| Literature DB >> 24998914 |
William P Cawthorn1,2, Erica L Scheller1, Brian S Learman1, Sebastian D Parlee1, Becky R Simon3, Hiroyuki Mori1, Xiaomin Ning1,4, Adam J Bree1, Benjamin Schell1, David T Broome1, Sandra S Soliman1, Jenifer L DelProposto5, Carey N Lumeng1,5, Aditi Mitra6, Sandeep V Pandit6, Katherine A Gallagher7, Joshua D Miller8, Venkatesh Krishnan2, Susanta K Hui9, Miriam A Bredella10, Pouneh K Fazeli11, Anne Klibanski11, Mark C Horowitz12, Clifford J Rosen13, Ormond A MacDougald1,3,14.
Abstract
The adipocyte-derived hormone adiponectin promotes metabolic and cardiovascular health. Circulating adiponectin increases in lean states such as caloric restriction (CR), but the reasons for this paradox remain unclear. Unlike white adipose tissue (WAT), bone marrow adipose tissue (MAT) increases during CR, and both MAT and serum adiponectin increase in many other clinical conditions. Thus, we investigated whether MAT contributes to circulating adiponectin. We find that adiponectin secretion is greater from MAT than WAT. Notably, specific inhibition of MAT formation in mice results in decreased circulating adiponectin during CR despite unaltered adiponectin expression in WAT. Inhibiting MAT formation also alters skeletal muscle adaptation to CR, suggesting that MAT exerts systemic effects. Finally, we reveal that both MAT and serum adiponectin increase during cancer therapy in humans. These observations identify MAT as an endocrine organ that contributes significantly to increased serum adiponectin during CR and perhaps in other adverse states.Entities:
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Year: 2014 PMID： 24998914 PMCID： PMC4126847 DOI： 10.1016/j.cmet.2014.06.003
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287