Data in Brief (Dec 2017)

Data on the expression and insulin-stimulated phosphorylation of IRS-1 by miR-96 in L6-GLUT4myc myocytes

  • Won-Mo Yang,
  • Kyung-Ho Min,
  • Yi-Seul Son,
  • Se-Whan Park,
  • Wan Lee

Journal volume & issue
Vol. 15
pp. 728 – 732

Abstract

Read online

Diets containing a high saturated fatty acid (SFA) increase the risk of metabolic diseases, and microRNAs (miRNAs) induced by SFA have been implicated in the pathogenesis of insulin resistance and type 2 diabetes. In a previous report, miR-96 is found to be upregulated by SFA and involved in the suppression of insulin signaling intermediates, leading to insulin resistance in hepatocytes (Yang et al., 2016) [1]. This article presents the accompanying data collected from L6-GLUT4myc myocytes to determine the effects of miR-96 on insulin signaling in skeletal muscle cells. The transfection of miR-96 decreased the expression of IRS-1 in myocytes. Accordingly, miR-96 inhibited the insulin-stimulated phosphorylation of IRS-1, which led to an impairment of insulin signaling. More detailed analysis and understanding of the roles of miR-96 in diet-induced insulin resistance can be found in 'Induction of miR-96 by dietary saturated fatty acids exacerbates hepatic insulin resistance through the suppression of INSR and IRS-1' (Yang et al., 2016) [1]. Keywords: MicroRNAs, miR-96, Myocyte, IRS-1, INSR