Peroxisome proliferator receptor gamma and the control of glucose metabolism: Insights from knockout mice

NICHOLAS J.G. WEBSTER; MARINA O FERNANDEZ

Molecular Nutrition: Carbohydrates

Academic Press

Lugar: Cambridge, Massachusets; Año: 2019; p. 115 - 125

Summary Points? Whole-body deletion of all PPARγ isoforms causes embryonic lethality.? Mice heterozygous for global PPARγ deletion were viable and were protected from high-fat diet-induced insulin resistance.? Whole-body deletion of the PPARγ2 isoform caused insulin resistance even for mice on a regular diet.? PPARγ deletion in adipose tissue showed that it is required for adipocyte survival and its loss caused lipodystrophy.? Deletion in macrophages predisposed mice to diet-induced obesity and insulin resistance.? When deleted in either the liver or skeletal muscle, animals were prone to glucose intolerance and insulin resistance.? Deletion in neurons had no effect on glucose homeostasis, although animals were protected from obesity-induced leptin resistance.? Astrocyte-specific knockout mice had impaired glucose tolerance and hepatic steatosis that did not worsen with HFD.? The studies reviewed here show that PPARγ acts in many tissues, not only adipose tissue, to regulate glucose metabolism