Dietary Fat Does Not Overcome trans-10, cis-12 Conjugated Linoleic Acid Inhibition of Milk Fat Synthesis in Lactating mice

Trans-10, cis-12 conjugated linoleic acid (CLA) is a potent inhibitor of milk fat synthesis in the cow and similarly reduces milk fat in rodents. The objective of this study was to determine whether dietary fat can overcome CLA inhibition of milk fat concentration in lactating mice. Wild type C57Bl/6J mice (n = 31) were fed semipurified diets containing either low fat (LF; 4% fat) or high fat (HF; 23.6% fat) starting 4–6 days postpartum. Dietary fat was increased by inclusion of high oleic sunflower oil. After 2 days on the experimental diets, lactating dams were orally dosed with either water (control) or trans-10, cis-12 CLA (20 mg/day) for 5 days. CLA treatment decreased pup growth similarly in both HF and LF diets. Milk fat percent was increased over 16% by the HF diet and decreased over 12% by CLA, but there was no interaction of dietary fat and CLA. Both CLA and the HF diet reduced the proportion of short- and medium-chain fatty acids that originate from de novo synthesis, and there was no interaction of diet and CLA. CLA had no effect on the percent of preformed fatty acids, but the HF diet increased their abundance. Dietary fat and CLA both modified mammary expression of lipogenic enzymes and regulators, but no interactions were observed. In conclusion, CLA reduced milk fat concentration and litter growth, but these effects were not overcome by increased dietary fat from high oleic sunflower oil. CLA inhibition of milk fat in the mammary gland is not substrate dependent, and the mechanism is independent from dietary supply of oleic acid.     

Maternal High‐Fat‐Diet Programs Rat Offspring Liver Fatty Acid Metabolism

In offspring exposed in utero to a maternal diet high in fat (HF), we have previously demonstrated that despite similar birth weights, HF adult offspring at 6 months of age had significantly higher body weights, greater adiposity, and increased triacylglycerol (TAG) levels as compared to controls. We hypothesized that a maternal HF diet predisposes to offspring adiposity via a programmed increase in the synthesis of monounsaturated fatty acids in the liver and hence increased substrate availability for liver TAG synthesis. We further hypothesized that programmed changes in offspring liver fatty acid metabolism are associated with increased liver expression of the lipogenic enzyme stearoyl‐CoA desaturase‐1 (SCD‐1). Female rats were maintained on a HF diet rich in monounsaturated fatty acids (MUFA) prior to and throughout pregnancy and lactation. After birth, newborns were nursed by the same dam, and all offspring were weaned to control diet. Plasma and liver fatty acid compositions were determined using gas chromatography/mass spectrometry. Fatty acid C16 desaturation indices of palmitoleic/palmitic and (vaccenic + palmitoleic)/palmitic and the C18 desaturation index of oleic/stearic were calculated. Liver protein abundance of SCD‐1 was analyzed in newborns and adult offspring. Plasma and liver C16 desaturation indices were decreased in HF newborns, but increased in the adult offspring. Liver SCD‐1 expression was increased in the HF adult offspring. These data show that the maternal HF diet during pregnancy and lactation increases offspring liver SCD‐1 protein abundance and alters the liver C16 desaturase pathway.     

Sex‐specific Alterations in Serology and the Expression of Liver FATP4 Protein in Offspring Exposed to High‐Fat Diet during Pregnancy and/or Lactation

Changes in dietary composition will have a significant impact on the nutritional status of the mother and the offspring. To examine the relevant hormone level changes during lactation and the expression of fatty acid transporters in the placenta and liver under the condition of a high‐fat (HF) diet, we established HF animal models and conducted a cross‐fostering program to mimic the shift in diet. On gestation day (GD)18, the weight of placenta in the HF group was significantly higher than that in the control group (p < 0.05). HF‐fed male pups had a significantly lower serum insulin level, but the same phenomenon was not found in females. On the contrary, serum triacylglycerol (TAG) level presented a tendency to decrease only in female offspring. Oil red O staining showed lipid accumulation in the HF diet offspring livers. The mRNA levels of FATP4 in the placenta in the HF diet group were significantly upregulated compared to the control diet group (p < 0.05). High‐fat diet (HFD) consumption also altered the liver mRNA levels of FATP4, SREBP‐1, and SCD‐1 in the male offspring, while the changes in protein levels of FATP4 were not observed in either sex. In conclusion, maternal HF diet has a profound impact on offspring growth, metabolism, and the risk of metabolic disorders, which would depend on the exposure period of pregnancy and lactation.     

Double Bond Position Plays an Important Role in Delta-9 Desaturation and Lipogenic Properties of Trans 18:1 Isomers in Mouse Adipocytes

The objective of this research was to study the delta‐9 desaturation of individual trans (t) fatty acids that can be found in ruminant fat or partially hydrogenated vegetable oils (PHVO) and determine their effects on lipogenic gene expression in adipocytes. It was hypothesized that delta‐9 desaturation and lipogenic properties of t‐18:1 isomers depend on the position of double bond. Differentiated 3T3‐L1 adipocytes were treated with 200 µM of t6–18:1, t9–18:1, t11–18:1, t13–18:1 or t16–18:1, cis (c)‐9 18:1 or bovine serum albumin (BSA) vehicle control for 48 h. Cells were then harvested for fatty acid and gene expression analyses using gas chromatography and quantitative PCR respectively. Among t‐18:1 isomers, t13–18:1 and t11–8:1 had the greatest percent delta‐9 desaturation (44 and 41 % respectively) followed by t16–18:1 and t6–18:1 (32 and 17 % respectively), while c9–18:1 and t9–18:1 did not undergo delta‐9 desaturation. Trans9–18:1 up‐regulated (P < 0.05) the expression of lipogenic genes including fatty acid synthase and stearoyl‐CoA desaturase‐1 (P < 0.05), whereas the expression of these genes were not affected with other t‐18:1 isomers (P > 0.05). Consistent with gene expression results, t9–18:1 increased the de novo lipogenic index (16:0/18:2n‐6) compared with control cells and increased delta‐9 desaturation index (c9–16:1/18:0) compared to other t‐18:1 isomers (P < 0.05). The current study provides further evidence that the predominant trans fatty acid in PHVO (t9–18:1) has isomer specific lipogenic properties.     

Metformin Reduces Lipogenesis Markers in Obese Mice Fed a Low-Carbohydrate and High-Fat Diet

Lipogenesis is the process by which fatty acids are synthesized. In metabolic syndrome, an insulin resistant state along with high plasma levels of free fatty acids (FFA) and hyperglycemia may contribute to the lipogenic process. The aim of the present study was to investigate the effects of oral administration of metformin on the expression of lipogenic genes and glycemic profile in mice fed with low‐carbohydrate high‐fat diet by evaluating their metabolic profile. SWISS male mice were divided into 4 groups (N = 7) that were fed with standard (ST), standard plus metformin (ST + MET), low‐carbohydrate high‐fat diet (LCHFD) and low‐carbohydrate high‐fat diet plus metformin (LCHFD + MET) (100 mg kg^?1 diet) diets respectively. Food intake, body weight and blood parameters, such as glucose tolerance, insulin sensitivity, glucose, HDL‐c, total cholesterol, triglycerides, ASL and ALT levels were assessed. Histological analyses were performed on hematoxylin and eosin‐stained epididymal adipose tissue histological specimens. The expression levels of peroxisome proliferator‐activated receptor (PPARγ), sterol regulatory element‐binding protein 1 (SREBP1), fatty acid synthase (FAS) and acetyl‐CoA carboxylase (ACC), were assessed by RT‐PCR. This study showed that metformin decreased adipocyte area, body weight and food consumption in obese animals when compared to the standard group. Furthermore, the expression of lipogenic markers in adipose tissue were diminished in obese animals treated with metformin. This data showed that oral administration of metformin improved glucose and lipid metabolic parameters in white adipose tissue by reducing the expression of lipogenesis markers, suggesting an important clinical application of MET in treating obesity‐related diseases in metabolic syndrome.     

High-Fat Diet Alters Serum Fatty Acid Profiles in Obesity Prone Rats: Implications for In Vitro Studies

High‐fat diets (HFD) are commonly used in rodents to induce obesity, increase serum fatty acids and induce lipotoxicity in various organs. Invitro studies commonly utilize individual free fatty acids (FFA) to study lipid exposure in an effort to model what is occurring in vivo; however, these approaches are not physiological as tissues are exposed to multiple fatty acids in vivo. Here we characterize circulating lipids in obesity‐prone rats fed an HFD in both fasted and fed states with the goal of developing physiologically relevant fatty acid mixtures for subsequent in vitro studies. Rats were fed an HFD (60 % kcal fat) or a control diet (10 % kcal fat) for 3 weeks; liver tissue and both portal and systemic blood were collected. Fatty acid profiles and absolute concentrations of triglycerides (TAG) and FFA in the serum and TAG, diacylglycerol (DAG) and phospholipids in the liver were measured. Surprisingly, both systemic and portal serum TAG were ~40 % lower in HFD‐fed compared to controls. Overall, compared to the control diet, HFD feeding consistently induced an increase in the proportion of circulating polyunsaturated fatty acids (PUFA) with a concomitant decline in monounsaturated fatty acids (MUFA) and saturated fatty acids (SFA) in both serum TAG and FFA. The elevations of PUFA were mostly attributed to increases in n‐6 PUFA, linoleic acid and arachidonic acid. In conclusion, fatty acid mixtures enriched with linoleic and arachidonic acid in addition to SFA and MUFA should be utilized for in vitro studies attempting to model lipid exposures that occur during in vivo HFD conditions.     

Effects of lovastatin on hepatic fatty acid metabolism

Thein vitro andin vivo effects of lovastatin on fatty acid metabolism were studied in isolated rat hepatocytes. When addedin vitro to cell incubations, lovastatin stimulatedde novo fatty acid synthesis and acetyl-CoA carboxylase activity, whereas fatty acid synthase, activity was unaffected. Lovastatin depressed palmitate, but not octanoate, oxidation. This may be attributed to the lovastatin-induced increase, in intracellular malonyl-CoA levels, as no concomitant changes of carnitine palmitoyltransferase I (CPT-I) specific activity was detected. Lovastatin had no effect on the synthesis and secretion of triacylglycerols and phospholipids in the form of very low density lipoproteins (VLDL). When rats were fed a diet supplemented with 0.1% (w/w) lovastatin for one week, both acetyl-CoA carboxylase activity andde novo fatty acid synthesis were reduced compared to pair-fed controls, whereas fatty acid synthase activity was unaffected. Palmitate oxidation was enhanced in the lovastatin-fed group. There was an increase in CPT-I activity but no change in intracellular concentration of malonyl-CoA. Lovastatin feeding and no significant effect either on the esterification of exogenous palmitic acid into both cellular and VLDL triacylglycerols and phospholipids or on hepatic lipid accumulation. Thein vitro andin vivo effects of lovastatin were not significantly different between periportal and perivenous hepatocytes. The results indicate that: (i) the administration of lovastatin increased the fatty acid-oxidative capacity of the liver at the expense of its lipogenic capacity, (ii) the rate ofde novo cholesterol synthesis did not seem to be a limiting factor in the synthesis and secretion of VLDL and (iii) lovastatin produced opposite effects on hepatic fatty acid metabolismin vitro andin vivo.     

Modification of the fat composition of the Iberian pig using Bacillus licheniformis and Bacillus subtilis

The aim of this work was to study the influence of a diet with probiotic bacteria on the lipid composition of different tissues from Iberian pigs. Cholesterol and fatty acid profiles were measured in liver, subcutaneous fat, and Serratus ventralis muscle samples. Feeding Iberian pigs a mixture of probiotic microorganisms for 45 days prior to slaughter affected the tissue composition. The feeds of the control and probiotic groups were identical except for the added Bacillus licheniformis and Bacillus subtilis (1.28 × 10⁹ cfu/kg feed) in the feed of the probiotic group. The diet with probiotics significantly affected the fatty acid profile of liver, subcutaneous fat and Serratus ventralis muscle samples, but no significant differences were found for the cholesterol content. The livers of the probiotic group contained lower levels of n‐6 fatty acids and higher levels of n‐3 fatty acids. The subcutaneous fat contained lower levels of n‐6 fatty acids. Serratus ventralis muscles from the probiotic group contained a significantly higher percentage of oleic acid than those of the control group. Practical applications: This study deals with the effect of the addition of probiotic bacteria to the diet of pigs on both the cholesterol and fatty acid content. B. subtilis and B. licheniformis can be used in pig feed (Regulation EC no. 2148/2004), but there are no studies about their effects on fresh meat or other tissues, particularly regarding the fat composition. Thus, it is interesting to study how feeding these microorganisms affects the different tissues. Including these microorganisms in the basic diet could serve as a strategy to modify the fat composition and to obtain healthier products from pigs.     

Effects of perfluorodecanoic acid onde novo fatty acid and cholesterol synthesis in the rat

Perfluorodecanoic acid (PFDA) is a peroxisome proliferator that causes a dose-dependent (20–80 mg/kg) increase in hepatic triacylglycerol and cholesteryl ester levels in the rat. We hypothesized that PFDA may cause an increase in thede novo synthesis of fatty acids and cholesterol in this species, which would explain observed effects. The incorporation of³H₂O into tissue lipids was examined 7 days after rats received vehicle or 20 or 80 mg/kg of PFDA. PFDA treatment decreased the rate of synthesis of cholesterol and fatty acids in the liver and in epididymal fat pad. At a PFDA dose (20 mg/kg) that decreasedde novo synthesis of fatty acids and cholesterol, there was no effect on the concentration of fatty acids and cholesterol in the liver, epididymal fat pads, and plasma. We conclude that PFDA induced fatty liver is due to either a decrease in the oxidation of fatty acids in the liver, or an impairment of triacylglycerol catabolism and/or export from the liver, and is not the result of an increase inde novo synthesis of fatty acids and cholesterol.     

Caloric Restriction Normalizes Obesity-Induced Alterations on Regulators of Skeletal Muscle Growth Signaling

The objective of this study was to establish the impact of caloric restriction on high fat diet‐induced alterations on regulators of skeletal muscle growth. We hypothesized that caloric restriction would reverse the negative effects of high fat diet‐induced obesity on REDD1 and mTOR‐related signaling. Following an initial 8 week period of HF diet‐induced obesity, caloric restriction (CR ~30 %) was employed while mice continued to consume either a low (LF) or high fat (HF) diet for 8 weeks. Western analysis of skeletal muscle showed that CR reduced (p < 0.05) the obesity‐related effects on the lipogenic protein, SREBP1. Likewise, CR reduced (p < 0.05) the obesity‐related effects on the hyperactivation of mTORC1 and ERK1/2 signaling to levels comparable to the LF mice. CR also reduced (p < 0.05) obesity‐induced expression of negative regulators of growth, REDD1 and cleaved caspase 3. These findings have implications for on the reversibility of dysregulated growth signaling in obese skeletal muscle, using short‐term caloric restriction.     

Origin of fatty acids in the body: endogenous synthesis versus dietary intakes

Fats, as fatty acids (FA), together with carbohydrates, represent a major substrate group for energy production. In contrast to carbohydrates FA are less efficiently used for energy and more easily stored in tissues. A major issue, still not completely solved, concerns the origin of FA in the organism. The two theoretical alternatives are a) endogenous de novo lipogenesis from carbohydrates, and b) supply through the diet. Various pieces of evidence indicate that the first option, while well‐documented in simple biological systems, plays a minimal role in vivo. The exogenous origin therefore represents the preferred, major route of FA supply to the body. This is also supported by the observation that only the enzymes involved in the production of long‐chain polyunsaturated FA from their precursors, and not those involved in the synthesis of the FA that are abundant in the diet, are operating in vivo. Finally, as a consequence of the load of fats in our diets, competition for esterification, and reciprocal replacements, of the unsaturated FA and FA classes, that are most abundantly provided by the diet, take place in plasma lipids.     

Liver Fatty Acid Binding Protein Gene-Ablation Exacerbates Weight Gain in High-Fat Fed Female Mice

Loss of liver fatty acid binding protein (L‐FABP) decreases long chain fatty acid uptake and oxidation in primary hepatocytes and in vivo. On this basis, L‐FABP gene ablation would potentiate high‐fat diet‐induced weight gain and weight gain/energy intake. While this was indeed the case when L‐FABP null (?/?) mice on the C57BL/6NCr background were pair‐fed a high‐fat diet, whether this would also be observed under high‐fat diet fed ad libitum was not known. Therefore, this possibility was examined in female L‐FABP (?/?) mice on the same background. L‐FABP (?/?) mice consumed equal amounts of defined high‐fat or isocaloric control diets fed ad libitum. However, on the ad libitum‐fed high‐fat diet the L‐FABP (?/?) mice exhibited: (1) decreased hepatic long chain fatty acid (LCFA) β‐oxidation as indicated by lower serum β‐hydroxybutyrate level; (2) decreased hepatic protein levels of key enzymes mitochondrial (rate limiting carnitine palmitoyl acyltransferase A1, CPT1A; HMG‐CoA synthase) and peroxisomal (acyl CoA oxidase 1, ACOX1) LCFA β‐oxidation; (3) increased fat tissue mass (FTM) and FTM/energy intake to the greatest extent; and (4) exacerbated body weight gain, weight gain/energy intake, liver weight, and liver weight/body weight to the greatest extent. Taken together, these findings showed that L‐FABP gene‐ablation exacerbated diet‐induced weight gain and fat tissue mass gain in mice fed high‐fat diet ad libitum—consistent with the known biochemistry and cell biology of L‐FABP.     

Downregulation of de Novo Fatty Acid Synthesis in Subcutaneous Adipose Tissue of Moderately Obese Women

The purpose of this work was to evaluate the expression of fatty acid metabolism-related genes in human adipose tissue from moderately obese women. We used qRT-PCR and Western Blot to analyze visceral (VAT) and subcutaneous (SAT) adipose tissue mRNA expression involved in de novo fatty acid synthesis (ACC1, FAS), fatty acid oxidation (PPARα, PPARδ) and inflammation (IL6, TNFα), in normal weight control women (BMI < 25 kg/m², n = 35) and moderately obese women (BMI 30–38 kg/m², n = 55). In SAT, ACC1, FAS and PPARα mRNA expression were significantly decreased in moderately obese women compared to controls. The downregulation reported in SAT was more pronounced when BMI increased. In VAT, lipogenic-related genes and PPARα were similar in both groups. Only PPARδ gene expression was significantly increased in moderately obese women. As far as inflammation is concerned, TNFα and IL6 were significantly increased in moderate obesity in both tissues. Our results indicate that there is a progressive downregulation in lipogenesis in SAT as BMI increases, which suggests that SAT decreases the synthesis of fatty acid de novo during the development of obesity, whereas in VAT lipogenesis remains active regardless of the degree of obesity.     

High Glucose and Liver Fatty Acid Binding Protein Gene Ablation Differentially Impact Whole Body and Liver Phenotype in High-Fat Pair-Fed Mice

Ad libitum-fed diets high in fat and carbohydrate (especially fructose) induce weight gain, obesity, and nonalcoholic fatty liver disease (NAFLD) in humans and animal models. However, interpretation is complicated since ad libitum feeding of such diets induces hyperphagia and upregulates expression of liver fatty acid binding protein (L-FABP)—a protein intimately involved in fatty acid and glucose regulation of lipid metabolism. Wild-type (WT) and L-fabp gene ablated (LKO) mice were pair-fed either high-fat diet (HFD) or high-fat/high-glucose diet (HFGD) wherein total carbohydrate was maintained constant but the proportion of glucose was increased at the expense of fructose. In LKO mice, the pair-fed HFD increased body weight and lean tissue mass (LTM) but had no effect on fat tissue mass (FTM) or hepatic fatty vacuolation as compared to pair-fed WT counterparts. These LKO mice exhibited upregulation of hepatic proteins in fatty acid uptake and cytosolic transport (caveolin and sterol carrier protein-2), but lower hepatic fatty acid oxidation (decreased serum β-hydroxybutyrate). LKO mice pair-fed HFGD also exhibited increased body weight; however, these mice had increased FTM, not LTM, and increased hepatic fatty vacuolation as compared to pair-fed WT counterparts. These LKO mice also exhibited upregulation of hepatic proteins in fatty acid uptake and cytosolic transport (caveolin and acyl-CoA binding protein, but not sterol carrier protein-2), but there was no change in hepatic fatty acid oxidation (serum β-hydroxybutyrate) as compared to pair-fed WT counterparts.     

Maternal and Postnatal High Linoleic Acid Diet Impacts Lipid Metabolism in Adult Rat Offspring in a Sex-Specific Manner

Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is essential for fetal growth and development. We aimed to investigate the effect of maternal and postnatal high LA (HLA) diet on plasma FA composition, plasma and hepatic lipids and genes involved in lipid metabolism in the liver of adult offspring. Female rats were fed with low LA (LLA; 1.44% LA) or HLA (6.21% LA) diets for 10 weeks before pregnancy, and during gestation/lactation. Offspring were weaned at postnatal day 25 (PN25), fed either LLA or HLA diets and sacrificed at PN180. Postnatal HLA diet decreased circulating total n-3 PUFA and alpha-linolenic acid (ALA), while increased total n-6 PUFA, LA and arachidonic acid (AA) in both male and female offspring. Maternal HLA diet increased circulating leptin in female offspring, but not in males. Maternal HLA diet decreased circulating adiponectin in males. Postnatal HLA diet significantly decreased aspartate transaminase (AST) in females and downregulated total cholesterol, HDL-cholesterol and triglycerides in the plasma of males. Maternal HLA diet downregulated the hepatic mRNA expression of Hmgcr in both male and female offspring and decreased the hepatic mRNA expression of Cpt1a and Acox1 in females. Both maternal and postnatal HLA diet decreased hepatic mRNA expression of Cyp27a1 in females. Postnatal diet significantly altered circulating fatty acid concentrations, with sex-specific differences in genes that control lipid metabolism in the adult offspring following exposure to high LA diet in utero.     

Dietary Linseed Oil Reduces Growth While Differentially Impacting LC-PUFA Synthesis and Accretion into Tissues in Eurasian Perch (Perca fluviatilis)

The aim of this study was to evaluate the impact of replacing dietary fish oil (FO) with linseed oil (LO) on growth, fatty acid composition and regulation of lipid metabolism in Eurasian perch (Perca fluviatilis) juveniles. Fish (17.5 g initial body weight) were fed isoproteic and isoenergetic diets containing 116 g/kg of lipid for 10 weeks. Fish fed the LO diet displayed lower growth rates and lower levels of DHA in the liver and muscle than fish fed the FO diet, while mortality was not affected by dietary treatment. However, DHA content recorded in the liver and muscle of fish fed the LO diet remained relatively high, despite a weight gain of 134 % and a reduced dietary level of long‐chain polyunsaturated fatty acids (LC‐PUFA), suggesting endogenous LC‐PUFA biosynthesis. This was supported by the higher amounts of pathway intermediates, including 18:4n‐3, 20:3n‐3, 20:4n‐3, 18:3n‐6 and 20:3n‐6, recorded in the liver of fish fed the LO diet in comparison with those fed the FO diet. However, fads2 and elovl5 gene expression and FADS2 enzyme activity were comparable between the two groups. Similarly, the expression of genes involved in eicosanoid synthesis was not modulated by dietary LO. Thus, the present study demonstrated that in fish fed LO for 10 weeks, growth was reduced but DHA levels in tissues were largely maintained compared to fish fed FO, suggesting a physiologically relevant rate of endogenous LC‐PUFA biosynthesis capacity.     

Reduced Maternal Erythrocyte Long Chain Polyunsaturated Fatty Acids Exist in Early Pregnancy in Preeclampsia

The present prospective study examines proportions of maternal erythrocyte fatty acids across gestation and their association with cord erythrocyte fatty acids in normotensive control (NC) and preeclamptic pregnancies. We hypothesize that maternal fatty acid status in early pregnancy influences fetal fatty acid stores in preeclampsia. 137 NC women and 58 women with preeclampsia were included in this study. Maternal blood was collected at 3 time points during pregnancy (16–20th weeks, 26–30th weeks and at delivery). Cord blood was collected at delivery. Fatty acids were analyzed using gas chromatography. The proportions of maternal erythrocyte α‐linolenic acid, docosahexaenoic acid, nervonic acid, and monounsaturated fatty acids (MUFA) (p < 0.05 for all) were lower while total n‐6 fatty acids were higher (p < 0.05) at 16–20th weeks of gestation in preeclampsia as compared with NC. Cord 18:3n‐3, 22:6n‐3, 24:1n‐9, MUFA, and total n‐3 fatty acids (p < 0.05 for all) were also lower in preeclampsia as compared with NC. A positive association was observed between maternal erythrocyte 22:6n‐3 and 24:1n‐9 at 16–20th weeks with the same fatty acids in cord erythrocytes (p < 0.05 for both) in preeclampsia. Our study for the first time indicates alteration in maternal erythrocyte fatty acids at 16th weeks of gestation which is further reflected in cord erythrocytes at delivery in preeclampsia.     

Effect of dietary organic selenium on fatty acid composition in nutria (Myocastor coypus Mol.) livers

Young, female nutrias (n = 13) were fed a diet supplemented with 0.36 mg/kg selenium in selenium‐enriched yeast (SeY; Sel‐Plex; Alltech, Inc., Nicholasville, KY) for 60 days (total Se concentration in the basal diet was ～0.1 mg/kg). Concentrations of fatty acids (FA) in the liver were compared to those of nutrias on a control diet (n = 11). Animals were sacrificed at 8 months of age and liver samples (approximately 30 g) were collected. The gas‐chromatographic analysis of tissue samples from the experimental group revealed a significant decrease in saturated fatty acids (p<0.001), monounsaturated fatty acid (p = 0.006), and polyunsaturated fatty acid (PUFA) (p = 0.02) compared to controls. The linoleic and linolenic acids, which are precursors of n‐6 and n‐3 PUFA, respectively, were significantly lower (p = 0.01 and p<0.001, respectively) in the supplemented group. The n‐6 to n‐3 PUFA ratio was significantly affected (p = 0.001) by the SeY dietary supplement (13.17 vs. 8.93, respectively).     

Individual trans 18:1 Isomers are Metabolised Differently and Have Distinct Effects on Lipogenesis in 3T3‐L1 Adipocytes

The objective of this research was to study the metabolism of individual trans fatty acids (FAs) that can be found in ruminant fat or partially hydrogenated vegetable oils (PHVO) and determine their effects on FA composition and lipogenic gene expression in adipocytes. Differentiated 3T3‐L1 adipocytes were treated with 200 µM of either trans‐9‐18:1, trans‐11‐18:1, trans‐13‐18:1, cis‐9‐18:1 or BSA vehicle control for 120 h. Trans‐9‐18:1 increased total cell FA content (µmole/well) compared to other FA treatments, which was mainly related to the accumulation of trans‐9‐18:1 in the cells. Adipocytes were able to desaturate a significant proportion of absorbed trans‐11‐18:1 and trans‐13‐18:1 (~20 and 30 % respectively) to cis‐9,trans‐11‐18:2 and cis‐9,trans‐13‐18:2, whereas trans‐9‐18:1 was mostly incorporated intact resulting in a greater lipophilic index (i.e. decreased mean FA fluidity) of adipocytes. Trans‐9‐18:1 up‐regulated (P < 0.05) the expression of lipogenic genes including acetyl‐CoA carboxylase (1.65 fold), FA synthase (1.45 fold), FA elongase‐5 (1.52 fold) and stearoyl‐CoA desaturase‐1 (1.49 fold), compared to the control, whereas trans‐11‐18:1 and trans‐13‐18:1 did not affect the expression of these genes compared to control. Our results suggest that the metabolism and lipogenic properties of trans‐11‐18:1 and trans‐13‐18:1, typically the most abundant trans FA in beef from cattle fed forage‐based diets, are similar and are different from those of trans‐9‐18:1, the predominant trans FA in PHVO.