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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