Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-4-8
pubmed:abstractText
A cDNA encoding a novel fatty acid transport protein (FATP) was identified recently using expression cloning methodologies. We have studied the expression of FATP in differentiating 3T3-L1 cells and adipose tissue in vivo. When 3T3-L1 preadipocytes are treated with a combination of methylisobutylxanthine, dexamethasone, and insulin to induce differentiation, the abundance of FATP mRNA decreases within 24 h to less than one-third that of preadipocytes and increases subsequently, such that mature adipocytes have 5-7 times more FATP mRNA than fibroblastic precursors. In fully differentiated 3T3-L1 adipocytes, insulin alone is sufficient to down-regulate FATP mRNA levels 10-fold. The concentration of insulin necessary for half-maximal repression (I0.5) is approximately 1 nM and is specific for insulin; insulin-like growth factor I (IGF-I) has little effect at similar concentrations. Kinetic analysis indicates that the reduction in expression of FATP mRNA by insulin is rapid (t1/2 = approximately 4 h) and reversible upon withdrawal of insulin. The half-lives of FATP mRNA are 2.9 h and 4.4 h in the absence and presence of insulin, respectively. The insulin-mediated decrease in FATP steady state mRNA level correlates with a decrease in its transcription rate as measured by nuclear run-on transcription assay. To determine whether physiological conditions that alter insulin concentration in vivo affect adipose FATP levels, feeding/fasting studies are employed. Fasting of C57BL/6J mice for 48 h results in an 11-fold up-regulation of FATP mRNA expression in adipose tissue. Refeeding of fasted animals for 72 h results in a return of FATP mRNA to basal levels. In sum, these results indicate that the expression of FATP gene is negatively regulated by insulin at the transcriptional level in cultured adipocytes and that transporter mRNA expression in murine adipose tissue is altered in a manner consistent with insulin being a negative regulator of gene activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1021-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:8843418-1-Methyl-3-isobutylxanthine, pubmed-meshheading:8843418-3T3 Cells, pubmed-meshheading:8843418-Adipocytes, pubmed-meshheading:8843418-Animals, pubmed-meshheading:8843418-Carrier Proteins, pubmed-meshheading:8843418-Cell Differentiation, pubmed-meshheading:8843418-Dexamethasone, pubmed-meshheading:8843418-Fasting, pubmed-meshheading:8843418-Fatty Acid-Binding Proteins, pubmed-meshheading:8843418-Food, pubmed-meshheading:8843418-Gene Expression Regulation, pubmed-meshheading:8843418-Insulin, pubmed-meshheading:8843418-Kinetics, pubmed-meshheading:8843418-Mice, pubmed-meshheading:8843418-Mice, Inbred C57BL, pubmed-meshheading:8843418-Myelin P2 Protein, pubmed-meshheading:8843418-Neoplasm Proteins, pubmed-meshheading:8843418-Nerve Tissue Proteins, pubmed-meshheading:8843418-RNA, Messenger
pubmed:year
1996
pubmed:articleTitle
Regulation of the murine adipocyte fatty acid transporter gene by insulin.
pubmed:affiliation
Whitehead Institute for Biomedical Research, Boston, Massachusetts, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't