The uniqueness of ruminant milk lipids is based on their high concentration of CLA. Maximal CLA concentrations in milk lipids require optimal conditions of ruminal fermentation and substrate availability, conditions like those present in pasture-fed cows. Our previous work showed that farm management (indoor feeding vs. pasture feeding) markedly influenced the CLA concentration. In this study, the objective was to evaluate the influence of the farm management system as dependent on different locations. Milk samples from different locations (Thuringia and the Alps, representing diverse altitudes) were collected during the summer months and analyzed for FA profile and CLA isomer distribution. The proportion of PUFA and total CLA in milk fat was significantly lower in milk from indoor cows compared with the pasture cows in the Alps. The trans-11 18:1 in milk fat of Alpine cows was elevated, in contrast to lower values for trans-10 18:1. Milk from cows grazing pasture in the Alps was higher in EPA and lower in arachidonic acid than milk from indoor-fed cows. The proportion of cis,trans/trans,cis isomers of CLA was 10 times higher from the indoor cows than from the Alpine cows. In addition to the major isomer cis-9,trans-11, this difference also occurred for the trans-11,cis-13 isomer, which represented more than a fourth of the total CLA present in milk fat. This is the first report showing a special isomer distribution in the milk fat of cows living under very natural conditions. We hypothesize that the CLA isomer trans-11,cis-13 is formed in large quantity as a result of grazing mountain pasture, which is rich in alpha-linolenic acid.

Milk consumption from early childhood on has been found to be inversely correlated with allergic sensitization and the onset of bronchial asthma. We tested whether cis-9,trans-11-conjugated linoleic acid (c9,t11-CLA), naturally occurring in milk fat, may prevent allergic sensitization and inhibit airway inflammation in a murine asthma model. BALB/c mice were fed a diet enriched in 1 wt% of c9,t11-CLA or a control diet 7 d prior to and for 32 d during sensitization [d 1 and 14, 100 mg/L ovalbumin (OVA) in adjuvant vs. PBS] and airway challenges (d 28-30, 1% OVA in PBS vs. PBS). Subgroups of mice were coadministered 20 micromol/L of the selective PPARgamma antagonist GW9662 during each OVA challenge. C9,t11-CLA feeding resulted in significantly reduced IgE production and allergen-induced in vivo airway hyperresponsiveness. Further, less mucous plugging of segmental bronchi and significantly reduced interleukin-5 and eosinophils were determined in bronchoalveolar lavage fluids of c9,t11-CLA-fed mice. C9,t11-CLA feeding prevented the downregulation of PPARgamma mRNA in the lung tissues observed after allergen sensitization and airway challenges in control mice. The inhibitory effects of c9,t11-CLA on airway inflammation were partially prevented by coadministration of GW9962. Further, c9,t11-CLA feeding resulted in a significantly lower concentration of the eicosanoid precursor, arachidonic acid, in tissue lipids. These findings demonstrate that dietary c9,t11-CLA can reduce allergic airway inflammation, most likely via a PPARgamma-related mechanism and by reducing eicosanoid precursors. They give new insights into the fatty acid-mediated mechanism of immunomodulation and may represent a step toward an attractive novel strategy in the dietary prevention and treatment of allergic asthma.

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The objective of the study was to investigate the influence of two roughage-to-concentrate ratios, with or without linseed oil supplementation, on the flow of fatty acids in the intestinal chyme and the secretion in milk fat in late lactating cows. Seven late lactating cows fitted with cannulae in the dorsal rumen and simple T-shaped cannulae in the proximal duodenum were randomly assigned to four experimental periods applying an incomplete replicated 2 x 2 Latin square design. The rations consisted of meadow hay and a concentrate mixture given in a ratio of 70:30 or 30:70 on dry matter basis. The basal rations were fed without or with 200 g linseed oil daily. After three weeks of adaptation, samples from the duodenal chyme were taken to study the flow of fatty acids. Additionally, milk samples were analysed for their milk fat composition. Decreasing roughage/concentrate ratio and linseed oil supplementation significantly increased the flow of monounsaturated fatty acids (MUFA), trans-fatty acids (tFA) and conjugated linoleic acids (CLA) in the duodenum. Furthermore, linseed oil increased the flow of saturated fatty acids (SFA) in the duodenum. Higher concentrate portion (H 30) and linseed oil supplementation significantly decreased the milk fat content. SFA were lower (p < 0.05) and MUFA were higher (p < 0.05) in milk fat after linseed oil supplementation; H 30 resulted in more polyunsaturated fatty acids (PUFA, p < 0.05) in the milk. Linseed oil supplementation significantly increased tFA and CLA in milk fat. The higher CLA content in milk fat as compared to that in the digesta suggests that a substantial endogenous synthesis of CLA in the mammary gland tissue through A9-desaturase took place. Between 21% and 48% of duodenal t11-C(18:1) were converted into c9, t11-CLA in milk fat.

The present study evaluated and compared the efficiency of the conversion of t11 18:1 and t12 18:1 to their corresponding dienoic acids (c9,tn 18:2) and assessed whether differences due to gender existed in several tissues of rats. Three groups of 4-wk-old male and female rats were fed for 3 wk a diet supplemented with 0, 0.5, or 1% of a trans-octadecenoic acid isomer mixture (tOIM) containing t11 18:1 and t12 18:1 in equal proportion. t11 18:1 and t12 18:1 were incorporated in a tissue-specific manner, and the accrual was significant with increased dietary intake of these trans fatty acid (tFA) isomers. The t12 18:1 isomer was more readily incorporated into the rat tissues than the t11 18:1 isomer. From t11 and t12 18:1, the respective desaturase products, c9,t11 18:2 and c9,t12 18:2, were formed. The calculated conversion rates varied greatly among the tissues of the rats but they were consistently lower for t12 18:1 than for t11 18:1, suggesting that t12 18:1 is a poorer substrate than t11 18:1 for Delta9-desaturase. For both fatty acids investigated, the calculated conversion rates in decreasing order of conversion efficiency were: testes = kidneys > adipose tissue > ovaries > muscle > liver > heart. Overall, there were distinct differences in the conversion of t11 18:1 and t12 18:1, indicating that these 2 fatty acids are metabolized differently despite their structural similarities. Such metabolic differences in tFA accumulation and metabolism may have potential implication in assessing the safety of these tFA isomers because there is a positive correlation between the intake of tFA and the incidence of various diseases.