|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
5
|
|
pubmed:dateCreated |
2011-2-1
|
|
pubmed:abstractText |
Glucose-stimulated insulin secretion (GSIS) by pancreatic ? cells is regulated by mitochondrial uncoupling protein-2 (UCP2), but opposing phenotypes, GSIS improvement and impairment, have been reported for different Ucp2-ablated mouse models. By measuring mitochondrial bioenergetics in attached INS-1E insulinoma cells with and without UCP2, we show that UCP2 contributes to proton leak and attenuates glucose-induced rises in both respiratory activity and the coupling efficiency of oxidative phosphorylation. Strikingly, the GSIS improvement seen upon UCP2 knockdown in INS-1E cells is annulled completely by the cell-permeative antioxidant MnTMPyP. Consistent with this observation, UCP2 lowers mitochondrial reactive oxygen species at high glucose levels. We conclude that UCP2 plays both regulatory and protective roles in ? cells by acutely lowering GSIS and chronically preventing oxidative stress. Our findings thus provide a mechanistic explanation for the apparently discrepant findings in the field.
|
|
pubmed:grant |
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-10389858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-10462758,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-10469130,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-11440717,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-11756659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-11780125,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-11890977,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-12011051,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-12401712,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-12525856,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-14592952,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-14679178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-14749279,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-15662004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-16005426,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-16098826,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-16137248,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-17015830,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-17209127,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-17400930,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-17437552,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-17728716,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-17824844,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-18006654,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-18433713,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-18626658,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-18692019,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19073765,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19246534,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19413946,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19426881,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19501608,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19539600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/21172424-19809798
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Mar
|
|
pubmed:issn |
1873-4596
|
|
pubmed:author |
|
|
pubmed:copyrightInfo |
2010 Elsevier Inc. All rights reserved.
|
|
pubmed:issnType |
Electronic
|
|
pubmed:day |
1
|
|
pubmed:volume |
50
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
609-16
|
|
pubmed:dateRevised |
2011-11-17
|
|
pubmed:meshHeading |
pubmed-meshheading:21172424-Animals,
pubmed-meshheading:21172424-Antioxidants,
pubmed-meshheading:21172424-Cell Line, Tumor,
pubmed-meshheading:21172424-Diabetes Mellitus, Type 2,
pubmed-meshheading:21172424-Energy Metabolism,
pubmed-meshheading:21172424-Gene Knockdown Techniques,
pubmed-meshheading:21172424-Glucose,
pubmed-meshheading:21172424-Insulin,
pubmed-meshheading:21172424-Insulin-Secreting Cells,
pubmed-meshheading:21172424-Ion Channels,
pubmed-meshheading:21172424-Metalloporphyrins,
pubmed-meshheading:21172424-Mice,
pubmed-meshheading:21172424-Mitochondria,
pubmed-meshheading:21172424-Mitochondrial Proteins,
pubmed-meshheading:21172424-Rats,
pubmed-meshheading:21172424-Reactive Oxygen Species
|
|
pubmed:year |
2011
|
|
pubmed:articleTitle |
Uncoupling protein-2 attenuates glucose-stimulated insulin secretion in INS-1E insulinoma cells by lowering mitochondrial reactive oxygen species.
|
|
pubmed:affiliation |
Mitochondrial Biology Unit, Medical Research Council, Cambridge CB2 0XY, UK.charles.affourtit@plymouth.ac.uk
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|
