Fat-specific transgenic expression of resistin in the spontaneously hypertensive rat impairs fatty acid re-esterification
M Pravenec, L Kazdová, M Cahová, V Landa… - International journal of …, 2006 - nature.com
M Pravenec, L Kazdová, M Cahová, V Landa, V Zidek, P Mlejnek, J Wang, N Qi, TW Kurtz
International journal of obesity, 2006•nature.comObjective: 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 …
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 …
Abstract
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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