pubmed-article:17438340 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0243192 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0166415 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0011847 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
pubmed-article:17438340 | lifeskim:mentions | umls-concept:C0087079 | lld:lifeskim |
pubmed-article:17438340 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:17438340 | pubmed:dateCreated | 2007-6-21 | lld:pubmed |
pubmed-article:17438340 | pubmed:abstractText | Peroxisome proliferator-activated receptor alpha (PPAR alpha) is a transcriptional regulator of the expression of mitochondrial thioesterase I (MTE-I) and uncoupling protein 3 (UCP3), which are induced in the heart at the mRNA level in response to diabetes. Little is known about the regulation of protein expression of MTE-I and UCP3 or about MTE-I activity; thus, we investigated the effects of diabetes and treatment with a PPAR alpha agonist on these parameters. Rats were either made diabetic with streptozotocin (55 mg/kg ip) and maintained for 10-14 days or treated with the PPAR alpha agonist fenofibrate (300 mg/kg/day) for 4 weeks. MTE-I and UCP3 protein expression, MTE-1 activity, palmitate export, and oxidative phosphorylation were measured in isolated cardiac mitochondria. Diabetes and fenofibrate increased cardiac MTE-I mRNA, protein, and activity ( approximately 4-fold compared with controls). This increase in activity was matched by a 6-fold increase in palmitate export in fenofibrate-treated animals, despite there being no effect in either group on UCP3 protein expression. Both diabetes and fenofibrate caused significant decreases in state III respiration of isolated mitochondria with pyruvate + malate as the substrate, but only diabetes reduced state III rates with palmitoylcarnitine. Both diabetes and specific PPAR alpha activation increased MTE-I protein, activity, and palmitate export in the heart, with little effect on UCP3 protein expression. | lld:pubmed |
pubmed-article:17438340 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:language | eng | lld:pubmed |
pubmed-article:17438340 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17438340 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17438340 | pubmed:month | Jul | lld:pubmed |
pubmed-article:17438340 | pubmed:issn | 0022-2275 | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:Moodley-Kunni... | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:AlexsonStefan... | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:StanleyWillia... | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:KernerJanosJ | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:YoungMartin... | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:HuangHazelH | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:KingKristen... | lld:pubmed |
pubmed-article:17438340 | pubmed:author | pubmed-author:O'SheaKaren... | lld:pubmed |
pubmed-article:17438340 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17438340 | pubmed:volume | 48 | lld:pubmed |
pubmed-article:17438340 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17438340 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17438340 | pubmed:pagination | 1511-7 | lld:pubmed |
pubmed-article:17438340 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:17438340 | pubmed:meshHeading | pubmed-meshheading:17438340... | lld:pubmed |
pubmed-article:17438340 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17438340 | pubmed:articleTitle | Diabetes or peroxisome proliferator-activated receptor alpha agonist increases mitochondrial thioesterase I activity in heart. | lld:pubmed |
pubmed-article:17438340 | pubmed:affiliation | Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106, USA. | lld:pubmed |
pubmed-article:17438340 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17438340 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:192272 | entrezgene:pubmed | pubmed-article:17438340 | lld:entrezgene |
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