Lipoatrophy and Severe Metabolic Disturbance in Mice with Fat-Specific Deletion of PPARγ

    Fenfen Wang, Shannon E. Mullican, Joanna R. DiSpirito, Lindsey C. Peed, Mitchell A. Lazar
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    TLDR Mice lacking the PPARγ gene in their fat cells had almost no fat tissue, severe metabolic problems, and abnormal development of other fat-related tissues.
    In the 2013 study, researchers found that mice with a fat-specific deletion of the PPARγ gene exhibited severe lipoatrophy, almost completely lacking both brown and white adipose tissue by 3 months of age, and suffered from severe metabolic disturbances, including insulin resistance. The PPARγ FKO mice also had delayed hair coat formation, disrupted mammary gland development, and high bone mass, highlighting the importance of adipose PPARγ in the development and function of fat-related tissues. Measurements supporting these findings included serum leptin, resistin, and adiponectin levels, liver weights, blood glucose, and insulin levels, with sample sizes ranging from 3 to 7 mice. The study concluded that adipocyte PPARγ is essential for the formation of healthy fat cells and plays a critical role in regulating the development of multiple tissues.
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