Fatty acid distribution of cord and maternal blood in human pregnancy: special focus on individual trans fatty acids and conjugated linoleic acids

<p>Abstract</p> <p>Background</p> <p>Maternal nutrition in pregnancy has a crucial impact on the development of the fetus. Dietary <it>trans </it>fatty acids (<it>t</it>FA) are known to have adverse health effects, especially during pregnancy. However, the distribution of <it>t</it>FA produced via partial hydrogenation of vegetable oils (mainly elaidic acid; <it>t</it>9) differs compared to ruminant-derived <it>t</it>FA (mainly vaccenic acid; <it>t</it>11). Recent findings indicate that they may have different impact on human health.</p> <p>Therefore, in this study, plasma and erythrocytes of mother-child pairs (n = 55) were sampled to investigate the distribution of <it>t</it>FA, including individual <it>trans </it>C18:1 fatty acids and conjugated linoleic acids (CLA) in fetal related to maternal lipids; with additional consideration of maternal dairy fat intake.</p> <p>Results</p> <p>Portion of <it>t</it>9 and <it>t</it>11, but also of <it>c</it>9,<it>t</it>11 CLA was higher in maternal than in fetal blood lipids. The portion of <it>t</it>9 in maternal and fetal lipids differed only slightly. In contrast, the portion of fetal <it>t</it>11 was only half of that in maternal blood. This led to a fetal <it>t</it>9/<it>t</it>11-index in plasma and erythrocytes being twice as high compared to the maternal values. A high dairy fat intake resulted in elevated portions of <it>t</it>11 and its Δ9-desaturation product <it>c</it>9,<it>t</it>11 CLA in maternal blood. In contrast, in the respective fetal blood lipids only <it>c</it>9,<it>t</it>11 CLA, but not <it>t</it>11 was increased. Nevertheless, a positive association between maternal and fetal plasma exists for both <it>t</it>11 and <it>c</it>9,<it>t</it>11 CLA. Furthermore, in contrast to <it>t</it>9, <it>t</it>11 was not negatively associated with n-3 LC-PUFA in fetal blood lipids.</p> <p>Conclusions</p> <p>Fetal blood fatty acid composition essentially depends on and is altered by the maternal fatty acid supply. However, in addition to dietary factors, other aspects also contribute to the individual fatty acid distribution (oxidation, conversion, incorporation). The lower portion of fetal <it>t</it>11 compared to maternal <it>t</it>11, possibly results from Δ9-desaturation to <it>c</it>9,<it>t</it>11 CLA and/or oxidation. Based on the fatty acid distribution, it can be concluded that <it>t</it>11 differs from <it>t</it>9 regarding its metabolism and their impact on fetal LC-PUFA.</p

High content of long-chain n-3 polyunsaturated fatty acids in red blood cells of Kenyan Maasai despite low dietary intake

<p>Abstract</p> <p>Background</p> <p>Increasing land restrictions and a reduced livestock-to-human ratio during the 20th century led the Maasai to lead a more sedentary, market-orientated lifestyle. Although plant-derived food nowadays contributes substantially to their diet, dairy products being high in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA) still are an important energy source. Since reliable data regarding the Maasai diet date back to the 1980s, the study objective was to document current diet practices in a Kenyan Maasai community and to investigate the fatty acid distribution in diet and red blood cells.</p> <p>Methods</p> <p>A cross-sectional study was conducted among 26 Maasai (20 women, 6 men) from Loodokilani, Kajiado District, Kenya. Food intake was described by the subjects via 24-h recall, and both food and blood samples were analysed.</p> <p>Results</p> <p>Two main foods - milk and <it>ugali </it>- constituted the Maasai diet in this region. A total of 0.9 L of milk and 0.6 kg of <it>ugali </it>were consumed per person and day to yield an energy intake of 7.6 MJ/d per person. A major proportion of ingested food contributing 58.3% to the total dietary energy (en%) was plant-derived, followed by dairy products representing 41.1 en%. Fat consumed (30.5 en%) was high in SFA (63.8%) and low in PUFA (9.2%). Long-chain n-3 PUFA (EPA, DPA and DHA) made up only 0.15% of the ingested fatty acids, but 5.9% of red blood cell fatty acids.</p> <p>Conclusion</p> <p>The study indicates the Maasai diet is rich in SFA and low in PUFA. Nevertheless, red blood cells are composed of comparable proportions of long-chain n-3 PUFA to populations consuming higher amounts of this fatty acid group.</p

The delta9-desaturation of dietary trans octadecenoic acids (trans11 and trans12 18:1) and the clinical relevance in humans

Als Folge der t11 und t12 Supplementation (S 6.0 g/d) stieg der Gehalt von t11, t12 und c9,t11 CLA in den Lipiden des Serums sowie in den Membranen der Erythrozyten und peripheren mononukleären Zellen signifikant an, wobei der Anteil von c9,t12 18:2 unverändert blieb. Die mittlere Konversionsrate von t11 lag bei 20 - 25 %. Die Serumlipide, Lipoproteine und Biomarker des Immunsystems und der Inflammation (Interleukine, TNFa, CRP, Prostacyclin, sPLA2, ICAM-1, Leptin, Adiponectin) unterlagen ebenfalls keinen Veränderungen. Die D9-Desaturation ist das Hauptkriterium, welches die t11 (natürliches trans-Isomere) von anderen trans 18:1 Isomeren wie t9- und t10-18:1, und resultierend aus den durchgeführten Studien, der t12 unterscheidet

Dietary supplementation with 11trans- and 12trans-18:1 and oxidative stress in humans

Background: High consumption of trans fat has been associated with high oxidative stress in humans, which could increase the risk of the development or acceleration of several diseases, such as atherosclerosis, cancer, and type 2 diabetes. Objective: Several urinary and blood biomarkers of oxidative stress [8-iso-prostaglandin-F2 (PGF2), 15-keto-dihydro-PGF2, and 7,8-dihydro-8-oxo-2'-deoxy-guanosine in urine and -, f-,-,-tocopherol, and retinol in plasma] were monitored to evaluate the oxidative stress induced by dietary supplementation of 11trans- and 12trans-18:1 isomers in humans during a 6-wk intervention. Design: After a 14-d adaptation period free of trans fatty acid supplementation (baseline), the test group (n =3D 12) received 3.0 g 11trans-18:1/d and 3.0 g 12trans-18:1/d ( 6.0 g/d), and the control group (n =3D 12) consumed a control oil free of trans fatty acids and conjugated linoleic acids for 6 wk. Results: The postintervention concentration of urinary 8-iso-PGF2 (free radical\u96induced lipid peroxidation) in the test group was significantly higher than baseline and significantly higher than that observed in the control group. The concentrations of 15-keto-dihydro-PGF2 (cyclooxygenase-mediated inflammatory response indicator) and 7,8-dihydro-8-oxo-2'-deoxy-guanosine (oxidative DNA damage) were not affected by the 11trans- and 12trans-18:1 supplementation. Conclusions: Although an increase in urinary 8-iso-PGF2 was observed and the effects of prolonged high (ie, >5.0 g/d) consumption of trans fat could be relevant to the development of disease, the mean intakes of 11trans- and 12trans-18:1 in Europeans are estimated to be significantly below the amounts administered in this study (ie, 6.0 g/d); such low intakes could minimize the possible risk of detrimental effects on human health

Influence of <it>in vitro </it>supplementation with lipids from conventional and Alpine milk on fatty acid distribution and cell growth of HT-29 cells

<p>Abstract</p> <p>Background</p> <p>To date, the influence of milk and dairy products on carcinogenesis remains controversial. However, lipids of ruminant origin such as conjugated linoleic acids (CLA) are known to exhibit beneficial effects <it>in vitro </it>and <it>in vivo</it>. The aim of the present study was to determine the influence of milk lipids of different origin and varying quality presenting as free fatty acid (FFA) solutions on cellular fatty acid distribution, cellular viability, and growth of human colon adenocarcinoma cells (HT-29).</p> <p>Methods</p> <p>FAME of conventional and Alpine milk lipids (ML_con, ML_alp) and cells treated with FFA derivatives of milk lipids were analyzed by means of GC-FID and Ag⁺-HPLC. Cellular viability and growth of the cells were determined by means of CellTiter-Blue^®-assay and DAPI-assay (4',6-diamidino-2-phenylindole dihydrochloride), respectively.</p> <p>Results</p> <p>Supplementation with milk lipids significantly decreased viability and growth of HT-29 cells in a dose- and time-dependent manner. ML_alpshowed a lower SFA/MUFA ratio, a 8 fold increased CLA content, and different CLA profile compared to ML_conbut did not demonstrate additional growth-inhibitory effects. In addition, total concentration and fatty acid distribution of cellular lipids were altered. In particular, treatment of the cells yielded highest amounts of two types of milk specific major fatty acids (μg FA/mg cellular protein) after 8 h of incubation compared to 24 h; 200 μM of ML_con(C16:0, 206 ± 43), 200 μM of ML_alp(C18:1 <it>c</it>9, (223 ± 19). Vaccenic acid (C18:1 <it>t</it>11) contained in milk lipids was converted to <it>c</it>9,<it>t</it>11-CLA in HT-29 cells. Notably, the ratio of <it>t</it>11,<it>c</it>13-CLA/<it>t</it>7,<it>c</it>9-CLA, a criterion for pasture feeding of the cows, was significantly changed after incubation for 8 h with lipids from ML_alp(3.6 - 4.8), compared to lipids from ML_con(0.3 - 0.6).</p> <p>Conclusions</p> <p>Natural lipids from conventional and Alpine milk showed similar growth inhibitory effects. However, different changes in cellular lipid composition suggested a milk lipid-depending influence on cell sensitivity. It is expected that similar changes may also be evident in other cell lines. To our knowledge, this is the first study showing a varied impact of complex milk lipids on fatty acid distribution in a colon cancer cell line.</p