| First Author | Kunath A | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 478 |
| Issue | 1 | Pages | 398-402 |
| PubMed ID | 27402271 | Mgi Jnum | J:238672 |
| Mgi Id | MGI:5823337 | Doi | 10.1016/j.bbrc.2016.07.038 |
| Citation | Kunath A, et al. (2016) Repin1 deficiency improves insulin sensitivity and glucose metabolism in db/db mice by reducing adipose tissue mass and inflammation. Biochem Biophys Res Commun 478(1):398-402 |
| abstractText | Replication initiator 1 (Repin1) is a zinc finger protein playing a role in insulin sensitivity, body fat mass and lipid metabolism by regulating the expression key genes of glucose and lipid metabolism. Here, we tested the hypothesis that introgression of a Repin1 deletion into db/db mice improves glucose metabolism in vivo. We generated a whole body Repin1 deficient db/db double knockout mouse (Rep1(-/-)x db/db) and systematically characterized the consequences of Repin1 deficiency on insulin sensitivity, glucose and lipid metabolism parameters and fat mass. Hyperinsulinemic-euglycemic clamp studies revealed significantly improved insulin sensitivity in Rep1(-/-)x db/db mice, which are also characterized by lower HbA1c, lower body fat mass and reduced adipose tissue (AT) inflammation area. Our study provides evidence that loss of Repin1 in db/db mice improves insulin sensitivity and reduces chronic hyperglycemia most likely by reducing fat mass and AT inflammation. |
