Source:http://linkedlifedata.com/resource/pubmed/id/17438340
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2007-6-21
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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.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Fenofibrate,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PPAR alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Palmitic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Palmitoyl-CoA Hydrolase,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 3
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-2275
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1511-7
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:17438340-Animals,
pubmed-meshheading:17438340-Diabetes Mellitus, Experimental,
pubmed-meshheading:17438340-Fenofibrate,
pubmed-meshheading:17438340-Ion Channels,
pubmed-meshheading:17438340-Male,
pubmed-meshheading:17438340-Mitochondria, Heart,
pubmed-meshheading:17438340-Mitochondrial Proteins,
pubmed-meshheading:17438340-Oxygen Consumption,
pubmed-meshheading:17438340-PPAR alpha,
pubmed-meshheading:17438340-Palmitic Acid,
pubmed-meshheading:17438340-Palmitoyl-CoA Hydrolase,
pubmed-meshheading:17438340-RNA, Messenger,
pubmed-meshheading:17438340-Rats,
pubmed-meshheading:17438340-Rats, Wistar
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pubmed:year |
2007
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pubmed:articleTitle |
Diabetes or peroxisome proliferator-activated receptor alpha agonist increases mitochondrial thioesterase I activity in heart.
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pubmed:affiliation |
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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