Source:http://linkedlifedata.com/resource/pubmed/id/11448938
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
14
|
| pubmed:dateCreated |
2001-7-12
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| pubmed:abstractText |
The bHLH-PAS transcription factor SIM1 is required for the development of the paraventricular nucleus (PVN) of the hypothalamus. Mice homozygous for a null allele of Sim1 (Sim1(-/-)) lack a PVN and die perinatally. In contrast, we show here that Sim1 heterozygous mice are viable but develop early-onset obesity, with increased linear growth, hyperinsulinemia and hyperleptinemia. Sim1(+/-) mice are hyperphagic but their energy expenditure is not decreased, distinguishing them from other mouse models of early-onset obesity such as deficiencies in leptin and melanocortin receptor 4. Quantitative histological comparison with normal littermates showed that the PVN of Sim1(+/-) mice contains on average 24% fewer cells without a selective loss of any identifiable major cell type. Since acquired lesions in the PVN also induce increased appetite without a decrease in energy expenditure, we propose that abnormalities of PVN development cause the obesity of Sim1(+/-) mice. Severe obesity was described recently in a patient with a balanced translocation disrupting SIM1. Pathways controlling the development of the PVN thus have the potential to cause obesity in both mice and humans.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Sim1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0964-6906
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
10
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1465-73
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:11448938-Adipose Tissue,
pubmed-meshheading:11448938-Adipose Tissue, Brown,
pubmed-meshheading:11448938-Age Factors,
pubmed-meshheading:11448938-Animals,
pubmed-meshheading:11448938-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:11448938-Body Constitution,
pubmed-meshheading:11448938-Female,
pubmed-meshheading:11448938-Helix-Loop-Helix Motifs,
pubmed-meshheading:11448938-Heterozygote,
pubmed-meshheading:11448938-Hyperphagia,
pubmed-meshheading:11448938-Insulin,
pubmed-meshheading:11448938-Male,
pubmed-meshheading:11448938-Mice,
pubmed-meshheading:11448938-Mice, Inbred Strains,
pubmed-meshheading:11448938-Neurons,
pubmed-meshheading:11448938-Obesity,
pubmed-meshheading:11448938-Paraventricular Hypothalamic Nucleus,
pubmed-meshheading:11448938-Repressor Proteins,
pubmed-meshheading:11448938-Sex Factors,
pubmed-meshheading:11448938-Transcription Factors
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
Sim1 haploinsufficiency causes hyperphagia, obesity and reduction of the paraventricular nucleus of the hypothalamus.
|
| pubmed:affiliation |
Research Center, Hôpital Sainte-Justine, 3175 Côte Sainte-Catherine, Montreal, Quebec, H3T 1C5, Canada. jmichaud@justine.umontreal.ca
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|