Gluteofemoral adipose tissue plays a major role in production of the lipokine palmitoleate in humans.
Pinnick, KE, Neville, MJ, Fielding, BA, Frayn, KN, Karpe, F and Hodson, L (2012) Gluteofemoral adipose tissue plays a major role in production of the lipokine palmitoleate in humans. Diabetes, 61 (6). pp. 1399-1403.
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The expansion of lower-body adipose tissue (AT) is paradoxically associated with reduced cardiovascular disease and diabetes risk. We examined whether the beneficial metabolic properties of lower-body AT are related to the production and release of the insulin-sensitizing lipokine palmitoleate (16:1n-7). Using venoarterial difference sampling, we investigated the relative release of 16:1n-7 from lower-body (gluteofemoral) and upper-body (abdominal subcutaneous) AT depots. Paired gluteofemoral and abdominal subcutaneous AT samples were analyzed for triglyceride fatty acid composition and mRNA expression. Finally, the triglyceride fatty acid composition of isolated human preadipocytes was determined. Relative release of 16:1n-7 was markedly higher from gluteofemoral AT compared with abdominal subcutaneous AT. Stearoyl-CoA desaturase 1 (SCD1), the key enzyme involved in endogenous 16:1n-7 production, was more highly expressed in gluteofemoral AT and was associated with greater enrichment of 16:1n-7. Furthermore, isolated human preadipocytes from gluteofemoral AT displayed a higher content of SCD1-derived fatty acids. We demonstrate that human gluteofemoral AT plays a major role in determining systemic concentrations of the lipokine palmitoleate. Moreover, this appears to be an inherent feature of gluteofemoral AT. We propose that the beneficial metabolic properties of lower-body AT may be partly explained by the intrinsically greater production and release of palmitoleate.
|Divisions :||Faculty of Health and Medical Sciences > School of Biosciences and Medicine > Department of Nutritional Sciences|
|Date :||June 2012|
|Identification Number :||https://doi.org/10.2337/db11-1810|
|Additional Information :||This is an author-created, uncopyedited electronic version of an article accepted for publication in Diabetes. The American Diabetes Association (ADA), publisher of Diabetes, is not responsible for any errors or omissions in this version of the manuscript or any version derived from it by third parties. The definitive publisher-authenticated version will be available in a future issue of Diabetes in print and online at http://diabetes.diabetesjournals.org.|
|Depositing User :||Symplectic Elements|
|Date Deposited :||15 Aug 2012 14:47|
|Last Modified :||23 Sep 2013 19:35|
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