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Fat-specific transgenic expression of resistin in the spontaneously hypertensive rat impairs fatty acid re-esterification

M Pravenec, L Kazdova, M Cahova, V Landa, V Zidek, P Mlejnek, M Simakova, J Wang, N Qi, TW Kurtz

. 2006 ; 30 (7) : 1157-1159.

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc13021023

Grantová podpora
NB7403 MZ0 CEP - Centrální evidence projektů

Digitální knihovna NLK
Plný text - Část
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Odkazy

PubMed 16432541
DOI 10.1038/sj.ijo.0803237
Knihovny.cz E-zdroje

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.

Citace poskytuje Crossref.org

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