肝脏维生素D代谢与非酒精性脂肪肝的关系

Title:The link between Hepatic Vitamin A Metabolism and Nonalcoholic Fatty Liver Disease

Volume: 16 Issue: 12

Author(s): Guoxun Chen

Affiliation:

关键词: 非酒精性脂肪性肝病，维生素A，维甲类物质，肝星状细胞，肝细胞，胰岛素。

摘要: The liver is essential for the control of glucose and lipid metabolism. Excessive accumulation of fat in the liver disturbs its function and leads to the development of fatty liver diseases. The nonalcoholic fatty liver disease (NAFLD) is a common type of fatty liver disease found in patients who have not consumed significant amount of alcohol. Multiple factors and cell types contribute to the development and progression of NAFLD. Diets contain macronutrients with energy and micronutrients with regulatory roles. As an essential micronutrient, vitamin A (VA), plays critical roles in various physiological functions including the regulation of glucose and lipid homeostasis in the liver. The body’s VA is mainly stored in quiescent hepatic stellate cells (HSCs) in the liver. Hepatocytes actively metabolize VA, and change glucose and lipid metabolism in response to VA metabolites. Interestingly, the activated HSCs lose their VA content and contribute to the NAFLD progression. Significant number of studies have been conducted to investigate the link between VA metabolism and NAFLD development. This review is to summarize current literatures that discuss the changes of VA metabolism occurring locally between hepatocytes and HSCs, and intracellularly in hepatocytes during the course of NAFLD development. It appears that factors derived from HSCs and hepatocytes mutually affect each other, which contributes to NAFLD development. Additionally, this review discusses the potential mechanism by which excessive VA metabolism increases lipogenesis and contributes to fat accumulation in hepatocytes. It offers potential future directions for the study of the role of VA metabolism in the NAFLD development.

Cite this article as:

Guoxun Chen , The link between Hepatic Vitamin A Metabolism and Nonalcoholic Fatty Liver Disease, Current Drug Targets 2015; 16 (12) . https://dx.doi.org/10.2174/1389450116666150325231015