In order to investigate the fatty acid composition and distribution in colostrum and mature milk, breast milk samples and 24 h food records were obtained from 65 lactating women across three regions in China (Inner Mongolia, North Jiangsu and Guangxi). Fatty acid methyl esters were prepared by standard methods and separated and identified by gas chromatography. Compared with the Chinese breast milk fatty acid data 10 years ago, SFA and trans fatty acids (TFA) in breast milk decreased, while PUFA increased in the present study. Most SFA (C16:0, C15:0, C14:0), cis-C16:1 and several LC-PUFA (C22:5n-3 and C22:6n-3) were predominantly acylated at the sn-2 position. The cis-C17:1 and C22:6n-3 were distributed equally in three positions of triacylglycerol (TAG). Whereas, TFA, conjugated linoleic acids (CLA), cis-C18:1, C18:2n-6, C18:3n-3 and C20:5n-3 were acylated at the sn-1, 3 positions of TAG in human milk. The composition of fatty acids in breast milk was closely related to the diet of lactating mothers. PUFA in breast milk was negatively correlated with the intake of protein, fat and meat, but positively correlated with the intake of carbohydrates. MUFA of human milk was negatively correlated with the intake of dairy products, eggs, fish and shrimp. SFA in breast milk was positively correlated with the maternal intake of meat. In addition, the present results showed that the composition of total fatty acids and sn-2 fatty acids in breast milk varied with the lactation period and the geographical regions in China; however, the regiospecific fatty acid profile seemed not to be affected by the lactation time and regions, although the quantities at each position could be changed.

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Endothelial inflammation is recognized as the initial stage of a multistep process leading to coronary heart disease (CHD). Recently, the different effects of industrial trans fatty acids (elaidic acid, 9t18:1) and ruminant trans fatty acids (vaccenic acid, 11t18:1) on CHD have been reported in epidemiological and animal studies, however, the mechanism was not fully studied. Therefore, the objective of this study was to explore the underlying mechanism by which 9t18:1 and 11t18:1 affect human umbilical vein endothelial cells (HUVECs) inflammation. We found that 9c11t-CLA modulated the inflammation of HUVECs induced by 9t18:1 and 11t18:1. Fatty acid composition, pro-inflammatory factors, phosphorylation of MAPKs, and the TLR4 level in HUVECs altered by 11t18:1 induction, collectively suggest that the bio-conversion of 11t18:1 to 9c11tCLA might be the cause why 11t18:1 and 9t18:1 have distinct influences on endothelial injuries. It was concluded that it is biosynthesis of 9c11t CLA from11t18:1, and the modulation of TLR4-MAPK pathway by 9c11t CLA, which at least partially account for the slight effect of 11t18:1 on endothelial inflammation.