AMPK activation by prolonged stimulation with interleukin-1 β contributes to the promotion of GLUT4 translocation in skeletal muscle cells.

AMPK activation by prolonged stimulation with interleukin-1β contributes to the promotion of GLUT4 translocation in skeletal muscle cells. Cell Biol Int. 2016 Aug 29; Authors: Takaguri A, Inoue S, Kubo T, Satoh K Abstract Impaired insulin signaling in skeletal muscle cells causes insulin resistance associated with the onset of type 2 diabetes. Although interleukin (IL)-1β has been considered to be implicated in the pathogenesis of type 2 diabetes, the action of prolonged stimulation with IL-1β on the insulin signaling pathway in skeletal muscle cells remains poorly understood. In the current study, we investigated the effect of IL-1β stimulation on insulin signal transduction from the insulin receptor (IR), resulting in glucose transporter 4 (GLUT4) translocation in skeletal muscle cells. In L6-GLUT4myc cells, stimulation with IL-1β for 24 h promoted GLUT4 translocation to the plasma membrane and increased glucose uptake in a concentration-dependent manner, whereas short-term stimulation with IL-1 for up to 6 h did not affect that. In addition, stimulation with IL-1β for 24 h further increased insulin-stimulated GLUT4 translocation. Interestingly, stimulation with IL-1β for 24 h did not cause any change in the phosphorylation of insulin signal molecules IR, insulin receptor substrate (IRS)-1, Akt, and p21-activated kinase (PAK1). Stimulation with IL-1β for 24 h significantly increased AMP-activated protein kinase (A...
Source: Cell Biology International - Category: Cytology Authors: Tags: Cell Biol Int Source Type: research