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Symbol PPARG contributors: mct/shn - updated : 12-01-2019
HGNC name peroxisome proliferative-activated receptor, gamma
HGNC id 9236
  • mouse PPAR gamma gene knockout leads to severe myocardial thinning and death by E10.0
  • Homozygous PPAR gamma-deficient embryos died at 10.5-11.5 dpc due to placental dysfunction
  • Heterozygous PPAR gamma-deficient mice showed overexpression and hypersecretion of leptin despite the smaller size of adipocytes and decreased fat mass
  • mice chimeric for wild-type and PPAR gamma null cells show little or no contribution of null cells to adipose tissue
  • PPAR-gamma(+/-) mice display no statistically significant differences in body weight, basal glucose, insulin, or FFA levels compared to wild-type
  • insulin-induced increase in glucose disposal rate was significantly increased and insulin-induced suppression of hepatic glucose production was significantly greater in the PPAR-gamma(+/-) mice
  • Pparg mutant mice exhibit impaired skin wound healing
  • deletion of the PPARgamma gene in mouse mammary epithelium and epithelial cells, B- and T-cells, and ovary does not affect mammary development and propensity for tumor formation but leads to reduced fertility
  • neither hemizygous deletion of Pparg nor complete ablation of Ppara influenced the development of prostate cancer in mouse model
  • elimination of expression of the PPARG gene in mouse beta cells leads to significant islet hyperplasia
  • knock out of Pparg in mouse skeletal muscle causes glucose intolerance and progressive insulin resistance
  • Targeted deletion of PPARgamma in adipose tissue results in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, decreased levels of plasma leptin and ACRP30, increased hepatic glucogenesis and insulin resistance
  • in contrast to the embryonic lethality of PPARgamma1-deficient mice, PPARgamma2(-/-) mice survived but exhibited an overall reduction in white adipose tissue, less lipid accumulation, and decreased expression of adipogenic genes in adipose tissue, and impairment of insulin sensitivity
  • homozygous mice with the equivalent P465L mutation die in utero while heterozygous mice grow normally with normal total adipose tissue weight but a reduced interscapular brown adipose tissue, intra-abdominal fat mass, increased extra-abdominal subcutaneous fat, and are hypertensive
  • disruption of PPARgamma in mouse myeloid cells impairs alternative macrophage activation, and predisposes to development of diet-induced obesity, insulin resistance, and glucose intolerance
  • targeted deletion of PPAR gamma in mice results in the production of "toxic milk" containing elevated levels of inflammatory lipids
  • Tie2Cre/flox mouse model in which PPAR-gamma is deleted in osteoclasts but not in osteoblasts develop osteopetrosis characterized by increased bone mass, reduced medullary cavity space and extramedullary hematopoiesis in the spleen
  • blocking the endogenous activation of central nervous system PPARG with pharmacological antagonists or reducing its expression with shRNA leads to negative energy balance, restored leptin sensitivity in high-fat-diet rats and blocked the hyperphagic response to oral thiazolidinedione treatment
  • food intake was reduced and energy expenditure increased
  • C3H mice do not express Pparg and Mgat1 in the liver and are protected against hepatic steatosis while being fed a HFD during high-fat diet in mice with neuron-specific Pparg knockout
  • over-expression of PPARG in cultured cortical neurons protects neurons from either HDAC4 over-expression- or H(2) O(2) -induced damage
  • C3H mice do not express Pparg and Mgat1 in the liver and are protected against hepatic steatosis while being fed a high-fat diet (HFD)