Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Choline Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed1986

Hepatic DNA methylation and liver tumor formation in male C3H mice fed methionine- and choline-deficient diets.

The effects of the chronic administration of methyl-deficient, amino acid-defined diets on liver tumor formation were examined in male weanling C3H/HeN mice previously treated with a single ip injection of 0 or 150 mg diethylnitrosamine/kg body weight [(DENA) CAS: 55-18-5]. Five diets were used: diet 1, adequate; diet 2, devoid of both methionine and choline; diet 3, devoid of methionine only; diet 4, devoid of choline only; and diet 5, devoid of methionine, choline, folic acid, and vitamin B12. Equimolar homocystine replaced methionine in all methionine-devoid diets. All diets were administered for 1 year. No hepatocellular carcinomas and only 3 liver adenomas were seen among the 129 animals at risk in the 5 groups that had received no DENA. Among the DENA-treated groups fed diets 1-4, the incidence of hepatocellular carcinomas in the mice at risk averaged 40%, with no significant differences noted among groups. A relatively low incidence of liver carcinomas (10%) was seen among DENA-treated mice subsequently fed diet 5; it could be ascribed to the enhanced mortality seen in these animals due to the dietary deficiencies. Lung tumors were seen in 44% of the DENA-treated mice surviving more than 35 experimental weeks and in only 2.5% of the corresponding DENA-untreated animals. Feeding diet 2, deficient in methionine and choline, to male C3H mice for 5-20 weeks decreased the hepatic ratio of S-adenosylmethionine (CAS: 29908-3-0) to S-adenosylhomocysteine (979-92-0) relative to that observed in mice fed the adequate diet 1. The 5-methyldeoxycytidine [(5-MC) CAS: 838-07-3] contents of liver DNA in animals fed diet 2 for 5, 10, and 20 weeks, however, were not significantly different from the corresponding levels in diet 1-fed mice. The results indicate that a methionine- and choline-deficient dietary regimen that lowers the 5-MC levels in DNA and enhances liver tumor formation in male F344 rats does not do so in male C3H mice.

Animals↗
PubMed2006

Mice fed a lipogenic methionine-choline-deficient diet develop hypermetabolism coincident with hepatic suppression of SCD-1.

Lipogenic diets that are completely devoid of methionine and choline (MCD) induce hepatic steatosis. MCD feeding also provokes systemic weight loss, for unclear reasons. In this study, we found that MCD feeding causes profound hepatic suppression of the gene encoding stearoyl-coenzyme A desaturase-1 (SCD-1), an enzyme whose regulation has significant effects on metabolic rate. Within 7 days of MCD exposure, hepatic SCD-1 mRNA decreased to nearly undetectable levels. By day 21, SCD-1 protein was absent from hepatic microsomes and fatty acids showed a decrease in monounsaturated species. These changes in hepatic SCD-1 were accompanied by signs of hypermetabolism. Calorimetry revealed that MCD-fed mice consumed 37% more energy than control mice (P = 0.0003). MCD feeding also stimulated fatty acid oxidation, although fatty oxidation genes were not significantly upregulated. Interestingly, despite their increased metabolic rate, MCD-fed mice did not increase their food consumption, and as a result, they lost 26% of their body weight in 21 days. In summary, MCD feeding suppresses SCD-1 in the liver, which likely contributes to hypermetabolism and weight loss. MCD feeding also induces hepatic steatosis, by an independent mechanism. Viewed together, these two disparate consequences of MCD feeding (weight loss and hepatic steatosis) give the appearance of an unusual form of lipodystrophy.

Animals↗