AICAR Inhibits Insulin-Stimulated Glucose Uptake in 3T3-L1 Adipocytes via an AMPK-Independent, ZMP-Dependent Mechanism.

ABSTRACT: AMP-activated protein kinase (AMPK) is activated by reduced cellular energy charge and mimics the action of insulin in muscle by stimulating increased trafficking of GLUT4 to the plasma membrane. In contrast, we have previously reported that short-term activation of AMPK in adipocytes has no effect on glucose uptake. Whether prolonged AMPK activation influences adipocyte glucose uptake remains poorly characterised. To investigate the effect of sustained AMPK activation on glucose uptake in adipocytes, glucose uptake and insulin signalling were assessed in 3T3-L1 adipocytes stimulated with AICAR and 991, which activate AMPK by different mechanisms, for 24 h. Furthermore, glucose uptake and GLUT4 levels were assessed in adipocytes or adipose tissue from mice lacking AMPKα1 as a model of prol

SUBMITTER: Alshuweishi Y 

PROVIDER: S-EPMC12651217 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature