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Updated: Dec 4, 2025

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
Published on: June 25, 2017
miR-150 regulates glucose utilization through targeting GLUT4 in insulin-resistant cardiomyocytes
Jin Ju1, Dan Xiao1,2, Nannan Shen1,3
1Department of Pharmacology, Harbin Medical University (The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), Harbin 150081, China.
Abstract:
MicroRNAs (miRNAs) play an important role in cardiac function and metabolism. However, whether they regulate insulin resistance (IR) of cardiomyocytes remains unclear. The aim of the present study was to shed light on this issue with a focus on miR-150. We found here that miR-150 level was elevated in myocardium of type 2 diabetes mellitus (T2DM) rat model and in insulin-resistant cardiomyocytes induced by high glucose (25 mM) and high insulin (1 μM). Deregulation of miR-150 downregulated the protein and mRNA levels of glucose transporter 4 (GLUT4) as assessed by western blot, real-time polymerase chain reaction (qPCR), and immunofluorescence assays. Overexpression of miR-150 inhibited glucose utilization in cardiomyocytes as detected by 2-deoxyglucose transport and glucose consumption assays. In contrast, knockdown of miR-150 significantly increased glucose uptake in cardiomyocytes. Moreover, GLUT4 translocation was increased after transfection of miR-150 inhibitor (AMO-150). Collectively, miR-150 reduced glucose utilization by directly decreasing the expression and translocation of GLUT4 in the cardiomyocytes with IR and therefore might be a new therapeutic target for metabolic diseases such as T2DM.
Insights
MicroRNAs (miRNAs) regulate glucose metabolism in heart cells. This study shows that elevated miR-150 in insulin resistance impairs glucose uptake by reducing glucose transporter 4 (GLUT4), suggesting miR-150 as a therapeutic target for type 2 diabetes mellitus.
Area of Science:
- Cardiovascular Biology
- Metabolic Regulation
- Molecular Genetics
Background:
- MicroRNAs (miRNAs) are crucial regulators of cardiac function and metabolism.
- The role of miRNAs in cardiomyocyte insulin resistance (IR) is not fully understood.
- Investigating specific miRNAs like miR-150 is key to understanding metabolic dysregulation in the heart.
Purpose of the Study:
- To investigate the role of miR-150 in cardiomyocyte insulin resistance.
- To determine the impact of miR-150 on glucose transporter 4 (GLUT4) expression and translocation.
- To explore miR-150 as a potential therapeutic target for type 2 diabetes mellitus (T2DM).
Main Methods:
- Western blot, real-time PCR, and immunofluorescence assays to assess GLUT4 levels.
- 2-deoxyglucose transport and glucose consumption assays to measure glucose utilization.
- In vitro models of insulin-resistant cardiomyocytes and in vivo T2DM rat models.
Main Results:
- miR-150 levels were elevated in T2DM rat hearts and insulin-resistant cardiomyocytes.
- miR-150 downregulation reduced GLUT4 protein and mRNA.
- Overexpression of miR-150 inhibited glucose uptake, while knockdown increased it.
- miR-150 inhibition promoted GLUT4 translocation.
Conclusions:
- miR-150 exacerbates insulin resistance in cardiomyocytes by decreasing GLUT4 expression and translocation.
- miR-150 is a potential therapeutic target for managing metabolic diseases like T2DM.
- Understanding miR-150's role provides insights into cardiac metabolic dysfunction.
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