Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
2002-5-28
pubmed:abstractText
Obesity is a common nutritional problem often associated with diabetes, insulin resistance, and fatty liver (excess fat deposition in liver). Leptin-deficient Lep(ob)/Lep(ob) mice develop obesity and those obesity-related syndromes. Increased lipogenesis in both liver and adipose tissue of these mice has been suggested. We have previously shown that the transcription factor sterol regulatory element-binding protein-1 (SREBP-1) plays a crucial role in the regulation of lipogenesis in vivo. To explore the possible involvement of SREBP-1 in the pathogenesis of obesity and its related syndromes, we generated mice deficient in both leptin and SREBP-1. In doubly mutant Lep(ob/ob) x Srebp-1(-/-) mice, fatty livers were markedly attenuated, but obesity and insulin resistance remained persistent. The mRNA levels of lipogenic enzymes such as fatty acid synthase were proportional to triglyceride accumulation in liver. In contrast, the mRNA abundance of SREBP-1 and lipogenic enzymes in the adipose tissue of Lep(ob)/Lep(ob) mice was profoundly decreased despite sustained fat, which could explain why the SREBP-1 disruption had little effect on obesity. In conclusion, SREBP-1 regulation of lipogenesis is highly involved in the development of fatty livers but does not seem to be a determinant of obesity in Lep(ob)/Lep(ob) mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
19353-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11923308-Adipose Tissue, pubmed-meshheading:11923308-Animals, pubmed-meshheading:11923308-Blotting, Northern, pubmed-meshheading:11923308-CCAAT-Enhancer-Binding Proteins, pubmed-meshheading:11923308-Crosses, Genetic, pubmed-meshheading:11923308-DNA-Binding Proteins, pubmed-meshheading:11923308-Fatty Liver, pubmed-meshheading:11923308-Genotype, pubmed-meshheading:11923308-Insulin Resistance, pubmed-meshheading:11923308-Leptin, pubmed-meshheading:11923308-Lipid Metabolism, pubmed-meshheading:11923308-Lipoprotein Lipase, pubmed-meshheading:11923308-Liver, pubmed-meshheading:11923308-Mice, pubmed-meshheading:11923308-Mice, Inbred C57BL, pubmed-meshheading:11923308-Mice, Transgenic, pubmed-meshheading:11923308-Obesity, pubmed-meshheading:11923308-Phenotype, pubmed-meshheading:11923308-RNA, Messenger, pubmed-meshheading:11923308-Sterol Regulatory Element Binding Protein 1, pubmed-meshheading:11923308-Transcription Factors, pubmed-meshheading:11923308-Triglycerides
pubmed:year
2002
pubmed:articleTitle
Absence of sterol regulatory element-binding protein-1 (SREBP-1) ameliorates fatty livers but not obesity or insulin resistance in Lep(ob)/Lep(ob) mice.
pubmed:affiliation
Department of Internal Medicine, University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't