Abstract

Fatty acids esterified into triacylglycerol (TAG) by mammary epithelial cells (MEC) of lactating animals are derived either from plasma lipid or by de novo biosynthesis from small molecule precursors. The major contribution to milk lipid from plasma arises by hydrolysis of the TAG components of VLDL and chylomicrons, catalysed by lipoprotein lipase (LPL) in the mammary capillary bed; a minor contribution may come from the direct uptake of plasma non-esterified fatty acids. In the mammary gland of ruminant animals, short and medium-chain saturated fatty acids are the major products of de novo lipogenesis whereas plasma lipids contribute longer-chain and mono-unsaturated species. Human populations consuming diets disproportionately rich in saturated fatty acids experience increased risk of atherosclerosis — this association is most probably causal. Conversely, the potential health benefits associated with minor lipid components of milk fat — in particular CLA — have also recently been highlighted. This presentation will focus on selected key enzyme reactions with potential to determine and/or influence the fatty acid composition of milk lipid: ACC, SCD and FAT. Recent advances in their enzymology and molecular biology will be reviewed, emphasizing those properties that are relevant to the regulation both of their catalytic activities and of their expression. The cell biology of lipid secretion by MEC will be examined. Mammary cell/tissue models of lipid secretion will be surveyed to assess their suitability as experimental platforms for monitoring the possible effectiveness of interventions aimed at altering the amount or composition of lipid output during lactation.

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