期刊
BIOCHEMICAL JOURNAL
卷 370, 期 -, 页码 987-993出版社
PORTLAND PRESS
DOI: 10.1042/BJ20021523
关键词
betaine; choline deficiency; liver steatosis; phosphatidylcholine; phosphocholine
资金
- NIA NIH HHS [AG09525] Funding Source: Medline
- NIDDK NIH HHS [DK55865, DK56350] Funding Source: Medline
- NIEHS NIH HHS [ES10126] Funding Source: Medline
Choline is an essential nutrient for humans and is derived from the diet as well as from de novo synthesis involving methylation of phosphatidylethanotamine catalysed by the enzyme phosphatidylethanolamine N-methyltransferase (PEMT). This is the only known pathway that produces new choline molecules. We used mice with a disrupted Pemt-2 gene (which encodes PEMT; Pemt(-/-)) that have previously been shown to possess no hepatic PEMT enzyme. Male, female and pregnant Pemt(-/-) and wildtype mice (n = 5-6 per diet group) were fed diets of different choline content (deficient, control, and supplemented). Livers were collected and analysed for choline metabolites, steatosis, and apoptotic [terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labelling (TUNEL)] positive cells. We found that, in livers of Pemt(-/-) mice fed any of the diets, there was hepatic steatosis and significantly higher occurrence of TUNEL positive cells compared with wild-type controls. In male, female and pregnant mice, liver phosphatidylcholine concentrations were significantly decreased in Pemt(-/-) choline deficient and in Pemt(-/-) choline control groups but returned to normal in Pemt(-/-) choline supplemented groups. Phosphocholine concentrations in liver were significantly diminished in knockout mice even when choline was supplemented to above dietary requirements. These results show that PEMT normally supplies a significant portion of the daily choline requirement in the mouse and, when this pathway is knocked out, mice are unable to attain normal concentrations of all choline metabolites even with a supplemental source of dietary choline.
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