Fat-specific transgenic expression of resistin in the spontaneously hypertensive rat impairs fatty acid re-esterification
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
HL63709
NHLBI NIH HHS - United States
TW01236
FIC NIH HHS - United States
PubMed
16432541
DOI
10.1038/sj.ijo.0803237
PII: 0803237
Knihovny.cz E-resources
- MeSH
- Epinephrine pharmacology MeSH
- Esterification MeSH
- Animals, Genetically Modified MeSH
- Glucose metabolism MeSH
- Glycerol metabolism MeSH
- Rats MeSH
- Fatty Acids, Nonesterified metabolism MeSH
- Lipolysis drug effects physiology MeSH
- Rats, Inbred SHR MeSH
- Resistin genetics metabolism physiology MeSH
- Adipose Tissue metabolism MeSH
- Adipocytes metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Names of Substances
- Epinephrine MeSH
- Glucose MeSH
- Glycerol MeSH
- Fatty Acids, Nonesterified MeSH
- Resistin MeSH
OBJECTIVE: To investigate the mechanism by which fat-specific transgenic expression of resistin affects fatty acid metabolism in the spontaneously hypertensive rat (SHR). DESIGN: Basal- and adrenaline-stimulated lipolysis, basal- and insulin-stimulated lipogenesis as well as the site (glycerol versus acyl moiety) of glucose incorporated into triglycerides were determined in adipose tissue isolated from SHR-Resistin transgenic and SHR control rats. RESULTS: A moderate expression of transgenic resistin in adipose tissue was associated with significant increase in the FFA/glycerol ratio during adrenaline-stimulated lipolysis in the SHR-Resistin transgenic rats (3.27+/-0.26) compared to SHR controls (2.11+/-0.10, P=0.0005). Transgenic SHR also exhibited a significant decrease in FFA re-esterification in adipose tissue (approximately by 23%). CONCLUSION: These findings raise the possibility that the prodiabetic effects of transgenic resistin may be partly mediated by increased FFA release from adipose tissue due to impaired FFA re-esterification in adipocytes.
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