The role of apolipoprotein C3 in the regulation of nonalcoholic fatty liver disease, glucose and lipid metabolism, and islet β cell function.
- Author:
Shan YAN
1
;
Zhi-Yong DING
2
;
Yuan GAO
3
;
Wang-Jia MAO
1
;
Xiao-Yun CHENG
1
Author Information
1. Department of Endocrinology and Metabolism, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
2. Department of Endocrinology and Metabolism, Chongming Branch, Tenth People's Hospital of Tongji University, Shanghai 202157, China.
3. School of Medicine, Tongji University, Shanghai 200092, China.
- Publication Type:Journal Article
- MeSH:
Apolipoprotein C-III/genetics*;
Non-alcoholic Fatty Liver Disease/pathology*;
Glucose/metabolism*;
Lipid Metabolism;
Humans;
Animals;
Hypertriglyceridemia/metabolism*;
Islets of Langerhans/metabolism*
- From:
Acta Physiologica Sinica
2023;75(6):767-778
- CountryChina
- Language:Chinese
-
Abstract:
As a member of the apolipoprotein C (ApoC) family with a relatively high content, ApoC3 plays a major role in the regulation of triglyceride metabolism, and plays an important role in the occurrence and development of cardiovascular diseases, glucose and lipid metabolism disorders. Nonalcoholic fatty liver disease (NAFLD) refers to the accumulation of a large amount of fat in the liver in the absence of a history of chronic alcohol consumption or other damage to the liver. A large number of previous studies have shown that there is a correlation between the gene polymorphism and high expression of ApoC3 and NAFLD. In the context of hypertriglyceridemia (HTG), this article reviews the relationship between ApoC3 and NAFLD, glucose and lipid metabolism, and islet β cell function, showing that ApoC3 can not only inhibit lipoprotein lipase (LPL) and hepatic lipase (HL) activity, delay the decomposition of triglyceride in plasma to maintain the body's energy metabolism during fasting, but also be significantly increased under insulin resistance, prompting the liver to secrete a large amount of very low-density lipoprotein (VLDL) to induce HTG. Therefore, targeting and inhibiting ApoC3 might become a new approach to treat HTG. Increasing evidence suggests that ApoC3 does not appear to be an independent "contributor" to NAFLD. Similarly, our previous studies have shown that ApoC3 is not an independent factor triggering islet β cell dysfunction in ApoC3 transgenic mice, but in a state of excess nutrition, HTG triggered by ApoC3 high expression may exacerbate the effects of hyperglycemia and insulin resistance on islet β cell function, and the underlying mechanism remains to be further discussed.
