| First Author | Elghazi L | Year | 2012 |
| Journal | Sci Rep | Volume | 2 |
| Pages | 693 | PubMed ID | 23012647 |
| Mgi Jnum | J:207267 | Mgi Id | MGI:5554999 |
| Doi | 10.1038/srep00693 | Citation | Elghazi L, et al. (2012) Importance of beta-Catenin in glucose and energy homeostasis. Sci Rep 2:693 |
| abstractText | In settings of increased insulin demand, failure to expand pancreatic beta-cells mass leads to diabetes. Genome-wide scans of diabetic populations have uncovered several genes associated with susceptibility to type 2 diabetes and a number of them are part of the Wnt signaling. beta-Catenin, a Wnt downstream effector participates in pancreatic development, however, little is known about its action in mature beta-cells. Deletion of beta-Catenin in Pdx1 pancreatic progenitors leads to a decreased beta-cell mass and impaired glucose tolerance. Surprisingly, loss of beta-catenin made these mice resistant to high fat diet because of their increased energy expenditure and insulin sensitivity due to hyperactivity. The complexity of this phenotype was also explained in part by ectopic expression of Cre recombinase in the hypothalamus. Our data implicates beta-Catenin in the regulation of metabolism and energy homeostasis and suggest that Wnt signaling modulates the susceptibility to diabetes by acting on different tissues. |
