High Intrinsic Aerobic Capacity Protects against Ethanol-Induced Hepatic Injury and Metabolic Dysfunction: Study Using High Capacity Runner Rat Model
| Autor: | Grace M. Uptergrove, John P. Thyfault, Nicholas M. Szary, Suzanne E. Ridenhour, Lauren G. Koch, R. Scott Rector, Jamal A. Ibdah, Shivendra D. Shukla, Steven L. Britton |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Blood Glucose
medicine.medical_specialty Liquid diet Physical Exertion Microvesicular Steatosis lcsh:QR1-502 Mitochondria Liver Biology Biochemistry Article Microsomal triglyceride transfer protein lcsh:Microbiology chemistry.chemical_compound mitochondrial function Internal medicine medicine Animals Aerobic exercise Molecular Biology Triglycerides Aerobic capacity Metabolic Syndrome Liver injury aerobic fitness fatty liver disease ethanol Triglyceride Superoxide Dismutase 3-Hydroxyacyl CoA Dehydrogenases medicine.disease Glutathione Rats Endocrinology chemistry Apolipoprotein B-100 biology.protein Steatosis human activities Fatty Liver Alcoholic |
| Zdroj: | Biomolecules; Volume 5; Issue 4; Pages: 3295-3308 Biomolecules, Vol 5, Iss 4, Pp 3295-3308 (2015) Biomolecules |
| ISSN: | 2218-273X |
| DOI: | 10.3390/biom5043295 |
| Popis: | Rats artificially selected over several generations for high intrinsic endurance/aerobic capacity resulting in high capacity runners (HCR) has been developed to study the links between high aerobic fitness and protection from metabolic diseases (Wisloff et al., Science, 2005). We have previously shown that the HCR strain have elevated hepatic mitochondrial content and oxidative capacity. In this study, we tested if the elevated hepatic mitochondrial content in the HCR rat would provide “metabolic protection” from chronic ethanol-induced hepatic steatosis and injury. The Leiber-Decarli liquid diet with ethanol (7% v/v; HCR-E) and without (HCR-C) was given to HCR rats (n = 8 per group) from 14 to 20 weeks of age that were weight matched and pair-fed to assure isocaloric intake. Hepatic triglyceride (TG) content and macro- and microvesicular steatosis were significantly greater in HCR-E compared with HCR-C (p < 0.05). In addition, hepatic superoxide dismutase activity and glutathione levels were significantly (p < 0.05) reduced in the HCR-E rats. This hepatic phenotype also was associated with reduced total hepatic fatty acid oxidation (p = 0.03) and ß-hydroxyacyl-CoA dehydrogenase activity (p = 0.01), and reductions in microsomal triglyceride transfer protein and apoB-100 protein content (p = 0.01) in HCR-E animals. However, despite these documented hepatic alterations, ethanol ingestion failed to induce significant hepatic liver injury, including no changes in hepatic inflammation, or serum alanine amino transferase (ALTs), free fatty acids (FFAs), triglycerides (TGs), insulin, or glucose. High intrinsic aerobic fitness did not reduce ethanol-induced hepatic steatosis, but protected against ethanol-induced hepatic injury and systemic metabolic dysfunction in a high aerobic capacity rat model. |
| Databáze: | OpenAIRE |
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