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.
journal_name
Curr Drug Targetsjournal_title
Current drug targetsauthors
Chen Gdoi
10.2174/1389450116666150325231015subject
Has Abstractpub_date
2015-01-01 00:00:00pages
1281-92issue
12eissn
1389-4501issn
1873-5592pii
CDT-EPUB-66164journal_volume
16pub_type
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journal_title:Current drug targets
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