Roles of PPARα and HNF4α within the emergence of fatty liver disease pathophysiology

Document Type : Review Article

Authors

1 physiology department faculty of medicine sohag university

2 Medical Physiology department, Sohag Faculty of Medicine, Sohag university

3 Department, of Histology, Facultyof Medicine, Sohag University.

4 lecturer in physiology department, Faculty of Medicine, Sohag university

5 Department of Physiology, Faculty of Medicine, Sohag University, Sohag, Egypt.

Abstract

Globally, non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent forms of persistent liver disease. It is regarded as a constituent of metabolic disease, which additionally comprises diabetes, overweight, resistance to insulin, hypertension, and dyslipidemia. The most common reason for NAFLD is disturbed whole-body energy balance brought on by consuming more calories than burning them. The extra energy is subsequently deposited in an aberrant fat stores. Alterations to the hepatic metabolic system are the hallmark of this disease. The characteristic feature underlying NAFLD is liver lipid accumulation in deficient excessive alcohol intake. PPARα is ligand-induced synthesis molecules that regulate the transcription of several processes primarily expressed in hepatic tissue, where it is involved in the fatty acid oxidation, regulation of many pathways implicated in metabolism, and regulates the energy and lipid balance. HNF4α is a multi-gene master regulator, that are involved in gluconeogenesis, and lipid homeostasis. Liver HNF4α not only controls VLDL secretion but also has a crucial influence in controlling liver lipolysis.

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Sohag Medical Journal
Volume 28, Issue 3. - Serial Number 3
Basic Science Volume
2024
Pages 27-34

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