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Effects of miR-152-Mediated Targeting of SOCS3 on Hepatic Insulin Resistance in Gestational Diabetes Mellitus Mice

SOCS3 妊娠期糖尿病 内科学 内分泌学 胰岛素抵抗 医学 小岛 甘油三酯 胰岛素 H&E染色 胆固醇 糖尿病 化学 妊娠期 生物 免疫组织化学 怀孕 抑制器 癌症 遗传学
作者
Yuanchun Li,Li Kang,Juanjuan Huang,Juan Zhang,Chunhua Liu,Wenjuan Shen
出处
期刊:The American Journal of the Medical Sciences [Elsevier BV]
卷期号:361 (3): 365-374 被引量:9
标识
DOI:10.1016/j.amjms.2020.06.032
摘要

Background The present study explored the effects of miR-152-mediated targeting of suppressor of cytokine signaling 3 (SOCS3) on hepatic insulin resistance (HIR) in mice with gestational diabetes mellitus (GDM). Healthy SPF C57BL/6J mice were selected to establish a GDM model. Methods Mice were divided into seven groups as follows: Normal group, Model group, NC-mimic group, miR-152 mimic group, NC-pcDNA3.0 group, pcDNA3.0-SOCS group, and miR-152 mimic + pcDNA3.0-SOCS3 group. The relationship between miR-152 and SOCS3 expression was analyzed by a dual-luciferase reporter system. Islet cell morphology and expression of miR-152 and SOCS3 mRNA and protein in the islet tissue were detected by hematoxylin and eosin (HE) staining, reverse-transcription quantitative polymerase chain reaction (RT-qPCR), and western blot analysis. Fasting blood glucose (FBG) level was measured by a glucose meter while triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and insulin levels were determined by an automatic biochemical analyzer. Insulin resistance index (HOMA-IR) was calculated by the formula FBG × FINS/22.5. Results The results showed that the levels of miR-152, SOCS3, FBG, fasting insulin (FINS), TG, and TC increased, and HDL-C content decreased in other groups as compared with those in the Normal group (all p < 0.05). Oral glucose tolerance test (OGTT), FBG, FINS, TG, TC, and HDL-C values showed an opposite trend in miR-152 mimic and pcDNA3.0-SOCS3 groups as compared with the Model group (all p < 0.05). Conclusions miR-152 can inhibit HIR in GDM mice by downregulating the expression of SOCS3.

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