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Dietary choline is required for proper structure and dynamics of cell membranes, lipoprotein synthesis, and methyl-group metabolism. In mammals, choline is synthesized via phosphatidylethanolamine N-methyltransferase (Pemt), which converts phosphatidylethanolamine to phosphatidylcholine. Pemt-/- mice have impaired VLDL secretion and developed fatty liver when fed a high-fat (HF) diet. Because of the reduction in plasma lipids, Pemt-/-/low-density lipoprotein receptor knockout (Ldlr-/-)miceare protected from atherosclerosis. The goal of this study was to investigate the importance of dietary choline in the metabolic phenotype of Pemt-/-/Ldlr-/- male mice. At 10-12 wk of age, Pemt+/+/Ldlr-/- (HF+/+) and half of the Pemt-/-/Ldlr-/- (HF/-) mice were fed an HF/-diet with normal (1.3g/kg) choline. The remaining Pemr/2/Ldlr/2 mice were fed an HF diet supplemented (5g/kg) with choline(HFCS--/- mice). The HF diet contained 60% of calories from fat and 1% cholesterol, and the mice were fed for 16 d. HF-/- mice lost weight and developed hepatomegaly, steatohepatitis, and liver damage. Hepatic concentrations of free cholesterol, cholesterol-esters, and triglyceride (TG) were elevated by 30%, 1.1-fold and 3.1-fold, respectively, in HF/- compared with HF+/+ mice. Choline supplementation normalized hepatic cholesterol, but not TG, and dramatically improved liver function. The expression of genes involved in cholesterol transport and esterification increased by 50% to 5.6-fold in HF-/- mice when compared with HF+/+ mice. Markers of macrophages, oxidative stress, and fibrosis were elevated in the HF--/- mice. Choline supplementation normalized the expression of these genes. In conclusion, HF--/- mice develop liver failure associated with altered cholesterol metabolism when fed an HF/normal choline diet. Choline supplementation normalized cholesterol metabolism, which was sufficient to prevent nonalcoholic steatohepatitis development and improve liver function. Our data suggest that choline can promote liver health by maintaining cholesterol homeostasis. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to investigate how maternal polyunsaturated fatty acid intake at different periods during pregnancy affects the composition of polyunsaturated fatty acids in mature human milk., Methods: A prospective study was conducted involving 45 pregnant women, aged between 18 and 35 y, who had full-term pregnancies and practiced exclusive or predominant breast-feeding. Mature breast milk samples were collected after the 5th postpartum week by manual expression; fatty acid composition was determined by gas chromatography. Fatty acid intake during pregnancy and puerperium was estimated through multiple 24-h dietary recalls. Linear regression models, adjusted by postpartum body mass index and deattenuated, were used to determine associations between estimated fatty acids in maternal diet during each trimester of pregnancy and fatty acid content in mature human milk., Results: A positive association was identified between maternal intake of eicosapentaenoic acid (β, 1.873; 95% confidence interval [CI], 0.545, 3.203) and docosahexaenoic acid (β, 0.464; 95% CI, 0.212-0.714) during the third trimester of pregnancy, as well as the maternal dietary ω-3 to ω-6 ratio (β, 0.093; 95% CI, 0.016-0.170) during the second and third trimesters and postpartum period, with these fatty acids content in mature breast milk., Conclusions: The maternal dietary docosahexaenoic acid and eicosapentaenoic acid content during late pregnancy may affect the fatty acid composition of mature breast milk. Additionally, the maternal dietary intake of ω-3 to ω-6 fatty acid ratio, during late pregnancy and the postpartum period, can affect the polyunsaturated fatty acid composition of breast milk., (Copyright © 2014 Elsevier Inc. All rights reserved.)