-1E respiration. UCP2 knock-down enhanced GSIS (glucose-stimulated insulin secretion), consistent with a role for UCP2 in beta-cell physiology. We propose that the high mitochondrial proton leak in beta-cells is a mechanism which amplifies the effect of physiological UCP2 regulators on cytoplasmic ATP/ADP and hence on insulin secretion. | lld:pubmed |
| pubmed-article:17824844 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17824844 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17824844 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17824844 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17824844 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17824844 | pubmed:issn | 1470-8728 | lld:pubmed |
| pubmed-article:17824844 | pubmed:author | pubmed-author:AffourtitChar... | lld:pubmed |
| pubmed-article:17824844 | pubmed:author | pubmed-author:BrandMartin... | lld:pubmed |
| pubmed-article:17824844 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17824844 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17824844 | pubmed:volume | 409 | lld:pubmed |
| pubmed-article:17824844 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17824844 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17824844 | pubmed:pagination | 199-204 | lld:pubmed |
| pubmed-article:17824844 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:17824844 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17824844 | pubmed:articleTitle | Uncoupling protein-2 contributes significantly to high mitochondrial proton leak in INS-1E insulinoma cells and attenuates glucose-stimulated insulin secretion. | lld:pubmed |
| pubmed-article:17824844 | pubmed:affiliation | MRC Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 0XY, UK. ca@mrc-dunn.cam.ac.uk | lld:pubmed |
| pubmed-article:17824844 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17824844 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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