Title:The link between Hepatic Vitamin A Metabolism and Nonalcoholic Fatty Liver Disease
Volume: 16
Issue: 12
Author(s): Guoxun Chen
Affiliation:
Keywords:
Nonalcoholic fatty liver disease, vitamin A, retinoids, hepatic stellate cells, hepatocytes, insulin.
Abstract: 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.
