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Cell Metab. 2013 May 7;17(5):644-656. doi: 10.1016/j.cmet.2013.03.008. Epub 2013 Apr 11.

Mechanisms and metabolic implications of regional differences among fat depots.

Author information

1
Robert and Arlene Kogod Center on Aging.
2
Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
3
Inflammatory Bowel Disease Center, Division of Digestive Diseases, Department of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA.
4
Endocrine Research Unit Mayo Clinic, Rochester, MN 55905, USA.
#
Contributed equally

Abstract

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.

PMID:
23583168
PMCID:
PMC3942783
DOI:
10.1016/j.cmet.2013.03.008
[Indexed for MEDLINE]
Free PMC Article

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