PUFA modulate immune function and have been associated with the risk of childhood atopy and asthma. We investigated the effect of maternal fat intake in mice on PUFA status, elongase and desaturase gene expression, inflammatory markers and lung function in the offspring. C57BL/6J mice (n 32) were fed either standard chow (C, 20·4 % energy as fat) or a high-fat diet (HFD, 39·9 % energy as fat) for 4 weeks prior to conception and during gestation and lactation. At 21 d of age, offspring were weaned onto either the HFD or C, generating four experimental groups: C/C, C/HF, HF/C and HF/HF. Plasma and liver fatty acid composition were measured by GC and gene expression by quantitative PCR. Lung resistance to methacholine was assessed. Arachidonic acid concentrations in offspring plasma and liver phospholipids were increased by HFD; this effect was greater in the post-natal HFD group. DHA concentration in offspring liver phospholipids was increased in response to HFD and was higher in the post-natal HFD group. Post-natal HFD increased hepatic fatty acid desaturase (FADS) 2 and elongation of very long-chain fatty acid 5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring compared with males. Post-natal HFD increased expression of IL-6 and C-C motif chemokine ligand 2 (CCL2) in perivascular adipose tissue. The HFD lowered lung resistance to methacholine. Excessive maternal fat intake during development modifies hepatic PUFA status in offspring through regulation of gene expression of enzymes that are involved in PUFA biosynthesis and modifies the development of the offspring lungs leading to respiratory dysfunction.

This research communications addresses the hypothesis that a part of iso 17:0 and anteiso 17:0 in milk fat could come from endogenous extraruminal tissue synthesis. In order to confirm this a linear regression model was applied to calculate the proportions of iso 17:0 and anteiso 17:0 in milk fat that could come from elongation of their putative precursors iso 15:0 and anteiso 15:0, respectively. Sixteen dairy goats were allocated to two simultaneous experiments, in a crossover design with four animals per treatment and two experimental periods of 25 d. In both experiments, alfalfa hay was the sole forage and the forage to concentrate ratio (33 : 67) remained constant. Experimental diets differed on the concentrate composition, either rich in starch or neutral detergent fibre, and they were administered alone or in combination with 30 g/d of linseed oil. Iso 15:0, anteiso 15:0, iso 17:0 and anteiso 17:0, the most abundant branched-chain fatty acids in milk fat, were determined by gas chromatography using two different capillary columns. The regression model resolved that 49% of iso 17:0 and 60% of anteiso 17:0 in milk fat was formed extraruminally from iso 15:0 and anteiso 15:0 elongation.

Humans can obtain pre-formed long-chain PUFA from the diet and are also able to convert essential fatty acids (EFA) to longer-chain PUFA. The metabolic pathway responsible for EFA interconversion involves alternating desaturation and carbon chain elongation reactions, and carbon chain shortening by peroxisomal β-oxidation. Studies using stable isotope tracers or diets supplemented with EFA show that capacity for PUFA synthesis is limited in humans, such that DHA (22 : 6n-3) synthesis in men is negligible. PUFA synthesis is higher in women of reproductive age compared with men. However, the magnitude of the contribution of hepatic PUFA synthesis to whole-body PUFA status remains unclear. A number of extra-hepatic tissues have been shown to synthesise PUFA or to express genes for enzymes involved in this pathway. The precise function of extra-hepatic PUFA synthesis is largely unknown, although in T lymphocytes PUFA synthesis is involved in the regulation of cell activation and proliferation. Local PUFA synthesis may also be important for spermatogenesis and fertility. One possible role of extra-hepatic PUFA synthesis is that it may provide PUFA in a timely manner to facilitate specific cell functions. If so, this may suggest novel insights into the effect of dietary PUFA and/or polymorphisms in genes involved in PUFA synthesis on health and tissue function.

Normal odd-chain SFA (OCSFA), particularly tridecanoic acid (n-13 : 0), pentadecanoic acid (n-15 : 0) and heptadecanoic acid (n-17 : 0), are normal components of dairy products, beef and seafood. The ratio of n-15 : 0:n-17 : 0 in ruminant foods (dairy products and beef) is 2:1, while in seafood and human tissues it is 1:2, and their appearance in plasma is often used as a marker for ruminant fat intake. Human elongases encoded by elongation of very long-chain fatty acid (ELOVL)1, ELOVL3, ELOVL6 and ELOVL7 catalyse biosynthesis of the dominant even-chain SFA; however, there are no reports of elongase function on OCSFA. ELOVL transfected MCF7 cells were treated with n-13 : 0, n-15 : 0 or n-17 : 0 (80 µm) and products analysed. ELOVL6 catalysed elongation of n-13 : 0→n-15 : 0 and n-15 : 0→n-17 : 0; and ELOVL7 had modest activity toward n-15 : 0 (n-15 : 0→n-17 : 0). No elongation activity was detected for n-17 : 0→n-19 : 0. Our data expand ELOVL specificity to OCSFA, providing the first molecular evidence demonstrating ELOVL6 as the major elongase acting on OCSFA n-13 : 0 and n-15 : 0 fatty acids. Studies of food intake relying on OCSFA as a biomarker should consider endogenous human metabolism when relying on OCSFA ratios to indicate specific food intake.

In salmon farming, the scarcity of fish oil has driven a shift towards the use of plant-based oil from vegetable or seed, leading to fish feed low in long-chain PUFA (LC-PUFA) and cholesterol. Atlantic salmon has the capacity to synthesise both LC-PUFA and cholesterol, but little is known about the regulation of synthesis and how it varies throughout salmon life span. Here, we present a systemic view of lipid metabolism pathways based on lipid analyses and transcriptomic data from salmon fed contrasting diets of plant or fish oil from first feeding. We analysed four tissues (stomach, pyloric caeca, hindgut and liver) at three life stages (initial feeding 0·16 g, 2·5 g fingerlings and 10 g juveniles). The strongest response to diets higher in plant oil was seen in pyloric caeca of fingerlings, with up-regulation of thirty genes in pathways for cholesterol uptake, transport and biosynthesis. In juveniles, only eleven genes showed differential expression in pyloric caeca. This indicates a higher requirement of dietary cholesterol in fingerlings, which could result in a more sensitive response to plant oil. The LC-PUFA elongation and desaturation pathway was down-regulated in pyloric caeca, probably regulated by srebp1 genes. In liver, cholesterol metabolism and elongation and desaturation genes were both higher on plant oil. Stomach and hindgut were not notably affected by dietary treatment. Plant oil also had a higher impact on fatty acid composition of fingerlings compared with juveniles, suggesting that fingerlings have less metabolic regulatory control when primed with plant oil diet compared with juveniles.

Human milk covers the infant’s nutrient requirements during the first 6 months of life. The composition of human milk progressively changes during lactation and it is influenced by maternal nutritional factors. Nowadays, it is well known that nutrients have the ability to interact with genes and modulate molecular mechanisms impacting physiological functions. This has led to a growing interest among researchers in exploring nutrition at a molecular level and to the development of two fields of study: nutrigenomics, which evaluates the influence of nutrients on gene expression, and nutrigenetics, which evaluates the heterogeneous individual response to nutrients due to genetic variation. Fatty acids are one of the nutrients most studied in relation to lactation given their biologically important roles during early postnatal life. Fatty acids modulate transcription factors involved in the regulation of lipid metabolism, which in turn causes a variation in the proportion of lipids in milk. This review focuses on understanding, on the one hand, the gene transcription mechanisms activated by maternal dietary fatty acids and, on the other hand, the interaction between dietary fatty acids and genetic variation in genes involved in lipid metabolism. Both of these mechanisms affect the fatty acid composition of human milk.

Five classes of herbicides (carbamothioates, chloroacetamides, substituted pyridazinones, cyclohexanediones, and aryloxyphenoxypropionic acids) have been reported to inhibit lipid biosynthesis in higher plants. Carbamothioates impair the synthesis of surface lipids (waxes, cutin, suberin). These effects have been attributed to the ability of this herbicide class to inhibit one or more acyl-CoA elongases. Though as yet poorly characterized, these enzymes are associated with the endoplasmic reticulum and catalyze the condensation of malonyl-CoA with fatty acid acyl-CoA substrates to form very long-chain fatty acids used in the synthesis of surface lipids. There is contradictory evidence regarding the effects of chloroacetamide herbicides on de novo fatty acid biosynthesis. Selected substituted pyridazinones decrease the degree of unsaturation of plastidic galactolipids. This effect is attributed to the ability of selected members of this herbicide class to inhibit fatty acid desaturases which are thought to be located in the chloroplast envelope. Aryloxyphenoxypropionic acid and cyclohexanedione herbicides inhibit de novo fatty acid biosynthesis in grasses. The target site for these herbicide classes is the enzyme acetyl-CoA carboxylase which is found in the stroma of plastids. In most cases, selectivity between grasses and dicots is expressed at this site. Aryloxyphenoxypropionic acids and cyclohexanediones are reversible, linear, noncompetitive inhibitors of acetyl-CoA carboxylase from grasses. Both classes are also mutually exclusive inhibitors of grass acetyl-CoA carboxylase which suggests that they bind at a common domain on the enzyme.

Most studies on dietary vegetable oil in rainbow trout (Oncorhynchus mykiss) have been conducted on a background of dietary EPA (20 : 5n-3) and DHA (22 : 6n-3) contained in the fishmeal used as a protein source in aquaculture feed. If dietary EPA and DHA repress their endogenous synthesis from α-linolenic acid (ALA, 18 : 3n-3), then the potential of ALA-containing vegetable oils to maintain tissue EPA and DHA has been underestimated. We examined the effect of individual dietary n-3 PUFA on the expression of the biosynthetic genes required for metabolism of ALA to DHA in rainbow trout. A total of 720 juvenile rainbow trout were allocated to twenty-four experimental tanks and assigned one of eight diets. The effect of dietary ALA, EPA or DHA, in isolation or in combination, on hepatic expression of fatty acyl desaturase (FADS)2a(Δ6), FADS2b(Δ5), elongation of very long-chain fatty acid (ELOVL)5 and ELOVL2 was examined after 3 weeks of dietary intervention. The effect of these diets on liver and muscle phospholipid PUFA composition was also examined. The expression levels of FADS2a(Δ6), ELOVL5 and ELOVL2 were highest when diets were high in ALA, with no added EPA or DHA. Under these conditions ALA was readily converted to tissue DHA. Dietary DHA had the largest and most consistent effect in down-regulating the gene expression of all four genes. The ELOVL5 expression was the least responsive of the four genes to dietary n-3 PUFA changes. These findings should be considered when optimising aquaculture feeds containing vegetable oils and/or fish oil or fishmeal to achieve maximum DHA synthesis.

There is now considerable evidence of the importance of n-3 long-chain PUFA in human health and development. At the same time, the marine fish stocks that serve as the primary sources of these fatty acids are threatened by continued over-exploitation. Thus, there is an urgent need to provide a sustainable alternative source of the n-3 long-chain PUFA normally found in fish oils. The possibility of using transgenic plants genetically engineered to synthesise these important fatty acids has recently been demonstrated. The approaches taken to realise this outcome will be discussed, as will their prospects for providing a sustainable resource for the future.

Plasmodium falciparum causes the most severe form of malaria. Utilization of fatty acids in serum is thought to be necessary for survival of this parasite in erythrocytes, and thus characterization of the parasite fatty acid metabolism is important in developing a new strategy for controlling malaria. Here, we examined which combinations of fatty acids present in human serum support the continuous culture of P. falciparum in serum-free medium. Metabolic labelling and gas chromatography analyses revealed that, despite the need for particular fatty acids for the growth of intraerythrocytic P. falciparum, it can metabolize a broad range of serum-derived fatty acids into the major lipid species of their membranes and lipid bodies. In addition, these analyses showed that the parasite's overall fatty acid composition reflects that of the medium, although the parasite has a limited capacity to desaturate and elongate serum-derived fatty acids. These results indicate that the Plasmodium parasite is distinct from most cells, which maintain their fatty acid composition by coordinating de novo biosynthesis, scavenging, and modification (desaturation and elongation).