Gluteofemoral Adipose Tissue Plays a Major Role in Production of the Lipokine Palmitoleate in Humans
- Katherine E. Pinnick1,
- Matt J. Neville1,
- Barbara A. Fielding1,2,
- Keith N. Frayn1,
- Fredrik Karpe1,3⇓ and
- Leanne Hodson1⇓
- 1Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), University of Oxford, Oxford, U.K.
- 2Postgraduate Medical School, University of Surrey, Surrey, U.K.
- 3National Institute for Health and Research Oxford Biomedical Research Centre, Oxford Radcliffe Hospitals Trust, Oxford, U.K.
- Corresponding author: Leanne Hodson, , or Fredrik Karpe, .
K.E.P. and M.J.N. contributed equally to this work.
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.
- Received December 22, 2011.
- Accepted February 15, 2012.
- © 2012 by the American Diabetes Association.
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