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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0025921,
umls-concept:C0026809,
umls-concept:C0028754,
umls-concept:C0185117,
umls-concept:C0299583,
umls-concept:C0443199,
umls-concept:C0542341,
umls-concept:C0851285,
umls-concept:C1510707,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2000-8-31
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pubmed:abstractText |
Obesity-resistant (A/J) and obesity-prone (C57BL/6J) mice were weaned onto low-fat (LF) or high-fat (HF) diets and studied after 2, 10, and 16 wk. Despite consuming the same amount of food, A/J mice on the HF diet deposited less carcass lipid and gained less weight than C57BL/6J mice over the course of the study. Leptin mRNA was increased in white adipose tissue (WAT) in both strains on the HF diet but to significantly higher levels in A/J compared with C57BL/6J mice. Uncoupling protein 1 (UCP1) and UCP2 mRNA were induced by the HF diet in brown adipose tissue (BAT) and WAT of A/J mice, respectively, but not in C57BL/6J mice. UCP1 mRNA was also significantly higher in retroperitoneal WAT of A/J compared with C57BL/6J mice. The ability of A/J mice to resist diet-induced obesity is associated with a strain-specific increase in leptin, UCP1, and UCP2 expression in adipose tissue. The findings indicate that the HF diet does not compromise leptin-dependent regulation of adipocyte gene expression in A/J mice and suggest that maintenance of leptin responsiveness confers resistance to diet-induced obesity.
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pubmed:grant |
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pubmed:commentsCorrections |
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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/Dietary Fats,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 2,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 3
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0193-1849
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
279
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E356-65
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10913036-Adipose Tissue,
pubmed-meshheading:10913036-Adipose Tissue, Brown,
pubmed-meshheading:10913036-Animals,
pubmed-meshheading:10913036-Body Weight,
pubmed-meshheading:10913036-Carrier Proteins,
pubmed-meshheading:10913036-Dietary Fats,
pubmed-meshheading:10913036-Eating,
pubmed-meshheading:10913036-Energy Intake,
pubmed-meshheading:10913036-Gene Expression,
pubmed-meshheading:10913036-Growth,
pubmed-meshheading:10913036-Ion Channels,
pubmed-meshheading:10913036-Leptin,
pubmed-meshheading:10913036-Membrane Proteins,
pubmed-meshheading:10913036-Membrane Transport Proteins,
pubmed-meshheading:10913036-Mice,
pubmed-meshheading:10913036-Mice, Inbred A,
pubmed-meshheading:10913036-Mice, Inbred C57BL,
pubmed-meshheading:10913036-Mitochondrial Proteins,
pubmed-meshheading:10913036-Obesity,
pubmed-meshheading:10913036-Proteins,
pubmed-meshheading:10913036-RNA, Messenger,
pubmed-meshheading:10913036-Species Specificity
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pubmed:year |
2000
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pubmed:articleTitle |
Differential regulation of leptin expression and function in A/J vs. C57BL/6J mice during diet-induced obesity.
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pubmed:affiliation |
Departments of Medicine and Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
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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