Prior AICAR Stimulation Increases Insulin Sensitivity in Mouse Skeletal Muscle in an AMPK-Dependent Manner

• DOI: 10.2337/db14-1402
• Publication Date: 2015-01-01T05:08:31Z
• Authors: Rasmus Kjøbsted; Jonas T. Treebak; Joachim Fentz; Louise Lantier; Benoit Viollet; Jesper B. Birk; Peter Schjerling; Marie Björnholm; Juleen R. Zierath; Jørgen F.P. Wojta...
• Keywords: GLUT4; AMP-Activated Protein Kinase

An acute bout of exercise increases glucose uptake in skeletal muscle by an insulin-independent mechanism. In the period after exercise, insulin sensitivity to increased is enhanced. The molecular mechanisms underpinning this phenomenon are poorly understood but appear involve cell surface abundance GLUT4. While proximal signaling does not seem mediate effect, elevated phosphorylation TBC1D4, a downstream target both (Akt) and (AMPK) signaling, appears play role. main purpose study was determine whether AMPK activation sensitivity. We found that prior AICAR stimulation wild-type mouse stimulate uptake. However, observed mice with reduced or ablated activity muscle. Furthermore, enhanced insulin-stimulated TBC1D4 at Thr(649) Ser(711) only. These events were positively correlated Our results provide evidence support sufficient increase Moreover, may facilitate effect enhance response insulin.