Case Control Study
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 14, 2015; 21(2): 511-516
Published online Jan 14, 2015. doi: 10.3748/wjg.v21.i2.511
miRNA-103: Molecular link between insulin resistance and nonalcoholic fatty liver disease
Qian Xu, Ying Li, Yong-Fang Shang, Hui-Ling Wang, Min-Xiu Yao
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
Author contributions: Xu Q and Yao MX performed the majority of experiments, designed the study and wrote the manuscript; Shang YF, Li Y and Wang HL collected part the clinical materials.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Min-Xiu Yao, Department of Endocrinology, the Second Affiliated Hospital of Medical College of Qingdao University, No. 127 Siliunan road, Qingdao 266042, Shandong Province, China. yaominxiu@medmail.com.cn
Telephone: +86-532-84961391 Fax: +86-532-84882721
Received: May 12, 2014
Peer-review started: May 12, 2014
First decision: June 18, 2014
Revised: June 20, 2014
Accepted: July 30, 2014
Article in press: July 30, 2014
Published online: January 14, 2015
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.

Keywords: miRNA-103, Insulin resistance, Nonalcoholic fatty liver disease

Core tip: Insulin resistance activates development of nonalcoholic fatty liver disease (NAFLD), however, the molecular mechanism is not fully understood. We determined fasting plasma glucose, fasting insulin, triglyceride (TG) and the levels of miRNA-103 (miR-103) in the serum of patients with NAFLD. We found that higher levels of miR-103 were expressed in the serum of patients with NAFLD. miR-103 was positively correlated with homeostasis model assessment and was used to evaluate basal insulin resistance (HOMA-IR), TG and BMI, respectively. miR-103 was an independent factor for HOMA-IR and a risk factor for NAFLD. We conclude that miR-103 is involved in insulin resistance and NAFLD.