| First Author | Welters HJ | Year | 2012 |
| Journal | Endocrinology | Volume | 153 |
| Issue | 10 | Pages | 4593-9 |
| PubMed ID | 22807489 | Mgi Jnum | J:189152 |
| Mgi Id | MGI:5444550 | Doi | 10.1210/en.2012-1243 |
| Citation | Welters HJ, et al. (2012) Rosiglitazone promotes PPARgamma-dependent and -independent alterations in gene expression in mouse islets. Endocrinology 153(10):4593-9 |
| abstractText | The glitazone class of insulin-sensitizing agents act, in part, by the activation of peroxisome proliferator-activated receptor (PPAR)-gamma in adipocytes. However, it is unclear whether the expression of PPARgamma in the islets is essential for their potential beta-cell-sparing properties. To investigate the in vivo effects of rosiglitazone on beta-cell biology, we used an inducible, pancreatic and duodenal homeobox-1 enhancer element-driven, Cre recombinase to knockout PPARgamma expression specifically in adult beta-cells (PPARgKO). Subjecting the PPARgKO mice to a chow diet led to virtually undetectable changes in glucose or insulin sensitivity, which was paralleled by minimal changes in islet gene expression. Similarly, challenging the mutant mice with a high-fat diet and treatment with rosiglitazone did not alter insulin sensitivity, glucose-stimulated insulin secretion, islet size, or proliferation in the knockout mice despite PPARgamma-dependent and -independent changes in islet gene expression. These data suggest that PPARgamma expression in the beta-cells is unlikely to be directly essential for normal beta-cell function or the insulin-sensitizing actions of rosiglitazone. |
