期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 16, 期 3, 页码 339-345出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e3283600d46
关键词
choline; DNA methylation; epigenetics; fatty liver; liver carcinoma
资金
- NIH [DK05595, DK36530]
- Pfizer Nutrition
- Balchem
- Egg Nutrition Research Center for studies
Purpose of review Humans eating diets low in choline develop fatty liver and liver damage. Rodents fed choline-methionine-deficient diets not only develop fatty liver, but also progress to develop fibrosis and hepatocarcinoma. This review focuses on the role of choline in liver function, with special emphasis on the epigenetic mechanisms of action. Recent findings Dietary intake of methyl donors like choline influences the methylation of DNA and histones, thereby altering the epigenetic regulation of gene expression. The liver is the major organ within which methylation reactions occur, and many of the hepatic genes involved in pathways for the development of fatty liver, hepatic fibrosis, and hepatocarcinomas are epigenetically regulated. Summary Dietary intake of choline varies over a three-fold range and many humans have genetic polymorphisms that increase their demand for choline. Choline is an important methyl donor needed for the generation of S-adenosylmethionine. Dietary choline intake is an important modifier of epigenetic marks on DNA and histones, and thereby modulates the gene expression in many of the pathways involved in liver function and dysfunction.
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