TY - JOUR
T1 - PPARγ
T2 - A critical determinant of body fat distribution in humans and mice
AU - Tsai, Yau Sheng
AU - Maeda, Nobuyo
N1 - Funding Information:
The authors thank Drs Raymond Givens, Nobuyuki Takahashi, Leighton James, and Terry Combs for critical reading and comments, and Dr Pei-Jane Tsai and Huei-Ru Tsai for the help in Figure 1 . This work was supported by grants from the National Institutes of Health to N. Maeda (HL42630 and HL70523) and the American Heart Association to Y.S. Tsai (0215270U).
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2005/4
Y1 - 2005/4
N2 - Evidence emerging from studies of humans and mice has indicated peroxisome proliferator-activated receptor γ (PPARγ) to be not only a key factor for adipogenesis but also a critical determinant of body fat distribution. Whereas genetically reduced PPARγ activity in adipose tissue leads to reduction of total fat mass in humans and in mice, mutations in the ligand-binding domain of PPARγ cause abnormal body fat distributions. It is less clear from mutation analysis how PPARγ is involved in metabolic disturbances such as insulin resistance and its cardiovascular complications. Nevertheless, similarities and differences in the phenotypes associated with PPARγ mutations in humans and in mouse models provide opportunities to dissect relationships between body fat distribution and its metabolic complications.
AB - Evidence emerging from studies of humans and mice has indicated peroxisome proliferator-activated receptor γ (PPARγ) to be not only a key factor for adipogenesis but also a critical determinant of body fat distribution. Whereas genetically reduced PPARγ activity in adipose tissue leads to reduction of total fat mass in humans and in mice, mutations in the ligand-binding domain of PPARγ cause abnormal body fat distributions. It is less clear from mutation analysis how PPARγ is involved in metabolic disturbances such as insulin resistance and its cardiovascular complications. Nevertheless, similarities and differences in the phenotypes associated with PPARγ mutations in humans and in mouse models provide opportunities to dissect relationships between body fat distribution and its metabolic complications.
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U2 - 10.1016/j.tcm.2005.04.002
DO - 10.1016/j.tcm.2005.04.002
M3 - Review article
C2 - 16039966
AN - SCOPUS:22544450826
SN - 1050-1738
VL - 15
SP - 81
EP - 85
JO - Trends in Cardiovascular Medicine
JF - Trends in Cardiovascular Medicine
IS - 3
ER -