activity in adipose tissue.The studies cannot resolve whether human PPARG mutations in FPLD3 might act in a dominant negative manner to interfere with function of the normal allele product or whether haploinsufficiency of PPARγ activity is more important.Interestingly, simple haploinsufficiency of PPARγ activity in mice by removal of one Pparg allele actually protects against insulin resistance (15), supporting the idea that missense mutations have distinct effects compared with simple reduction in PPARγ.In any event, the findings of Tsai et al. reinforce the importance of PPARγ in adipogenesis (4), highlight the role of adipose tissue as an endocrine organ (16), and also support the idea that PPARG mutations affect metabolic and vascular phenotypes through multiple mechanisms, some of which are distinct from effects on adipose tissue mass or distribution.
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Strieter et al. (2004) studied this question.
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