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

Won-Mo Yang1, Kyung-Ho Min1, Yi-Seul Son1

  • 1Department of Biochemistry, Dongguk University College of Medicine, Gyeongju-si, Gyeongsangbuk-do 38067, Republic of Korea.

Data in Brief
|November 11, 2017
PubMed

Insights

High saturated fatty acids (SFAs) increase metabolic disease risk. This study shows that microRNA-96 (miR-96) impairs insulin signaling in skeletal muscle cells, contributing to insulin resistance.

Area of Science:

  • Molecular Biology
  • Metabolic Diseases
  • Endocrinology

Background:

  • High saturated fatty acid (SFA) intake is linked to metabolic diseases, including insulin resistance and type 2 diabetes.
  • MicroRNAs (miRNAs) are implicated in SFA-induced insulin resistance, with miR-96 previously shown to impair hepatic insulin signaling.

Purpose of the Study:

  • To investigate the role of miR-96 in insulin signaling within skeletal muscle cells (myocytes).
  • To determine the impact of miR-96 on insulin resistance in the context of SFA-rich diets.

Main Methods:

  • Utilized L6-GLUT4myc myocytes, a skeletal muscle cell model.
  • Transfected myocytes with miR-96 to assess its effects on insulin signaling pathways.
  • Measured IRS-1 expression and insulin-stimulated IRS-1 phosphorylation.

Main Results:

  • miR-96 transfection led to decreased expression of Insulin Receptor Substrate-1 (IRS-1) in myocytes.
  • miR-96 inhibited the insulin-stimulated phosphorylation of IRS-1.
  • These molecular changes resulted in impaired insulin signaling in skeletal muscle cells.

Conclusions:

  • miR-96 plays a significant role in regulating insulin signaling in skeletal muscle.
  • The upregulation of miR-96 by SFAs contributes to insulin resistance in skeletal muscle, similar to its effects in the liver.
  • Targeting miR-96 may offer a therapeutic strategy for managing diet-induced insulin resistance.
Keywords:
INSRIRS-1MicroRNAsMyocytemiR-96

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