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dc.contributor.authorHarrison D. Stierwalt
dc.contributor.authorE. Matthew Morris
dc.contributor.authorAdrianna Maurer
dc.contributor.authorUdayan Apte
dc.contributor.authorKathryn Phillips
dc.contributor.authorTiangang Li
dc.contributor.authorGrace M. E. Meers
dc.contributor.authorLauren G. Koch
dc.contributor.authorSteven L. Britton
dc.contributor.authorGreg Graf
dc.contributor.authorR. Scott Rector
dc.contributor.authorKelly Mercer
dc.contributor.authorKartik Shankar
dc.contributor.authorJohn P. Thyfault
dc.contributor.otherMolecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA
dc.contributor.otherMolecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA
dc.contributor.otherMolecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA
dc.contributor.otherDepartment of Pharmacology, Toxicology, and Therapeutics University of Kansas Medical Center Kansas City Missouri USA
dc.contributor.otherDepartment of Pediatrics Cornell Medicine New York New York USA
dc.contributor.otherDepartment of Physiology University of Oklahoma Health Sciences Center Oklahoma City Oklahoma USA
dc.contributor.otherDivision of Gastroenterology and Hepatology University of Missouri Columbia Missouri USA
dc.contributor.otherPhysiology and Pharmacology The University of Toledo Toledo Ohio USA
dc.contributor.otherAnesthesiology University of Michigan Ann Arbor Michigan USA
dc.contributor.otherDepartment of Pharmaceutical Sciences Saha Cardiovascular Research Center, University of Kentucky Lexington Kentucky USA
dc.contributor.otherDivision of Gastroenterology and Hepatology University of Missouri Columbia Missouri USA
dc.contributor.otherArkansas Children's Nutrition Center University of Arkansas for Medical Sciences Little Rock Arkansas USA
dc.contributor.otherSection of Nutrition, Department of Pediatrics University of Colorado School of Medicine Anschutz Medical Campus Aurora Colorado USA
dc.contributor.otherMolecular and Integrative Physiology University of Kansas Medical Center Kansas City Missouri USA
dc.date.accessioned2022-08-11T07:18:31Z
dc.date.accessioned2025-10-08T08:27:16Z
dc.date.available2025-10-08T08:27:16Z
dc.date.issued01-08-2022
dc.identifier.urihttp://digilib.fisipol.ugm.ac.id/repo/handle/15717717/35936
dc.description.abstractAbstract 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.isoEN
dc.publisherWiley
dc.subject.lccPhysiology
dc.titleRats with high aerobic capacity display enhanced transcriptional adaptability and upregulation of bile acid metabolism in response to an acute high‐fat diet
dc.typeArticle
dc.description.keywordsaerobic capacity
dc.description.keywordsbile acids
dc.description.keywordscholesterol
dc.description.keywordsfatty liver
dc.description.pagesn/a-n/a
dc.description.doi10.14814/phy2.15405
dc.title.journalPhysiological Reports
dc.identifier.e-issn2051-817X
dc.identifier.oaif8e93ebdad734679b7f4c777c1e5d38b
dc.journal.infoVolume 10, Issue 15


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