| First Author | O'Donnell PE | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 8 | Pages | e0160636 |
| PubMed ID | 27505464 | Mgi Jnum | J:254580 |
| Mgi Id | MGI:6100413 | Doi | 10.1371/journal.pone.0160636 |
| Citation | O'Donnell PE, et al. (2016) Lipodystrophy, Diabetes and Normal Serum Insulin in PPARgamma-Deficient Neonatal Mice. PLoS One 11(8):e0160636 |
| abstractText | Peroxisome proliferator activated receptor gamma (PPARgamma) is a pleiotropic ligand activated transcription factor that acts in several tissues to regulate adipocyte differentiation, lipid metabolism, insulin sensitivity and glucose homeostasis. PPARgamma also regulates cardiomyocyte homeostasis and by virtue of its obligate role in placental development is required for embryonic survival. To determine the postnatal functions of PPARgamma in vivo we studied globally deficient neonatal mice produced by epiblast-restricted elimination of PPARgamma. PPARgamma-rescued placentas support development of PPARgamma-deficient embryos that are viable and born in near normal numbers. However, PPARgamma-deficient neonatal mice show severe lipodystrophy, lipemia, hepatic steatosis with focal hepatitis, relative insulin deficiency and diabetes beginning soon after birth and culminating in failure to thrive and neonatal lethality between 4 and 10 days of age. These abnormalities are not observed with selective PPARgamma2 deficiency or with deficiency restricted to hepatocytes, skeletal muscle, adipocytes, cardiomyocytes, endothelium or pancreatic beta cells. These observations suggest important but previously unappreciated functions for PPARgamma1 in the neonatal period either alone or in combination with PPARgamma2 in lipid metabolism, glucose homeostasis and insulin sensitivity. |
