Significant experimental evidence supports fat as a taste modality; however, the associated peripheral mechanisms are not well established. Several candidate taste receptors have been identified, but their expression pattern and potential functions in human fungiform papillae remain unknown. The aim of this study is to identify the fat taste candidate receptors and ion channels that were expressed in human fungiform taste buds and their association with oral sensory of fatty acids. For the expression analysis, quantitative RT-PCR (qRT-PCR) from RNA extracted from human fungiform papillae samples was used to determine the expression of candidate fatty acid receptors and ion channels. Western blotting analysis was used to confirm the presence of the proteins in fungiform papillae. Immunohistochemistry analysis was used to localise the expressed receptors or ion channels in the taste buds of fungiform papillae. The correlation study was analysed between the expression level of the expressed fat taste receptors or ion channels indicated by qRT-PCR and fat taste threshold, liking of fatty food and fat intake. As a result, qRT-PCR and western blotting indicated that mRNA and protein of CD36, FFAR4, FFAR2, GPR84 and delayed rectifying K+ channels are expressed in human fungiform taste buds. The expression level of CD36 was associated with the liking difference score (R −0·567, β=−0·04, P=0·04) between high-fat and low-fat food and FFAR2 was associated with total fat intake (ρ=−0·535, β=−0·01, P=0·003) and saturated fat intake (ρ=−0·641, β=−0·02, P=0·008).

Nutritional strategies are currently developed to produce farmed fish rich in n-3 long-chain PUFA (LC-PUFA) whilst replacing fish oil by plant-derived oils in aquafeeds. The optimisation of such strategies requires a thorough understanding of fish lipid metabolism and its nutritional modulation. The present study evaluated the fatty acid bioconversion capacity of rainbow trout (Oncorhynchus mykiss) fry previously depleted in n-3 PUFA through a 60-d pre-experimental feeding period with a sunflower oil-based diet (SO) followed by a 36-d experimental period during which fish were fed either a linseed oil-based diet (LO) (this treatment being called SO/LO) or a fish oil-based diet (FO) (this treatment being called SO/FO). These treatments were compared with fish continuously fed on SO, LO or FO for 96 d. At the end of the 36-d experimental period, SO/LO and SO/FO fish recovered >80 % of the n-3 LC-PUFA reported for LO and FO fish, respectively. Fish fed on LO showed high apparent in vivo elongation and desaturation activities along the n-3 biosynthesis pathway. However, at the end of the experimental period, no impact of the fish n-3 PUFA depletion was observed on apparent in vivo elongation and desaturation activities of SO/LO fish as compared with LO fish. In contrast, the fish n-3 PUFA depletion negatively modulated the n-6 PUFA bioconversion capacity of fish in terms of reduced apparent in vivo elongation and desaturation activities. The effects were similar after 10 or 36 d of the experimental period, indicating the absence of short-term effects.

The present study was conducted to evaluate the effect of different dietary lipid sources, age and sex on the SFA and MUFA metabolism in broiler chickens using a whole body fatty acid balance method. Four dietary lipid sources (palm fat, Palm; soyabean oil, Soya; linseed oil, Lin; and fish oil, Fish) were added at 3 % to a basal diet containing 5 % Palm. Diets were fed to female and male chickens from day 1 to either day 21 or day 42 of age. The accumulation (percentage of net intake and ex novo production) of SFA and MUFA was significantly lower in broilers fed on Palm than in broilers fed on the other diets (85·7 v. 97·4 %). Conversely, β-oxidation was significantly higher in Palm-fed birds than the average of the other dietary treatments (14·3 v. 2·6 %). On average, 33·1 % of total SFA and MUFA accumulated in the body were elongated, and 13·8 % were Δ-9 desaturated to longer chain or more unsaturated metabolites, with lower proportions being elongated and desaturated for the Palm and Fish diets than for the Soya and Lin diets. Total in vivo apparent elongase activity decreased exponentially in relation to the net intake of SFA and MUFA, while it increased with age. Total in vivo apparent Δ-9 desaturase activity was not significantly affected by dietary treatment or age. Total ex novo production and β-oxidation of SFA and MUFA showed a negative and positive curvilinear relationship with net intake of SFA and MUFA, respectively. Sex had no effect on SFA and MUFA metabolism.

In consideration of economical and environmental concerns, fish oil (FO) substitution in aquaculture is the focus of many fish nutritionists. The most stringent drawback of FO replacement in aquafeeds is the consequential modification to the final fatty acid (FA) make-up of the fish fillet. However, it is envisaged that a solution may be achieved through a better understanding of fish FA metabolism. Therefore, the present study investigated the fate of individual dietary FA in rainbow trout (Oncorhynchus mykiss) fed a FO-based diet (rich in 20 : 5n-3) or a linseed oil-based diet (LO; rich in 18 : 3n-3). The study demonstrated that much of the 18 : 3n-3 content from the LO diet was oxidised and, despite the significantly increased accretion of Δ-6 and Δ-5 desaturated FA, a 2- and 3-fold reduction in the fish body content of 20 : 5n-3 and 22 : 6n-3, respectively, compared with the FO-fed fish, was recorded. The accretion of longer-chain FA was unaffected by the dietary treatments, while there was a greater net disappearance of FA provided in dietary surplus. SFA and MUFA recorded a net accretion of FA produced ex novo. In the fish fed the FO diet, the majority of dietary 20 : 5n-3 was accumulated (53·8 %), some was oxidised (14·7 %) and a large proportion (31·6 %) was elongated and desaturated up to 22 : 6n-3. In the fish fed the LO diet, the majority of dietary 18 : 3n-3 was accumulated (58·1 %), a large proportion was oxidised (29·5 %) and a limited amount (12·4 %) was bio-converted to longer and more unsaturated homologues.

The physiological function of the mitochondrial uncoupling protein (UCP), UCP3, is still under debate. There is, however, ample evidence to indicate that, in contrast to UCP1, the primary function of UCP3 is not the dissipation of energy. Rather, several lines of evidence suggest that UCP3 is associated with cellular fatty acid metabolism. The highest levels of expression of UCP3 have been found in type 2 glycolytic muscle fibres, and fasting and high-fat diets up regulate UCP3. This up-regulation is most pronounced in muscle with a low fat oxidative capacity. Acute exercise also up regulates UCP3, and this effect has been shown to be a result of the exercise-induced increase in plasma fatty acid levels. In contrast, regular physical activity, which increases fat oxidative capacity, reduces UCP3 content. Based on these data it has been postulated that UCP3 functions to export those fatty acids that cannot be oxidized from the mitochondrial matrix, in order to prevent fatty acid accumulation inside the matrix. Several experiments have been conducted to test this hypothesis. Blocking carnitine palmitoyltransferase 1, thereby reducing fat oxidative capacity, rapidly induces UCP3. High-fat diets, which increase the mitochondrial supply of fatty acids, also up regulate UCP. However, feeding a similar amount of medium-chain fatty acids, which can be oxidized inside the mitochondrial matrix and therefore does not need to be exported from the matrix, does not affect UCP3 protein levels. In addition, UCP3 is increased in patients with defective β-oxidation and is reduced after restoring oxidative capacity. In conclusion, it is suggested that UCP3 has an important physiological function in facilitating outward transport from the mitochondrial matrix of fatty acid anions that cannot be oxidized, thereby protecting against lipid-induced mitochondrial damage.

Disturbances in pathways of lipolysis and fatty acid handling are of importance in the aetiology of obesity and type 2 diabetes mellitus. There is evidence that a lowered catecholamine-mediated lipolytic response may play a role in the development and maintenance of increased adipose tissue stores. Increased adipose tissue stores, a disturbed insulin-mediated regulation of lipolysis and subnormal skeletal muscle non-esterified fatty acid (NEFA) uptake under conditions of high lipolytic rate may increase circulating NEFA concentrations, which may promote insulin resistance and cardiovascular complications. In addition, a disturbance of NEFA uptake by adipose tissue postprandially is also a critical determinant of plasma NEFA concentration. Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. A dysbalance between fatty acid uptake and fatty acid oxidation may in turn be a factor promoting accumulation of lipid intermediates and triacylglycerols within skeletal muscle, which is strongly associated with skeletal muscle insulin resistance. The present review describes the reported disturbances in pathways of lipolysis and skeletal muscle fatty acid handling, and discusses underlying mechanisms and metabolic consequences of these disturbances.

The present article addresses the hypothesis that disturbances in skeletal muscle fatty acid handling in abdominal obesity and type 2 diabetes mellitus may play a role in the aetiology of increased adipose tissue stores, increased triacylglycerol storage in skeletal muscle and skeletal muscle insulin resistance. The uptake and/or oxidation of fatty acids have been shown to be impaired during post-absorptive conditions in abdominally-obese subjects and/or subjects with type 2 diabetes. Also, human studies have shown that muscle of subjects that are (abdominally) obese and/or have type 2 diabetes is characterized by an inability to increase fatty acid uptake and/or fatty acid oxidation during β-adrenergic stimulation and exercise. This disturbance in fat oxidation may promote, on one hand, the development of increased adipose tissue stores and obesity. On the other hand, fatty acids that are taken up by muscle and not oxidized may increase triacylglycerol storage in muscle, which has been associated with skeletal-muscle insulin resistance. Disturbances in the capacity to increase fat oxidation during post-absorptive conditions, β-adrenergic stimulation and exercise in subjects who are obese and/or have type 2 diabetes persist after weight reduction, indicating that the diminished fat oxidation may be a primary factor leading to the obese and/or insulin-resistant state rather than an adaptational response. Clearly, the precise sequence of events leading to an increased adiposity and insulin resistance in obesity and type 2 diabetes mellitus is not yet fully understood.

Maternal adipose tissue is a major contributor to breast milk long-chain fatty acids, probably through the pool of plasma NEFA. The fatty acid composition of the erythrocyte membrane (EM) is a biochemical index of the intake of fatty acids not synthesized endogenously and of PUFA and long-chain PUFA fatty acid status. The present study investigated the associations between breast milk fatty acid composition and the composition of plasma NEFA and of EM fatty acids with special reference to PUFA, long-chain PUFA and conjugated linoleic acid (CLA). The detailed fatty acid composition of mature breast milk was also reported. Thirty-three healthy, lactating Brazilian women donated milk samples; of these, twenty-four also donated blood samples in an observational cross-sectional study. Breast milk fatty acid composition presented several associations with NEFA and EM composition, which explained most (≥50%) of the variability of selected milk PUFA, long-chain PUFA and CLA. Milk CLA was associated with fatty acids that are markers of dairy fat intake in the diet, NEFA and EM. In general, breast milk n-3 fatty acids and CLA, but not n-6 fatty acids, were associated with EM composition, whereas both the n-6 and n-3 fatty acids and CLA in milk were associated with NEFA composition, possibly owing to its role as a direct source of fatty acids for breast milk. These findings emphasize the contribution of the NEFA pool derived from the adipose tissue to the long-chain fatty acid composition of breast milk.

The effect of sesame (Sesamum orientale) lignan preparation containing equivalent amounts of sesamin and episesamin on hepatic fatty acid metabolism was compared in rats, mice and hamsters. Animals were fed on either a diet free of lignan or a diet containing 2glignan/kg for 15d. The lignan preparation greatly increased hepatic activity and the mRNA levels of enzymes involved in fatty acid oxidation, while it strongly down-regulated those of enzymes involved in lipogenesis in rats. In contrast, lignan did not modify these variables in mice and hamsters. Changes observed, if any, were more attenuated in these mice and hamsters than in rats. Sesamin and episesamin concentrations in serum and liver of animals fed on lignan-containing diets were significantly greater (P<0·05) in rats than in mice and hamsters. Moreover, sesamin:episesamin values in tissues were far from that expected from the value in the lignan preparation given to the animals and were dependent on the animal species. Liver microsomes from each animal species degraded sesamin and episesamin in the presence of NADPH. The combined value of sesamin and episesamin degradation rates was lower in rats than in mice and hamsters. In addition, there was considerable diversity in the specificity of the enzyme reaction toward sesamin and episesamin among animal species. The differences in the amounts of lignan remaining in the tissues may account for the species dependence of the physiological activity of sesame lignan in affecting hepatic fatty acid oxidation and synthesis.

Coconut oil (CO) induces a triacylglycerol infiltration in the hepatocytes of preruminant calves when given as the sole source of fat in the milk diet over a long-term period. Metabolic pathways potentially involved in this hepatic triacylglycerol accumulation were studied by in vitro methods on liver slices from preruminant Holstein × Friesian male calves fed a conventional milk diet containing CO (n 5) or beef tallow (BT, n 5) for 19 d. Liver slices were incubated for 12 h in the presence of 0·8 mM-[14C] oleate or -[14C] laurate added to the medium. Fatty acid oxidation was determined by measuring the production of CO2 (total oxidation) and acid-soluble products (partial oxidation). Production of CO2 was 1·7–3·6-fold lower (P 0·0490) and production of acid-soluble products tended to be lower (P = 0·0625) in liver slices of CO- than BT-fed calves. Fatty acid esterification as neutral lipids was 2·6– to 3·1–fold higher (P = 0·0088) in liver slices prepared from calves fed the CO diet compared with calves fed the BT diet. By contrast with what occurs in the liver of rats fed CO, the increase in neutral lipid production did not stimulate VLDL secretion by the hepatocytes of calves fed with CO, leading to a triacylglycerol accumulation in the cytosol. It could be explained by the reduction of fatty acid oxidation favouring esterification in the form of triacylglycerols, in association with a limited availability of triacylglycerols and/or apolipoprotein B for VLDL packaging and subsequent secretion.