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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2002-8-1
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pubmed:abstractText |
Mice with a targeted null mutation of the serotonin 5-HT(2C) receptor gene exhibit hyperphagia that leads to a late-onset obesity. Here we show that oxygen consumption was decreased in fed and fasted obese mutants. No phenotypic differences were observed in uncoupling protein-1 (UCP-1) mRNA levels in brown adipose tissues and UCP-3 mRNA in skeletal muscle. UCP-2 mRNA levels were significantly increased in white adipose tissue (4-fold) and skeletal muscle (47%) in older obese mutant mice, whereas UCP-2 mRNA in liver are significantly increased in both young lean (54% increase) and older obese (52% increase) mutant mice. In contrast, 5-HT(2C) receptor mutants displayed age-dependent decreases in beta 3-adrenergic receptor (beta 3-AR) mRNA levels in white adipose tissue, however, no such changes were observed in brown adipose tissue. These results indicate that a mutation of 5-HT(2C) receptor gene leads to a secondary decrease in beta 3-AR gene expression that is related to enhanced adiposity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Serotonin, 5-HT2C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein,
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 |
0006-291X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
12
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pubmed:volume |
295
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
249-54
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12150939-Animals,
pubmed-meshheading:12150939-Base Sequence,
pubmed-meshheading:12150939-Carrier Proteins,
pubmed-meshheading:12150939-DNA Primers,
pubmed-meshheading:12150939-Energy Metabolism,
pubmed-meshheading:12150939-Gene Expression,
pubmed-meshheading:12150939-Hyperphagia,
pubmed-meshheading:12150939-Ion Channels,
pubmed-meshheading:12150939-Membrane Proteins,
pubmed-meshheading:12150939-Mice,
pubmed-meshheading:12150939-Mice, Mutant Strains,
pubmed-meshheading:12150939-Mitochondrial Proteins,
pubmed-meshheading:12150939-Obesity,
pubmed-meshheading:12150939-Oxygen Consumption,
pubmed-meshheading:12150939-RNA, Messenger,
pubmed-meshheading:12150939-Receptor, Serotonin, 5-HT2C,
pubmed-meshheading:12150939-Receptors, Adrenergic, beta-3,
pubmed-meshheading:12150939-Receptors, Serotonin
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pubmed:year |
2002
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pubmed:articleTitle |
Altered gene expressions involved in energy expenditure in 5-HT(2C) receptor mutant mice.
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pubmed:affiliation |
Department of Psychiatry and Center for Neurobiology and Psychiatry, University of California, San Francisco, CA 94143, USA. nonogaki@med.nagoya-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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