Research Article Details
| Article ID: | A50590 |
| PMID: | 35331900 |
| Source: | J Nutr Biochem |
| Title: | Intermittent fasting, high-intensity interval training, or a combination of both have beneficial effects in obese mice with nonalcoholic fatty liver disease. |
| Abstract: | Intermittent fasting (IF) and high-intensity interval training (HIIT) are procedures that might mitigate the effects of nonalcoholic fatty liver disease. Two groups of 3-month-old C57BL/6 male mice were fed for 16 weeks with a control (C) or high-fat (HF) diet. In the last 4 weeks of the study, IF, HIIT, and IF/HIIT were implemented. Obese HF animals showed liver fat accumulation with macro-, and micro-vesicular steatosis and inflammatory infiltrate. IF and HIIT successfully reduced liver steatosis in the HF-derived groups. IF, HIIT, and IF/HIIT were beneficial in improving glucose metabolism in both C-derived and HF-derived groups. High levels observed in plasmatic and liver levels of total cholesterol and triacylglycerol in the HF group compared to the C group were mitigated by IF, HIIT, and IF/HIIT. IF decreased adiponectin and increased leptin and insulin in the HF group. HIIT improved adiponectin and leptin. IF chances liver gene expressions: increased interleukin-6 (IL-6) in the C IF group, reduced IL-6, and PAI-1 in the HF group. IF/HIIT reduced IL-6, MCP-1, and PAI-1. IF and HIIT enhanced hepatic beta-oxidation. However, lipogenesis was reduced by IF and HIIT in the HF-derived groups. In conclusion, IF and HIIT benefit weight loss, hormones, glucose tolerance/insulin resistance, liver steatosis/inflammation, fatty acid oxidation, and lipogenesis. Furthermore, the IF groups showed beneficial effects more often and intensely than HIIT ones. The IF/HIIT combination was slightly more efficient than IF, indicating that IF is the primary intervening factor benefiting the obese mouse liver. |
| DOI: | 10.1016/j.jnutbio.2022.108997 |
| 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 |
| S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | 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 |
| I14 | 9970 | Obesity | An overnutrition that is characterized by excess body fat, traditionally defined as an elevated ratio of weight to height (specifically 30 kilograms per meter squared), has_material_basis_in a multifactorial etiology related to excess nutrition intake, decreased caloric utilization, and genetic susceptibility, and possibly medications and certain disorders of metabolism, endocrine function, and mental illness. https://en.wikipedia.org/wiki/Obesity | disease of metabolism/acquired metabolic disease/ nutrition disease/overnutrition | Details |