Current intakes of trans-palmitoleic (trans-C16:1 n-7) and trans-vaccenic (trans-C18:1 n-7) acids in France are exclusively ensured by ruminant milk and ruminant meat: A market basket investigation.

High circulating levels of trans-palmitoleic acid (TPA) are associated with a lower risk of type 2 diabetes in humans. Thus, the origin of circulating TPA matters. Direct intakes of TPA are ensured by dairy products, and perhaps by partially hydrogenated oils (PHOs). Indirect intakes of TPA rely on dietary trans-vaccenic acid (TVA), which occurs in ruminant-derived foods and PHOs. As it is usually assumed that PHOs are not used any longer, we analyzed here a wide range of foods currently available at retail in France. We report that TPA and TVA (1) do occur in ruminant milk and meat, dairy products and in foreign PHOs, (2) do occur in dairy fat-containing foods and (3) do not occur in dairy fat-free foods. Together, our findings demonstrate that ruminant fats are the only contributors to circulating levels of TPA in humans.

Trans-palmitoleic acid (trans-9-C16:1, or trans-C16:1 n-7): Nutritional impacts, metabolism, origin, compositional data, analytical methods and chemical synthesis. A review.

Since the early 2010s, dietary trans-palmitoleic acid (trans-9-hexadecenoic acid, trans-9-C16:1 in the Δ-nomenclature, trans-C16:1 n-7 in the Ω-nomenclature, TPA) has been epidemiologically associated with a lower risk of type 2 diabetes in humans. Thanks to these findings, TPA has become a nutrient of interest. However, there is a lot of unresolved crucial questions about this dietary fatty acid. Is TPA a natural trans fatty acid? What kind of foods ensures intakes in TPA? What about its metabolism? How does dietary TPA act to prevent type 2 diabetes? What are the biological mechanisms involved in this physiological effect? Clearly, it is high time to answer all these questions with the very first review specifically dedicated to this intriguing fatty acid. Aiming at getting an overview, we shall try to give an answer to all these questions, relying on appropriate and accurate scientific results. Briefly, this review underlines that TPA is indeed a natural trans fatty acid which is metabolically linked to other well-known natural trans fatty acids. Knowledge on physiological impacts of dietary TPA is limited so far to epidemiological data, awaiting for supplementation studies. In this multidisciplinary review, we also emphasize on methodological topics related to TPA, particularly when it comes to the quantification of TPA in foods and human plasma. As a conclusion, we highlight promising health benefits of dietary TPA; however, there is a strong lack in well-designed studies in both the nutritional and the analytical area.

Trans-fatty acids aggravate anabolic steroid-induced metabolic disturbances and differential gene expression in muscle, pancreas and adipose tissue.

AIMS: Although anabolic steroids (AS) and trans-fatty acids overload exerts systemic toxicity and are independent risk factors for metabolic and cardiovascular disorders, their interaction remains poorly understood. Thus, we investigated the impact of a diet rich in trans-fatty acids (HFD) combined with AS on glycemic control, lipid profile, adipose tissue, skeletal muscle and pancreas microstructure and expression of genes involved in energy metabolism. MAIN METHODS: Forty-eight C57BL/6 mice were randomized into 6 groups treated for 12 weeks with a standard diet (SD) or a diet rich in C18:1 trans-fatty isomers (HFD), alone or combined with 10 or 20 mg/kg testosterone cypionate (AS). KEY FINDINGS: Our results indicated that AS improved glycemic control, upregulated gene expression of Glut-4 and CPT-1 in skeletal muscle, FAS, ACC and UCP-1 in adipose tissue. AS also reduced total and LDL cholesterol in mice fed a SD. When combined with the HFD, AS was unable to induce microstructural adaptations in adipose tissue, pancreatic islets and ß-cells, but potentiated GCK and Glut-2 (pancreas) and Glut-4 and CPT-1 (skeletal muscle) upregulation. HFD plus AS also downregulated FAS and ACC gene expression in adipose tissue. Combined with HFD, AS increased triacylglycerol circulating levels, improved insulin sensitivity and glycemic control in mice. SIGNIFICANCE: Our findings indicated that HFD and AS can interact to modulates glycemic control and lipid profile by a mechanism potentially related with a reprogramming of genes expression in organs such as the pancreas, adipose tissue and skeletal muscle.

Retroconversion of dietary trans-vaccenic (trans-C18:1 n-7) acid to trans-palmitoleic acid (trans-C16:1 n-7): proof of concept and quantification in both cultured rat hepatocytes and pregnant rats.

Trans-palmitoleic acid (trans-C16:1 n-7 or trans-Δ9-C16:1, TPA) is believed to improve several metabolic parameters according to epidemiological data. TPA may mainly come from direct intakes: however, data are inconsistent due to its very low amount in foods. Instead, TPA might arise from dietary trans-vaccenic acid (trans-C18:1 n-7, TVA), which is more abundant in foods. TVA chain-shortening would be involved, but formal proof of concept is still lacking to our knowledge. Therefore, the present study aimed at providing in vitro and in vivo evidence of TVA retroconversion to TPA. First, fresh rat hepatocytes cultured with growing doses of TVA were able to synthesize growing amounts of TPA, according to a 10% conversion rate. In addition, TPA was found in secreted triacylglycerols (TAG). Inhibiting peroxisomal ß-oxidation significantly reduced TPA synthesis, whereas no effect was observed when mitochondrial ß-oxidation was blocked. Second, pregnant female rats fed a TVA-supplemented diet free of TPA did metabolize dietary TVA, leading to detectable amounts of TPA in the liver. Apart from the brain, TPA was also found in all analyzed tissues, including the mammary gland. Hepatic peroxisomal ß-oxidation of dietary TVA, combined with exportation of TPA under VLDL-TAG, may explain amounts of TPA in other tissues. In conclusion, dietary TVA undergoes peroxisomal ß-oxidation and yields TPA. Thus, not only TPA circulating levels in humans can be explained by dietary TPA itself, but dietary TVA is also of importance.

Comparative effects of dietary n-3 docosapentaenoic acid (DPA), DHA and EPA on plasma lipid parameters, oxidative status and fatty acid tissue composition.

The specific and shared physiologic and metabolic effects of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and even more of n-3 docosapentaenoic acid (DPA) are poorly known. We investigated the physiological effects and the overall fatty acid tissue composition of a nutritional supplementation of DPA compared both to EPA and DHA in healthy adult rats. Rats (n=32) were fed with semisynthetic diets supplemented or not with 1% of total lipids as EPA, DPA or DHA in ethyl esters form from weaning for 6 weeks. Fatty acid tissue composition was determined by gas chromatography-mass spectrometry, and blood assays were performed. The DPA supplementation was the only one that led to a decrease in plasma triglycerides, total cholesterol, non-high-density lipoprotein (HDL)-cholesterol, cholesterol esters and total cholesterol/HDL-cholesterol ratio compared to the nonsupplemented control group. The three supplemented groups had increased plasma total antioxidant status and superoxide dismutase activity. In all supplemented groups, the n-3 polyunsaturated fatty acid level increased in all studied tissues (liver, heart, lung, spleen, kidney, red blood cells, splenocytes, peripheral mononucleated cells) except in the brain. We showed that the DPA supplementation affected the overall fatty acid composition and increased DPA, EPA and DHA tissue contents in a similar way than with EPA. However, liver and heart DHA contents increased in DPA-fed rats at the same levels than in DHA-fed rats. Moreover, a large part of DPA seemed to be retroconverted into EPA in the liver (38.5%) and in the kidney (68.6%). In addition, the digestibility of DPA was lower than that of DHA and EPA.

Conversion of dietary trans-vaccenic acid to trans11,cis13-conjugated linoleic acid in the rat lactating mammary gland by Fatty Acid Desaturase 3-catalyzed methyl-end Δ13-desaturation.

In vitro, the rat Fatty Acid Desaturase 3 (FADS3) gene was shown to code for an enzyme able to catalyze the unexpected Δ13-desaturation of trans-vaccenic acid, producing the trans11,cis13-conjugated linoleic acid (CLA) isomer. FADS3 may therefore be the first methyl-end trans-vaccenate Δ13-desaturase functionally characterized in mammals, but the proof of this concept is so far lacking in vivo. The present study therefore aimed at investigating further the putative in vivo synthesis of trans11,cis13-CLA from dietary trans-vaccenic acid in rodents. During one week of pregnancy and two weeks post-partum, Sprague-Dawley female rats were fed two diets either high (10.0% of fatty acids and 3.8% of energy intake) or low (0.4% of fatty acids and 0.2% of energy intake) in trans-vaccenic acid. The trans11,cis13-CLA was specifically detected, formally identified and reproducibly quantified (0.06% of total fatty acids) in the mammary gland phospholipids of lactating female rats fed the high trans-vaccenic acid-enriched diet. This result was consistent with FADS3 mRNA expression being significantly higher in the lactating mammary gland than in the liver. Although the apparent metabolic conversion is low, this physiological evidence demonstrates the existence of this new pathway described in the lactating mammary gland and establishes the FADS3 enzyme as a reliable mammalian trans-vaccenate Δ13-desaturase in vivo.

Impact of n-3 Docosapentaenoic Acid Supplementation on Fatty Acid Composition in Rat Differs Depending upon Tissues and Is Influenced by the Presence of Dairy Lipids in the Diet.

The n-3 docosapentaenoic acid (n-3 DPA) could be a novel source of n-3 long-chain polyunsaturated fatty acids (LCPUFA) with beneficial physiological effects. Following the supplementation of 0.5% purified n-3 DPA for 3 weeks from weaning, the n-3 DPA content increased in one-half of the 18 studied tissues (from +50% to +110%, p < 0.05) and mostly affected the spleen, lung, heart, liver, and bone marrow. The n-3 DPA was slightly converted into DHA (+20% in affected tissues, p < 0.05) and mostly retroconverted into EPA (35-46% of n-3 DPA intake in liver and kidney) showing an increased content of these LCPUFA in specific tissues. The partial incorporation of dairy lipids in the diet for 6 weeks increased overall n-3 PUFA status and brain DHA status. Furthermore, the n-3 DPA supplementation and dairy lipids had an additive effect on the increase of n-3 PUFA tissue contents. Moreover, n-3 DPA supplementation decreased plasma cholesterol.

Expected satiation alone does not predict actual intake of desserts.

The degree to which consumers expect foods to satisfy hunger, referred to as expected satiation, has been reported to predict food intake. Yet this relationship has not been established precisely, at a quantitative level. We sought to explore this relationship in detail by determining whether expected satiation predicts the actual intake of semi-solid desserts. Two separate experiments were performed: the first used variations of a given food (eight apple purées), while the second involved a panel of different foods within a given category (eight desserts). Both experiments studied the consumption of two products assigned to volunteers based on their individual liking and expected satiation ratings, given ad libitum at the end of a standardised meal. A linear model was used to find predictors of food intake and included expected satiation scores, palatability scores, BMI, age, sex, TFEQ-R, TFEQ-D, water consumption during the meal, reported frequency of eating desserts, and reported frequency of consuming tested products as explanatory variables. Expected satiation was a significant predictor of actual food intake in both experiments (apple purée: F(1,97) = 18.60, P < .001; desserts: F(1,106) = 9.05, P < .01), along with other parameters such as product palatability and the volunteers' age, sex and food restriction (variation explained by the model/expected satiation in the experiments: 57%/23% and 36%/17%, respectively). However, we found a significant gap between expected and actual consumption of desserts, on group and on individual level. Our results confirm the importance of expected satiation as a predictor of subsequent food intake, but highlight the need to study individual consumption behaviour and preferences in order to fully understand the role of expected satiation.