Modulation of Fibroblast Growth Factor-21 and βklotho Proteins Expression in Type 2 Diabetic Women with Non-alcoholic Fatty Liver Disease Following Endurance and Strength Training
Open Access
- 11 October 2021
- journal article
- research article
- Published by Briefland in Hepatitis Monthly
- Vol. 21 (7)
- https://doi.org/10.5812/hepatmon.116513
Abstract
Background: There is limited research on the effects of physical activity with moderate intensity on βklotho (BKL) and fibroblast growth factor-21 (FGF-21) proteins expression in diabetic patients with non-alcoholic fatty liver disease (NAFLD). Objectives: This study was aimed to determine the effects of eight weeks of endurance and resistance training on BKL and FGF-21 proteins expression in diabetic women with NAFLD. Methods: Forty-five diabetic women (age: 51 ± 8 years, height: 158 ± 2 cm, weight: 75 ± 8 kg) with NAFLD participated. The subjects were randomly divided into three groups, including control (n = 15), endurance training (n = 15), and resistance training (n = 15). The enzyme-linked immunosorbent assay (ELISA) was used to measure BKL and FGF-21 proteins. Two-way ANOVA with repeated measures was applied to determine differences at a significant level of P < 0.05. Results: Eight weeks of endurance and resistance training reduced AST, ALT, and FGF-21 (25, 26, 19% and 13, 16, 13%, respectively) and increased BKL (16% and 18, respectively). However, in the variables of HDL, insulin, AST, ALT, FGF-21, and BKL, a significant difference was observed in the control group (P < 0.05). Also, there was a significant difference between the control and training groups in BKL and FGF21 proteins expression (P < 0.05), but no significant difference was observed between the two training groups (P > 0.05). Conclusions: The results suggest that both moderate-intensity endurance and resistance training can modulate the destructive effects of type 2 diabetes and NAFLD on BKL and FGF-21 proteins expression, and there is no difference between the two training methods.Keywords
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