The effect of aerobic, resistance, and combined training on PPAR-α, SIRT1 gene expression, and insulin resistance in high-fat diet-induced NAFLD male rats.
Aerobic training
Combined training
NAFLD
PPAR-α
Resistance training
SIRT1
Journal
Physiology & behavior
ISSN: 1873-507X
Titre abrégé: Physiol Behav
Pays: United States
ID NLM: 0151504
Informations de publication
Date de publication:
01 12 2020
01 12 2020
Historique:
received:
30
04
2020
revised:
20
08
2020
accepted:
20
08
2020
pubmed:
6
9
2020
medline:
22
6
2021
entrez:
5
9
2020
Statut:
ppublish
Résumé
Insulin resistance (IR) is known as the most important cause of Non-alcoholic Fatty Liver Disease (NAFLD), which is accompanied by a decline in gene expression of hepatic's peroxisomes Proliferator-Activated Receptors-alpha (PPAR-α) and Sirtuin-1 (SIRT1). This study aimed to investigate the effect of eight weeks of aerobic, resistance, and combined training on hepatic PPAR-α and SIRT1 expression, IR, serum Alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in rats of NAFLD induced by high-fat diet (HFD). A total of 37 male NAFLD rats induced 12 weeks of HFD were randomly divided into 4 groups: control, aerobic, resistance, and combined training. All groups continued the HFD until the end of the study. The training groups carried out exercise training with moderate intensity by 8 weeks of running on a treadmill and climbing a ladder for 5 sessions/week. At the end of the trainings, PPAR-α and SIRT1 expressions were examined via qPCR technique in the liver tissue. The 3 types of trainings controlled the weight gain caused by HFD and showed a significant decrease in serum ALT (P<0.05). Post-hoc test results indicated a significant reduction in AST and IR between the control group and HFD+AT, as well as the control group and HFD+RT (P<0.05). Despite a notable increase in hepatic PPAR-α and SIRT1 expression, it was not statistically significant (P ≥ 0.05). Doing any aerobic, resistance, and combined training for 8 weeks can control body weight, improve IR, decrease ALT; nevertheless, resistance training is more effective in improving NAFLD.
Sections du résumé
BACKGROUND
Insulin resistance (IR) is known as the most important cause of Non-alcoholic Fatty Liver Disease (NAFLD), which is accompanied by a decline in gene expression of hepatic's peroxisomes Proliferator-Activated Receptors-alpha (PPAR-α) and Sirtuin-1 (SIRT1). This study aimed to investigate the effect of eight weeks of aerobic, resistance, and combined training on hepatic PPAR-α and SIRT1 expression, IR, serum Alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in rats of NAFLD induced by high-fat diet (HFD).
METHODS
A total of 37 male NAFLD rats induced 12 weeks of HFD were randomly divided into 4 groups: control, aerobic, resistance, and combined training. All groups continued the HFD until the end of the study. The training groups carried out exercise training with moderate intensity by 8 weeks of running on a treadmill and climbing a ladder for 5 sessions/week. At the end of the trainings, PPAR-α and SIRT1 expressions were examined via qPCR technique in the liver tissue.
RESULTS
The 3 types of trainings controlled the weight gain caused by HFD and showed a significant decrease in serum ALT (P<0.05). Post-hoc test results indicated a significant reduction in AST and IR between the control group and HFD+AT, as well as the control group and HFD+RT (P<0.05). Despite a notable increase in hepatic PPAR-α and SIRT1 expression, it was not statistically significant (P ≥ 0.05).
CONCLUSION
Doing any aerobic, resistance, and combined training for 8 weeks can control body weight, improve IR, decrease ALT; nevertheless, resistance training is more effective in improving NAFLD.
Identifiants
pubmed: 32888948
pii: S0031-9384(20)30463-7
doi: 10.1016/j.physbeh.2020.113149
pii:
doi:
Substances chimiques
PPAR alpha
0
Sirt1 protein, rat
EC 3.5.1.-
Sirtuin 1
EC 3.5.1.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
113149Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.