High-fat diet induces fibrosis in mice lacking CYP2A5 and PPARα: a new model for steatohepatitis-associated fibrosis

Author:

Chen Xue1,Acquaah-Mensah George K.2,Denning Krista L.3,Peterson Jonathan M.4,Wang Kesheng5,Denvir James1,Hong Feng6,Cederbaum Arthur I.7,Lu Yongke18

Affiliation:

1. Department of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia

2. Department of Pharmaceutical Sciences, Massachusetts College of Pharmacy and Health Sciences, Worcester, Massachusetts

3. Department of Pathology, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia

4. Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, Tennessee

5. Department of Family and Community Health, School of Nursing, Health Sciences Center, West Virginia University, Morgantown, West Virginia

6. Institute of Liver Diseases, Affiliated Hospital of Jining Medical University, Jining, China

7. Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York

8. Department of Clinical and Translational Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia

Abstract

PPARα is upregulated in cyp2a5−/− mice, but HFD-induced steatosis is still deteriorated. PPARα abrogation makes cyp2a5−/− mice more sensitive to HFD-induced steatosis, liver inflammation, and fibrosis, suggesting that PPARα upregulation in cyp2a5−/− mice is a compensation response. HFD-induced liver inflammation, fibrosis, and nitrotyrosine formation in pparα−/−/cyp2a5−/− mice are all within clusters of lipid droplets, and lipid droplets are all within CYP2E1-positive area.

Funder

HHS | NIH | National Institute on Alcohol Abuse and Alcoholism

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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