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PPAR gamma mediates high-fat diet-induced adipocyte hypertrophy and insulin resistance.

Molecular cell | Oct 26, 1999

http://www.ncbi.nlm.nih.gov/pubmed/10549291

Agonist-induced activation of peroxisome proliferator-activated receptor gamma (PPAR gamma) is known to cause adipocyte differentiation and insulin sensitivity. The biological role of PPAR gamma was investigated by gene targeting. Homozygous PPAR gamma-deficient embryos died at 10.5-11.5 dpc due to placental dysfunction. Quite unexpectedly, heterozygous PPAR gamma-deficient mice were protected from the development of insulin resistance due to adipocyte hypertrophy under a high-fat diet. These phenotypes were abrogated by PPAR gamma agonist treatment. Heterozygous PPAR gamma-deficient mice showed overexpression and hypersecretion of leptin despite the smaller size of adipocytes and decreased fat mass, which may explain these phenotypes at least in part. This study reveals a hitherto unpredicted role for PPAR gamma in high-fat diet-induced obesity due to adipocyte hypertrophy and insulin resistance, which requires both alleles of PPAR gamma.

Pubmed ID: 10549291 RIS Download

Mesh terms: Adipocytes | Animals | Blood Glucose | Body Weight | Cell Differentiation | Cell Size | Diet | Eating | Energy Metabolism | Fats | Fetal Viability | Hypoglycemic Agents | Insulin Resistance | Leptin | Mice | Mice, Knockout | Myocardium | Placenta | Receptors, Cytoplasmic and Nuclear | Thiazoles | Thiazolidinediones | Transcription Factors

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