Fat-specific transgenic expression of resistin in the spontaneously hypertensive rat impairs fatty acid re-esterification
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
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-zdroje
- MeSH
- adrenalin farmakologie MeSH
- esterifikace MeSH
- geneticky modifikovaná zvířata MeSH
- glukosa metabolismus MeSH
- glycerol metabolismus MeSH
- krysa rodu Rattus MeSH
- kyseliny mastné neesterifikované metabolismus MeSH
- lipolýza účinky léků fyziologie MeSH
- potkani inbrední SHR MeSH
- resistin genetika metabolismus fyziologie MeSH
- tuková tkáň metabolismus MeSH
- tukové buňky metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Názvy látek
- adrenalin MeSH
- glukosa MeSH
- glycerol MeSH
- kyseliny mastné neesterifikované 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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