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Updated: Mar 21, 2026

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

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Regulation of Insulin Resistance by Multiple MiRNAs via Targeting the GLUT4 Signalling Pathway

Tong Zhou, Xianhong Meng, Hui Che

    Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
    |May 12, 2016
    PubMed
    Abstract

    Insights

    This study shows that specific microRNAs (miRNAs) like miR-106b, miR-27a, and miR-30d are key regulators of glucose metabolism in insulin resistance. A novel multiple-target anti-miRNA strategy effectively improved glucose uptake and key protein levels.

    Area of Science:

    • Molecular Biology
    • Endocrinology
    • Biochemistry

    Background:

    • Type 2 Diabetes Mellitus (T2DM) involves insulin resistance (IR), with poorly understood molecular drivers.
    • MicroRNAs (miRNAs) are implicated in glucose metabolism signaling pathways relevant to IR.

    Purpose of the Study:

    • To evaluate the efficacy of multiple-target anti-miRNA antisense oligonucleotides (MTg-AMO) technology in modulating miRNAs critical for IR.
    • To investigate the role of specific miRNAs (miR-106b, miR-27a, miR-30d) in glucose metabolism and insulin resistance.

    Main Methods:

    • Construction of a novel MTg-AMO targeting miR-106b, miR-27a, and miR-30d (MTg-AMO106b/27a/30d).
    • Assessment of protein and mRNA levels using Western blot and qRT-PCR.
    • Analysis of insulin resistance via glucose consumption and uptake assays in diabetic rat skeletal muscle and insulin-resistant L6 cells.

    Main Results:

    • Down-regulation of glucose transporter 4 (GLUT4), MAPK 14, and PI3K regulatory subunit beta (and their corresponding mRNAs) in diabetic rat skeletal muscle and insulin-resistant L6 cells.
    • Overexpression of miR-106b, miR-27a, and miR-30d impaired glucose uptake and reduced key protein expression.
    • Silencing these miRNAs in insulin-resistant L6 cells enhanced glucose uptake and increased key protein expression.
    • MTg-AMO106b/27a/30d treatment significantly up-regulated GLUT4, MAPK 14, and PI3K regulatory subunit beta, improving glucose consumption and uptake.

    Conclusions:

    • miR-106b, miR-27a, and miR-30d play significant roles in regulating glucose metabolism through the GLUT4 signaling pathway in L6 cells.
    • The MTg-AMO106b/27a/30d strategy demonstrates potent therapeutic potential for insulin resistance, outperforming singular anti-miRNA approaches.

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