| First Author | Fernandez MO | Year | 2017 |
| Journal | J Endocr Soc | Volume | 1 |
| Issue | 11 | Pages | 1332-1350 |
| PubMed ID | 29264458 | Mgi Jnum | J:307568 |
| Mgi Id | MGI:6723957 | Doi | 10.1210/js.2017-00242 |
| Citation | Fernandez MO, et al. (2017) Astrocyte-Specific Deletion of Peroxisome-Proliferator Activated Receptor-gamma Impairs Glucose Metabolism and Estrous Cycling in Female Mice. J Endocr Soc 1(11):1332-1350 |
| abstractText | Mice lacking peroxisome-proliferator activated receptor-gamma (PPARgamma) in neurons do not become leptin resistant when placed on a high-fat diet (HFD). In male mice, this results in decreased food intake and increased energy expenditure, causing reduced body weight, but this difference in body weight is not observed in female mice. In addition, estrous cycles are disturbed and the ovaries present with hemorrhagic follicles. We observed that PPARgamma was more highly expressed in astrocytes than neurons, so we created an inducible, conditional knockout of PPARgamma in astrocytes (AKO). The AKO mice had impaired glucose tolerance and hepatic steatosis that did not worsen with HFD. Expression of gluconeogenic genes was elevated in the mouse livers, as was expression of several genes involved in lipogenesis, lipid transport, and storage. The AKO mice also had a reproductive phenotype with fewer estrous cycles, elevated plasma testosterone levels, reduced corpora lutea formation, and alterations in hypothalamic and ovarian gene expression. Thus, the phenotypes of the AKO mice were very different from those seen in the neuronal knockout mice, suggesting distinct roles for PPARgamma in these two cell types. |
