Mechanisms and Metabolic Implications of Regional Differences among Fat Depots

被引：525

作者：

Tchkonia, Tamara ^{[1
]}

Thomou, Thomas ^{[3
]}

Zhu, Yi ^{[1
]}

Karagiannides, Iordanes ^{[4
]}

Pothoulakis, Charalabos ^{[4
]}

Jensen, Michael D. ^{[2
]}

Kirkland, James L. ^{[1
]}

机构：

[1] Mayo Clin, Robert & Arlene Kogod Ctr Aging, Rochester, MN 55905 USA

[2] Mayo Clin, Endocrine Res Unit, Rochester, MN 55905 USA

[3] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA

[4] Univ Calif Los Angeles, Inflammatory Bowel Dis Ctr, Dept Med, Div Digest Dis, Los Angeles, CA 90095 USA

来源：

CELL METABOLISM | 2013年 / 17卷 / 05期

关键词：

HUMAN ADIPOSE-TISSUE; ACTIVATED RECEPTOR-GAMMA; GENE-EXPRESSION; BODY-FAT; INSULIN-RESISTANCE; SUBCUTANEOUS FAT; ACID-METABOLISM; VISCERAL FAT; SUBSTANCE-P; ADIPOCYTE DIFFERENTIATION;

D O I：

10.1016/j.cmet.2013.03.008

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：644 / 656

页数：13

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