Table of Contents Author Guidelines Submit a Manuscript
Journal of Diabetes Research
Volume 2016, Article ID 1564386, 9 pages
Research Article

Swimming Exercise Alleviated Insulin Resistance by Regulating Tripartite Motif Family Protein 72 Expression and AKT Signal Pathway in Sprague-Dawley Rats Fed with High-Fat Diet

1College of Physical Education, Shanghai Normal University, Shanghai 200234, China
2Department of Food Science and Nutrition, Zhejiang University, Hangzhou 310053, China
3Rehabilitation College of Gannan Medical University, Jiangxi 341000, China
4College of Physical Education, Yangzhou University, Jiangsu 225009, China

Received 27 May 2016; Revised 14 August 2016; Accepted 3 October 2016

Academic Editor: Hassan Dashti

Copyright © 2016 Jie Qi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We aimed to investigate whether swimming exercise could improve insulin resistance (IR) by regulating tripartite motif family protein 72 (TRIM72) expression and AKT signal pathway in rats fed with high-fat diet. Five-week-old rats were classified into 3 groups: standard diet as control (CON), high-fat diet (HFD), and HFD plus swimming exercise (Ex-HFD). After 8 weeks, glucose infusion rate (GIR), markers of oxidative stress, mRNA and protein expression of TRIM72, protein of IRS, p-AK, and AKT were determined in quadriceps muscles. Compared with HFD, the GIR, muscle SOD, and GSH-Px were significantly increased (, resp.), whereas muscle MDA and 8-OHdG levels were significantly decreased ( and ) in Ex-HFD. Expression levels of TRIM72 mRNA and protein in muscles were significantly reduced ( and ), whereas protein expression levels of IRS-1, p-AK, and AKT were significantly increased in Ex-HFD compared with HFD (, , and ). These results suggest that an 8-week swimming exercise improves HFD-induced insulin resistance maybe through a reduction of TRIM72 in skeletal muscle and enhancement of AKT signal transduction.