TY - JOUR
T1 - Mechanisms and metabolic implications of regional differences among fat depots
AU - Tchkonia, Tamara
AU - Thomou, Thomas
AU - Zhu, Yi
AU - Karagiannides, Iordanes
AU - Pothoulakis, Charalabos
AU - Jensen, Michael D.
AU - Kirkland, James L.
N1 - Funding Information:
The authors are grateful for the administrative support of L. Wadum and J. Armstrong. This work was funded by NIH grants AG41122 (J.K.), AG13925 (J.K.), AG31736 (J.K.), DK50456 (J.K. and M.D.J.), DK40484 (M.D.J.), DK45343 (M.D.J.), DK47343 (C.P.), DK60729 (C.P.), and DK86150 (C.P.); the Noaber, Ellison, and Broad Medical Foundations; and the Crohn’s and Colitis Foundation of America.
PY - 2013/5/7
Y1 - 2013/5/7
N2 - 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.
AB - 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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U2 - 10.1016/j.cmet.2013.03.008
DO - 10.1016/j.cmet.2013.03.008
M3 - Review article
C2 - 23583168
AN - SCOPUS:84877580638
SN - 1550-4131
VL - 17
SP - 644
EP - 656
JO - Cell Metabolism
JF - Cell Metabolism
IS - 5
ER -