Adipose tissue expandability in the maintenance of metabolic homeostasis

被引：54

作者：

Gray, Sarah L. ^{[1
]}

Vidal-Puig, Antonio J. ^{[1
]}

机构：

[1] Univ Cambridge, Dept Clin Biochem, Cambridge CB2 1TN, England

来源：

NUTRITION REVIEWS | 2007年 / 65卷 / 06期

基金：

英国医学研究理事会;

关键词：

adipokines; adipose tissue; expandability; lipotoxicity; metabolic homeostasis;

D O I：

10.1301/nr.2007.jun.S7-S12

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

Adipose tissue expands to accommodate increased lipid through hypertrophy of existing adipocytes and by initiating differentiation of preadipocytes. The capacity of adipose tissue to expand is critical for accommodating changes in energy availability, but this capacity is not an unlimited process and likely varies between individuals. We suggest that it is not the absolute amount of adipose tissue but rather the capacity of adipose tissue to expand that affects metabolic homeostasis. Here we highlight examples of disease states and transgenic animal models with altered adipose tissue function that support this hypothesis and discuss possible mechanisms by which altered adipose tissue expandability impairs metabolic homeostasis.

引用

页码：S7 / S12

页数：6

共 47 条

[1] PPARγ is required for placental, cardiac, and adipose tissue development [J].

Barak, Y ;

Nelson, MC ;

Ong, ES ;

Jones, YZ ;

Ruiz-Lozano, P ;

Chien, KR ;

Koder, A ;

Evans, RM .

MOLECULAR CELL, 1999, 4 (04) :585-595

[2] Dominant negative mutations in human PPARγ associated with severe insulin resistance, diabetes mellitus and hypertension [J].

Barroso, I ;

Gurnell, M ;

Crowley, VEF ;

Agostini, M ;

Schwabe, JW ;

Soos, MA ;

Maslen, GL ;

Williams, TDM ;

Lewis, H ;

Schafer, AJ ;

Chatterjee, VKK ;

O'Rahilly, S .

NATURE, 1999, 402 (6764) :880-883

[3] Transgenic animal models for the study of adipose tissue biology [J].

Blüher, M .

BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 19 (04) :605-623

[4] Direct metabolic regulation in skeletal muscle and fat tissue by leptin: implications for glucose and fatty acids homeostasis [J].

Ceddia, RB .

INTERNATIONAL JOURNAL OF OBESITY, 2005, 29 (10) :1175-1183

[5] The adipose organ [J].

Cinti, S .

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS, 2005, 73 (01) :9-15

[6] Mechanisms of pancreatic β-cell death in type 1 and type 2 diabetes -: Many differences, few similarities [J].

Cnop, M ;

Welsh, N ;

Jonas, JC ;

Jörns, A ;

Lenzen, S ;

Eizirik, DL .

DIABETES, 2005, 54 :S97-S107

[7] Keystone meeting summary: 'Adipogenesis, obesity, and inflammation' and 'Diabetes mellitus and the control of cellular energy metabolism,' January 21-26, 2006, Vancouver, Canada [J].

Corvera, Silvia ;

Burkart, Alison ;

Kim, Ja-Young ;

Christianson, Jennifer ;

Wang, Zhao ;

Scherer, Philipp E. .

GENES & DEVELOPMENT, 2006, 20 (16) :2193-2201

[8] A dominant negative peroxisome proliferator-activated receptor-γ knock-in mouse exhibits features of the metabolic syndrome [J].

Freedman, BD ;

Lee, EJ ;

Park, Y ;

Jameson, JL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (17) :17118-17125

[9] Lipodystrophies: rare disorders causing metabolic syndrome [J].

Garg, A ;

Misra, A .

ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA, 2004, 33 (02) :305-+

[10] Liver peroxisome proliferator-activated receptor γ contributes to hepatic steatosis, triglyceride clearance, and regulation of body fat mass [J].

Gavrilova, O ;

Haluzik, M ;

Matsusue, K ;

Cutson, JJ ;

Johnson, L ;

Dietz, KR ;

Nicol, CJ ;

Vinson, C ;

Gonzalez, FJ ;

Reitman, ML .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (36) :34268-34276

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