| First Author | Eldar-Finkelman H | Year | 1999 |
| Journal | Diabetes | Volume | 48 |
| Issue | 8 | Pages | 1662-6 |
| PubMed ID | 10426388 | Mgi Jnum | J:56435 |
| Mgi Id | MGI:1340955 | Doi | 10.2337/diabetes.48.8.1662 |
| Citation | Eldar-Finkelman H, et al. (1999) Increased glycogen synthase kinase-3 activity in diabetes- and obesity-prone C57BL/6J mice. Diabetes 48(8):1662-6 |
| abstractText | Although the precise mechanisms contributing to insulin resistance and type 2 diabetes are unknown, it is believed that defects in downstream components of the insulin signaling pathway may be involved. In this work, we hypothesize that a serine/threonine kinase, glycogen synthase kinase-3 (GSK-3), may be pertinent in this regard. To test this hypothesis, we examined GSK-3 activity in two inbred mouse strains known to be susceptible (C57BL/6J) or resistant (A/J) to diet-induced obesity and diabetes. Examination of GSK-3 in fat, liver, and muscle tissues of C57BL/6J mice revealed that GSK-3 activity increased twofold in the epididymal fat tissue and remained unchanged in muscle and liver of mice fed a high-fat diet, compared with their low-fat diet-fed counterparts. In contrast, GSK-3 activity did not change in the epididymal fat tissue of A/J mice, regardless of the type of diet they were fed. In addition, both basal and diet-induced GSK-3 activity tvas higher (2.3- and 3.2- fold, respectively) in the adipose tissue of C57BL/6J mice compared with that in A/J mice, Taken together, our studies suggest an unsuspected Link between increased GSK- 3 activity and development of insulin resistance and type 2 diabetes in fat tissue of C57BL/6J mice, and implicate GSK-3 as a potential factor contributing to susceptibility of C57BL/6J mice to diet-induced diabetes. |
