| Autor: |
Eldar-Finkelman, Hagit, Schreyer, Sandra A., Shinohara, Michi M., LeBoeuf, Renee C., Krebs, Edwin G., Eldar-Finkelman, H, Schreyer, S A, Shinohara, M M, LeBoeuf, R C, Krebs, E G |
| Předmět: |
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| Zdroj: |
Diabetes; Aug99, Vol. 48 Issue 8, p1662-1666, 5p, 1 Diagram, 1 Chart, 3 Graphs |
| Abstrakt: |
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 was 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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