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Published on: November 27, 2019
Increased apolipoprotein A5 expression in human and rat non-alcoholic fatty livers
Qin Feng1, Susan S Baker, Wensheng Liu
11Institute of Hepatology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China 2Digestive Diseases and Nutrition Center, Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York at Buffalo, Buffalo, NY 3Center for Prevention of Obesity, Diabetes and Cardiovascular Disease, Children's Hospital Oakland Research Institute, Oakland, CA, United States 4Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China *these senior authors contributed equally to this work.
Apolipoprotein A5 (apoA5) expression is elevated in non-alcoholic fatty liver disease (NAFLD) livers, promoting fat storage and contributing to disease pathogenesis. This suggests apoA5 may be a therapeutic target for NAFLD.
Area of Science:
- Hepatology
- Metabolic Disease Research
- Molecular Biology
Background:
- Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes.
- Apolipoprotein A5 (apoA5) is a key regulator of triglyceride (TG) metabolism.
- The role of apoA5 in NAFLD pathogenesis requires further investigation.
Purpose of the Study:
- To investigate the role of apoA5 in the pathogenesis of NAFLD.
- To examine apoA5 mRNA expression in human paediatric NAFLD livers and a NAFLD rat model.
- To determine the correlation between apoA5 expression and hepatic TG content.
Main Methods:
- Microarray analysis and quantitative real-time PCR were used to assess apoA5 mRNA expression.
- Hepatic TG content and perilipin expression were measured.
- A NAFLD rat model and cultured HepG2 cells were utilized.
Main Results:
- Human NAFLD livers showed significantly elevated apoA5 mRNA expression compared to healthy controls.
- ApoA5 expression positively correlated with hepatic TG storage and perilipin levels in NAFLD livers.
- ApoA5 expression was not induced by fat accumulation in cultured HepG2 cells, but was elevated in NAFLD rat models.
Conclusions:
- Apolipoprotein A5 promotes intracellular hepatic TG storage, contributing to NAFLD pathogenesis.
- Elevated apoA5 expression in NAFLD may be linked to insulin resistance.
- ApoA5 represents a potential therapeutic target for non-alcoholic fatty liver disease.
