| dc.contributor.author | Harrison D. Stierwalt | |
| dc.contributor.author | E. Matthew Morris | |
| dc.contributor.author | Adrianna Maurer | |
| dc.contributor.author | Udayan Apte | |
| dc.contributor.author | Kathryn Phillips | |
| dc.contributor.author | Tiangang Li | |
| dc.contributor.author | Grace M. E. Meers | |
| dc.contributor.author | Lauren G. Koch | |
| dc.contributor.author | Steven L. Britton | |
| dc.contributor.author | Greg Graf | |
| dc.contributor.author | R. Scott Rector | |
| dc.contributor.author | Kelly Mercer | |
| dc.contributor.author | Kartik Shankar | |
| dc.contributor.author | John P. Thyfault | |
| dc.contributor.other | Molecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA | |
| dc.contributor.other | Molecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA | |
| dc.contributor.other | Molecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA | |
| dc.contributor.other | Department of Pharmacology, Toxicology, and Therapeutics University of Kansas Medical Center Kansas City Missouri USA | |
| dc.contributor.other | Department of Pediatrics Cornell Medicine New York New York USA | |
| dc.contributor.other | Department of Physiology University of Oklahoma Health Sciences Center Oklahoma City Oklahoma USA | |
| dc.contributor.other | Division of Gastroenterology and Hepatology University of Missouri Columbia Missouri USA | |
| dc.contributor.other | Physiology and Pharmacology The University of Toledo Toledo Ohio USA | |
| dc.contributor.other | Anesthesiology University of Michigan Ann Arbor Michigan USA | |
| dc.contributor.other | Department of Pharmaceutical Sciences Saha Cardiovascular Research Center, University of Kentucky Lexington Kentucky USA | |
| dc.contributor.other | Division of Gastroenterology and Hepatology University of Missouri Columbia Missouri USA | |
| dc.contributor.other | Arkansas Children's Nutrition Center University of Arkansas for Medical Sciences Little Rock Arkansas USA | |
| dc.contributor.other | Section of Nutrition, Department of Pediatrics University of Colorado School of Medicine Anschutz Medical Campus Aurora Colorado USA | |
| dc.contributor.other | Molecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA | |
| dc.date.accessioned | 2022-08-11T07:18:31Z | |
| dc.date.accessioned | 2025-10-08T08:27:16Z | |
| dc.date.available | 2025-10-08T08:27:16Z | |
| dc.date.issued | 01-08-2022 | |
| dc.identifier.uri | http://digilib.fisipol.ugm.ac.id/repo/handle/15717717/35936 | |
| dc.description.abstract | Abstract Rats selectively bred for the high intrinsic aerobic capacity runner (HCR) or low aerobic capacity runner (LCR) show pronounced differences in susceptibility for high‐fat/high sucrose (HFHS) diet‐induced hepatic steatosis and insulin resistance, replicating the protective effect of high aerobic capacity in humans. We have previously shown multiple systemic differences in energy and substrate metabolism that impacts steatosis between HCR and LCR rats. This study aimed to investigate hepatic‐specific mechanisms of action via changes in gene transcription. Livers of HCR rats had a greater number of genes that significantly changed in response to 3‐day HFHS compared with LCR rats (171 vs. 75 genes: >1.5‐fold, p < 0.05). HCR and LCR rats displayed numerous baseline differences in gene expression while on a low‐fat control diet (CON). A 3‐day HFHS diet resulted in greater expression of genes involved in the conversion of excess acetyl‐CoA to cholesterol and bile acid (BA) synthesis compared with the CON diet in HCR, but not LCR rats. These results were associated with higher fecal BA loss and lower serum BA concentrations in HCR rats. Exercise studies in rats and mice also revealed higher hepatic expression of cholesterol and BA synthesis genes. Overall, these results suggest that high aerobic capacity and exercise are associated with upregulated BA synthesis paired with greater fecal excretion of cholesterol and BA, an effect that may play a role in protection against hepatic steatosis in rodents. | |
| dc.language.iso | EN | |
| dc.publisher | Wiley | |
| dc.subject.lcc | Physiology | |
| dc.title | Rats with high aerobic capacity display enhanced transcriptional adaptability and upregulation of bile acid metabolism in response to an acute high‐fat diet | |
| dc.type | Article | |
| dc.description.keywords | aerobic capacity | |
| dc.description.keywords | bile acids | |
| dc.description.keywords | cholesterol | |
| dc.description.keywords | fatty liver | |
| dc.description.pages | n/a-n/a | |
| dc.description.doi | 10.14814/phy2.15405 | |
| dc.title.journal | Physiological Reports | |
| dc.identifier.e-issn | 2051-817X | |
| dc.identifier.oai | f8e93ebdad734679b7f4c777c1e5d38b | |
| dc.journal.info | Volume 10, Issue 15 | |