Dataset Information

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

ABSTRACT: 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].

SUBMITTER: Yang WM

PROVIDER: S-EPMC5671482 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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

Yang Won-Mo WM Min Kyung-Ho KH Son Yi-Seul YS Park Se-Whan SW Lee Wan W

Data in brief 20171028

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 de ...[more]

PMID: 29124099

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Project description:ObjectiveTo explore the possible mechanism of electroacupuncture to improve insulin sensitivity in type 2 diabetes rats.MethodsFourteen Zucker Diabetic Fatty (ZDF) rats were randomly divided into two groups: a model group and an electroacupuncture group, with 7 rats in each group. Seven Zucker Lean (ZL) rats served as a control group. All rats were fed with Purina #5008 for 4 weeks, and the electroacupuncture group received 4-week electroacupuncture intervention, while the control group and model group received no intervention. We measured fasting blood glucose (FBG) on the fourth weekend. After 4 weeks of intervention, the expression levels of insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, IRS-1 serine/threonine phosphorylation, and GLUT4 in quadriceps femoris muscles were detected by western Blot.ResultsCompared with the model group, the electroacupuncture group had a lower level of fasting blood glucose, serum insulin level, and insulin resistance index (P < 0.05). The electroacupuncture group had lower IRS-1 serine/threonine phosphorylation than the model group, with the difference showing statistical significance (P < 0.05). Furthermore, the mean score (MS) of the control group showed the lowest phosphorylation expression, followed by the electroacupuncture group, while the model group had the highest level of phosphorylated protein expression. The level of IRS-1 tyrosine phosphorylation at Tyr895 sites was compared, and the result showed that there was no significant difference between the electroacupuncture group and the control group (P > 0.05), and the electroacupuncture group had higher phosphorylation expression than the model group (P < 0.05). Compared with the control group and the model group, the expression level of GLUT4 protein in the electroacupuncture group was significantly increased (P < 0.05).ConclusionElectroacupuncture has the effect to improve the insulin sensitivity of type 2 diabetic ZDF rats by reducing fasting blood glucose, insulin level, and insulin resistance index, effectively up regulating the expression of GLUT4 protein in quadriceps femoris muscle. The mechanism is related to the regulation of skeletal muscle IRS-1 serine/threonine and tyrosine phosphorylation levels.

Dataset Information

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

Publications

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

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