Qian Xu1, Ying Li1, Yong-Fang Shang1, Hui-Ling Wang1, Min-Xiu Yao1. 1. Qian Xu, Ying Li, Yong-Fang Shang, Hui-Ling Wang, Min-Xiu Yao, Department of Endocrinology, the Second Affiliated Hospital of Medical College of Qingdao University, Qingdao 266042, Shandong Province, China.
Abstract
AIM: To investigate the associations between miRNA-103 (miR-103) and insulin resistance and nonalcoholic fatty liver disease (NAFLD). METHODS: Serum samples were collected from 50 NAFLD patients who were overweight or obese (NAFLD group) and from 30 healthy subjects who served as controls (normal control group). Quantitative polymerase chain reaction was used to detect expression of miR-103. Fasting plasma glucose, fasting insulin, and triglyceride (TG) levels were measured. Homeostasis model assessment was used to evaluate basal insulin resistance (HOMA-IR). Patient height and weight were measured to calculate body mass index (BMI). RESULTS: Compared with the normal control group, higher serum levels of miR-103 were expressed in the NAFLD group (8.18 ± 0.73 vs 4.23 ± 0.81, P = 0.000). When P = 0.01 (bilateral), miR-103 was positively correlated with HOMA-IR (r = 0.881), TG (r = 0.774) and BMI (r = 0.878), respectively. miR-103, TG and BMI were all independent factors for HOMA-IR (β = 0.438/0.657/0.251, P = 0.000/0.007/0.001). miR-103, TG, BMI and HOMA-IR were all risk factors for NAFLD (odds ratio = 2.411/16.196/1.574/19.11, P = 0.009/0.022/0.01/0.014). CONCLUSION: miR-103 is involved in insulin resistance and NAFLD, and may be a molecular link between insulin resistance and NAFLD and a therapeutic target for these disorders.
AIM: To investigate the associations between miRNA-103 (miR-103) and insulin resistance and nonalcoholic fatty liver disease (NAFLD). METHODS: Serum samples were collected from 50 NAFLD patients who were overweight or obese (NAFLD group) and from 30 healthy subjects who served as controls (normal control group). Quantitative polymerase chain reaction was used to detect expression of miR-103. Fasting plasma glucose, fasting insulin, and triglyceride (TG) levels were measured. Homeostasis model assessment was used to evaluate basal insulin resistance (HOMA-IR). Patient height and weight were measured to calculate body mass index (BMI). RESULTS: Compared with the normal control group, higher serum levels of miR-103 were expressed in the NAFLD group (8.18 ± 0.73 vs 4.23 ± 0.81, P = 0.000). When P = 0.01 (bilateral), miR-103 was positively correlated with HOMA-IR (r = 0.881), TG (r = 0.774) and BMI (r = 0.878), respectively. miR-103, TG and BMI were all independent factors for HOMA-IR (β = 0.438/0.657/0.251, P = 0.000/0.007/0.001). miR-103, TG, BMI and HOMA-IR were all risk factors for NAFLD (odds ratio = 2.411/16.196/1.574/19.11, P = 0.009/0.022/0.01/0.014). CONCLUSION:miR-103 is involved in insulin resistance and NAFLD, and may be a molecular link between insulin resistance and NAFLD and a therapeutic target for these disorders.
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