Figure 2.

Relationship between Lipodystrophy and Adipose Tissue Inflammation. In adipocytes, lipid metabolism is well balanced by several genes, including Srebp1c, Atgl, Hsl, Cgi-58, Plin1, and Fsp27. However, lean subjects with lipodystrophy show dysregulated lipid metabolism with increased inflammation and insulin resistance. Evidence suggests that dysregulation of lipid metabolism could influence adipose tissue inflammation in lipodystrophy. aP2-nuclear form of SREBP1c transgenic (aP2-nSREBP1c Tg) mice and Caveolin1 KO mice show significantly reduced fat mass and display metabolic dysregulation including insulin resistance and dyslipidemia. In addition, Plin1 deficiency induces partial fat loss, leakage of FFAs, ATM accumulation, dyslipidemia and systemic insulin resistance. In these lipodystrophic models, several lipid metabolites such as FFA and PGE2 recruit monocytes into adipose tissue and worsen adipose tissue inflammation.