Research Article Details
Article ID: | A06413 |
PMID: | 32888948 |
Source: | Physiol Behav |
Title: | 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. |
Abstract: | 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. |
DOI: | 10.1016/j.physbeh.2020.113149 |

Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
---|---|---|---|---|---|
S08 | Lifestyle measures | Lifestyle intervention; weight loss; diet adaptation; dietary interventions; lifestyle modifications; Exercise | -- | -- | Details |
S01 | Improve insulin resistance | insulin sensitizer; insulin resistance; glucose tolerance | Biguanide: increases 5-AMP activated protein kinase signaling; SGLT-2 inhibitor; Thiazalidinedione: selective PPAR-γ agonists; GLP-1 agonist | Metformin; Empagliflozin; Canagliflozin; Rosiglitazone; Pioglitazone; Liraglutide | Details |
Diseases ID | DO ID | Disease Name | Definition | Class | |
---|---|---|---|---|---|
I05 | 9352 | Type 2 diabetes mellitus | A diabetes that is characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. A diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. http://en.wikipedia.org/wiki/Diabetes, http://en.wikipedia.org/wiki/Diabetes_mellitus_type_2 | disease of metabolism/inherited metabolic disorder/ carbohydrate metabolic disorder/glucose metabolism disease/diabetes/ diabetes mellitus | Details |
Drug ID | Drug Name | Type | DrugBank ID | Targets | Category | Latest Progress | |
---|---|---|---|---|---|---|---|
D328 | Serine | Chemical drug | DB00133 | SRR | Improve insulin resistance | Under clinical trials | Details |
D579 | Emfilermin | Miscellany | -- | adipocytes | Enhance lipid metabolism | Under investigation | Details |
D182 | Insulin | Biological drug | DB00030 | INSR agonist; CPE modulator&product of | -- | Under clinical trials | Details |
D199 | L-alanine | Chemical drug | DB00160 | KYNU | -- | Failed in clinical trials | Details |