Journal
CELL METABOLISM
Volume 17, Issue 5, Pages 644-656Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2013.03.008
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Funding
- NIH [AG41122, AG13925, AG31736, DK50456, DK40484, DK45343, DK47343, DK60729, DK86150]
- Noaber Medical Foundation
- Ellison Medical Foundation
- Broad Medical Foundation
- Crohn's and Colitis Foundation of America
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Fat distribution is closely linked to metabolic disease risk. Distribution varies with sex, genetic background, disease state, certain drugs and hormones, development, and aging. Preadipocyte replication and differentiation, developmental gene expression, susceptibility to apoptosis and cellular senescence, vascularity, inflammatory cell infiltration, and adipokine secretion vary among depots, as do fatty-acid handling and mechanisms of enlargement with positive-energy and loss with negative-energy balance. How interdepot differences in these molecular, cellular, and pathophysiological properties are related is incompletely understood. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.
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