The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
Deregulated miR-487b-3p in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance.
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Chen Mingtao, Tan Jie, Huang Min, Zhan Ting, Han Zheng, Liu Meng, Lu Yuanyuan, Tian Xia
Аннотация
BACKGROUND/AIMS: This study aims to elucidate both the diagnostic potential of miR-487b-3p for insulin resistance and its regulatory mechanisms in patients with nonalcoholic fatty liver disease (NAFLD).
MATERIALS AND METHODS: The study group included 60 NAFLD patients and 60 healthy controls. The expression levels of miR-487b-3p and insulin receptor substrate 1 (IRS1) in serum and cells were quantified by RT-qPCR. The diagnostic utility of the microRNA was evaluated through receiver operating characteristic (ROC) analysis. Glucose uptake in HepG2 was measured using fluorescence-based assays. The interaction between miR-487b-3p and IRS1 was confirmed by dual-luciferase reporter assay.
RESULTS: Compared with controls, NAFLD patients exhibited significantly elevated serum miR-487b-3p levels (P < .05). The ROC analysis demonstrated high diagnostic accuracy of miR-487b-3p in distinguishing between healthy controls and NAFLD patients. Functional analyses demonstrated that miR-487b-3p overexpression suppressed both glucose uptake and IRS1 expression (P < .05), whereas miR487b-3p inhibition enhanced glucose uptake and IRS1 expression (P < .05). Mechanistically, miR-487b-3p negatively regulated IRS1 to modulate glucose uptake.
CONCLUSION: miR-487b-3p may serve as a potential diagnostic biomarker for NAFLD, and miR-487b-3p negatively regulates IRS1 to modulate glucose uptake, thereby impairing insulin sensitivity in NAFLD patients.
MATERIALS AND METHODS: The study group included 60 NAFLD patients and 60 healthy controls. The expression levels of miR-487b-3p and insulin receptor substrate 1 (IRS1) in serum and cells were quantified by RT-qPCR. The diagnostic utility of the microRNA was evaluated through receiver operating characteristic (ROC) analysis. Glucose uptake in HepG2 was measured using fluorescence-based assays. The interaction between miR-487b-3p and IRS1 was confirmed by dual-luciferase reporter assay.
RESULTS: Compared with controls, NAFLD patients exhibited significantly elevated serum miR-487b-3p levels (P < .05). The ROC analysis demonstrated high diagnostic accuracy of miR-487b-3p in distinguishing between healthy controls and NAFLD patients. Functional analyses demonstrated that miR-487b-3p overexpression suppressed both glucose uptake and IRS1 expression (P < .05), whereas miR487b-3p inhibition enhanced glucose uptake and IRS1 expression (P < .05). Mechanistically, miR-487b-3p negatively regulated IRS1 to modulate glucose uptake.
CONCLUSION: miR-487b-3p may serve as a potential diagnostic biomarker for NAFLD, and miR-487b-3p negatively regulates IRS1 to modulate glucose uptake, thereby impairing insulin sensitivity in NAFLD patients.