Search

In addition to providing complete postnatal nutrition, breast milk is a complex biofluid that delivers bioactive components for the growth and development of the intestinal and immune systems. Lactation is a unique opportunity to understand the role of diet in shaping the intestinal environment including the infant microbiome. Of considerable interest is the diversity and abundance of milk glycans that are energetically costly for the mammary gland to produce yet indigestible by infants. Milk glycans comprise free oligosaccharides, glycoproteins, glycopeptides, and glycolipids. Emerging technological advances are enabling more comprehensive, sensitive, and rapid analyses of these different classes of milk glycans. Understanding the impact of inter- and intraindividual glycan diversity on function is an important step toward interventions aimed at improving health and preventing disease. This review discusses the state of technology for glycan analysis and how specific structure-function knowledge is enhancing our understanding of early nutrition in the neonate. [ABSTRACT FROM AUTHOR]

Maternal fat intake and adipose reserves are major sources of PUFA during lactation. The present study examined the cross-sectional relationship between prolonged breast-feeding and maternal BMI, assessed adequacy of fat intake among lactating and non-lactating mothers of children 24–48 months of age and determined breast-milk fatty acid composition. Multi-stage sampling was used to select a representative sample of mothers from two rural districts in Bangladesh (n 474). Dietary data were collected during two non-consecutive 24 h periods via 12 h in-home daytime observations and recall. The National Cancer Institute method for episodically consumed foods was used to estimate usual intake distributions. Breast milk samples were collected from ninety-eight women, and breast-milk fatty acid methyl esters were quantified using GC. Approximately 42 % of lactating v. 26 % of non-lactating mothers were underweight (BMI < 18·5 kg/m2; P = 0·0003). The maternal diet was low in total fat (approximately 8 % of mean total energy) and food sources of PUFA, including oil and animal source foods, resulting in a low estimated mean total consumption of PUFA (5·1 g/d). Almost all women were estimated to consume less than the recommended intake levels for total fat, total PUFA, α-linolenic acid (ALA) and DHA. Median breast-milk linoleic acid (8·5 % weight) and ALA (0·2 %) concentrations were among the lowest reported in the literature, in contrast with arachidonic acid (0·5 %) and DHA (0·3 %) concentrations, which were mid-range. Bangladeshi women in general, and especially those who practise prolonged breast-feeding, may benefit from increased consumption of food sources of PUFA. [ABSTRACT FROM PUBLISHER]

Background: Chronic ethanol consumption coupled with folate deficiency leads to rapid liver fat accumulation and progression to alcoholic steatohepatitis (ASH). However, the specific effects of alcohol on key liver lipid metabolic pathways involved in fat accumulation are unknown. It is unclear whether lipid synthesis, lipid export, or a combination of both is contributing to hepatic steatosis in ASH. Methods: In this study we estimated the flux of fatty acids (FA) through the stearoyl-CoA desaturase (SCD), phosphatidylethanolamine- N-methyltransferase (PEMT), and FA elongation pathways in relation to liver triacylglycerol (TG) content in Yucatan micropigs fed a 40% ethanol folate-deficient diet with or without supplementation with S-adenosyl methionine (SAM) compared with controls. Flux through the SCD and PEMT pathways was used to assess the contribution of lipid synthesis and lipid export respectively on the accumulation of fat in the liver. Liver FA composition within TG, cholesterol ester (CE), phosphatidylethanolamine, and phosphatidylcholine classes was quantified by gas chromatography. Results: Alcoholic pigs had increased liver TG content relative to controls, accompanied by increased flux through the SCD pathway as indicated by increases in the ratios of 16:1n7 to 16:0 and 18:1n9 to 18:0. Conversely, flux through the elongation and PEMT pathways was suppressed by alcohol, as indicated by multiple metabolite ratios. SAM supplementation attenuated the TG accumulation associated with alcohol. Conclusions: These data provide an in vivo examination of liver lipid metabolic pathways confirming that both increased de novo lipogenesis (e.g., lipid synthesis) and altered phospholipid metabolism (e.g., lipid export) contribute to the excessive accumulation of lipids in liver affected by ASH. [ABSTRACT FROM AUTHOR]