The replacement of fish oil (FO) with vegetable oil (VO) in feed formulations reduces the availability of n-3 long-chain PUFA (LC-PUFA) to marine fish such as gilthead seabream. The aim of this study was to examine compositional and physiological responses to a dietary gradient of n-3 LC-PUFA. Six iso-energetic and iso-nitrogenous diets (D1–D6) were fed to seabream, with the added oil being a blend of FO and VO to achieve a dietary gradient of n-3 LC-PUFA. Fish were sampled after 4 months feeding, to determine biochemical composition, tissue fatty acid concentrations and lipid metabolic gene expression. The results indicated a disturbance to lipid metabolism, with fat in the liver increased and fat deposits in the viscera reduced. Tissue fatty acid profiles were altered towards the fatty acid compositions of the diets. There was evidence of endogenous modification of dietary PUFA in the liver which correlated with the expression of fatty acid desaturase 2 (fads2). Expression of sterol regulatory element binding protein 1 (srebp1), fads2 and fatty acid synthase increased in the liver, whereas PPARα1 pathways appeared to be supressed by dietary VO in a concentration-dependent manner. The effects in lipogenic genes appear to become measurable in D1–D3, which agrees with the weight gain data suggesting that disturbances to energy metabolism and lipogenesis may be related to performance differences. These findings suggested that suppression of β-oxidation and stimulation of srebp1-mediated lipogenesis may play a role in contributing toward steatosis in fish fed n-3 LC-PUFA deficient diets.

Asthma is one of the most common and prevalent problems worldwide affecting over 300 million individuals. There is some evidence from observational and intervention studies to suggest a beneficial effect of n-3 PUFA in inflammatory diseases, specifically asthma. Marine-based n-3 PUFA have therefore been proposed as a possible complementary/alternative therapy for asthma. The proposed anti-inflammatory effects of n-3 fatty acids may be linked to a change in cell membrane composition. This altered membrane composition following n-3 fatty acid supplementation (primarily EPA and DHA) can modify lipid mediator generation via the production of eicosanoids with a reduced inflammatory potential/impact. A recently identified group of lipid mediators derived from EPA including E-series resolvins are proposed to be important in the resolution of inflammation. Reduced inflammation attenuates the severity of asthma including symptoms (dyspnoea) and exerts a bronchodilatory effect. There have been no major health side effects reported with the dietary supplementation of n-3 fatty acids or their mediators; consequently supplementing with n-3 fatty acids is an attractive non-pharmacological intervention which may benefit asthma.

Humans who eat fish are exposed to mixtures of healthful nutrients and harmful contaminants that are influenced by environmental and ecological factors. Marine fisheries are composed of a multitude of species with varying life histories, and harvested in oceans, coastal waters and estuaries where environmental and ecological conditions determine fish exposure to both nutrients and contaminants. Many of these nutrients and contaminants are thought to influence similar health outcomes (i.e., neurological, cardiovascular, immunological systems). Therefore, our understanding of the risks and benefits of consuming seafood require balanced assessments of contaminants and nutrients found in fish and shellfish. In this paper, we review some of the reported benefits of fish consumption with a focus on the potential hazards of mercury exposure, and compare the environmental variability of fish oils, selenium and mercury in fish. A major scientific gap identified is that fish tissue concentrations are rarely measured for both contaminants and nutrients across a range of species and geographic regions. Interpreting the implications of seafood for human health will require a better understanding of these multiple exposures, particularly as environmental conditions in the oceans change.

Dietary fish consumption contributes to a reduced risk of cardiac mortality. In the present study, the effect of low-dose fish oil (FO) supplementation on heart rate (HR) response to intense exercise and recovery was investigated in physically fit males. The subjects (n 26) were supplemented (double-blind, parallel design) with (2 × 1 g/d) soya bean oil (control) or tuna FO providing the long-chain n-3 PUFA DHA (560 mg) and EPA (140 mg). Erythrocyte omega-3 index (%EPA+DHA), HR, HR variability and HR recovery were analysed during rest, intense exercise and recovery at baseline and after 8 weeks of supplementation. The mean erythrocyte omega-3 index, which did not differ between the groups at baseline (control 4·2 (sem 0·2), n 13; FO 4·7 (sem 0·2), n 13), remained unchanged in the control group (3·9 (sem 0·2)), but increased in the FO group (6·3 (sem 0·3); P< 0·01). The mean HR during supine resting conditions (control 56 (sem 10); FO 59 (sem 9)) was not affected by FO supplementation. Poincaré analysis of HR variability at rest exhibited a decreasing trend in parasympathetic activity in the FO group (SD1 (standard deviation of points perpendicular to the axis of line of identity)/SD2 (standard deviation of points along the axis of line of identity): control 0·02 (sem 0·01); FO − 0·05 (sem 0·02); P= 0·18). Peak HR was not affected by supplementation. However, during submaximal exercise over 5 min, fewer total heart beats were recorded in the FO group ( − 22 (sem 6) ( = − 4·5 beats/min)), but not in the control group (+1 (sem 4)) (P< 0·05). Supine HR recovery (half-time) after cycling was significantly faster after FO supplementation (control − 0·4 (sem 1·2) s; FO − 8·0 (sem 1·7) s; P< 0·05). A low intake of FO increased the omega-3 index and reduced the mean exercise HR and improved HR recovery without compromising the peak HR. A direct influence of DHA via reductions in the cardiac intrinsic beat rate was balanced by a reciprocal decrease in vagal tone.

In the present study, salmon products available from UK retailers were analysed to determine the levels of n-3 long-chain PUFA (LC-PUFA), a key determinant of nutritional quality. There was a wide variation in the proportions and absolute contents of EPA and DHA in the products. Relatively high contents of 18 : 1n-9, 18 : 2n-6 and 18 : 3n-3, characteristic of vegetable oils (VO), were found in several farmed salmon products, which also had generally lower proportions of EPA and DHA. In contrast, farmed salmon products with higher levels of 16 : 0 and 22 : 1, characteristic of fish oil (FO), had higher proportions of EPA and DHA. Therefore, there was a clear correlation between the levels of VO and FO in feeds and the proportions of n-3 LC-PUFA in products. Although wild salmon products were characterised by higher proportions of n-3 LC-PUFA (20–40 %) compared with farmed fish (9–26 %), they contained lower total lipid contents (1–6 % compared with 7–17 % in farmed salmon products). As a result, farmed salmon products invariably had higher levels of n-3 LC-PUFA in absolute terms (g/100 g fillet) and, therefore, delivered a higher ‘dose’ of EPA and DHA per portion. Overall, despite the finite and limiting supply of FO and increasing use of VO, farmed salmon continue to be an excellent source of and delivery system for n-3 LC-PUFA to consumers.

Many clinical and epidemiological studies have shown that the polyunsaturated n-3 fatty acids EPA and DHA from fish and fish oils, provide cardiovascular protection, particularly in the setting of secondary prevention. n-3 Fatty acids beneficially influence a number of cardiometabolic risk factors including blood pressure, cardiac function, vascular reactivity and lipids, as well as having anti-platelet, anti-inflammatory and anti-oxidative actions. They do not appear to adversely interact with other medications such as statins and other lipid-lowering drugs or antihypertensive medications. n-3 Fatty acids have gained widespread usage by general practitioners and clinicians in a number of clinical settings such as pregnancy and infant development, secondary prevention in CHD patients, treatment of dyslipidaemias and haemodialysis patients. Small doses are achievable with consumption of two to three oily fish meals per week or via purified encapsulated preparations now readily available. n-3 Fatty acids, particularly when consumed as fish, should be considered an important component of a healthy diet. The present paper reviews the effects of n-3 fatty acids on cardiometabolic risk factors, concentrating particularly on the evidence from randomised controlled studies in human subjects.

The erythrocyte and plasma fatty acid compositions of children with autism were compared in a case–control study with typically developing (TD) children and with children showing developmental delay (DD). Forty-five autism subjects were age-matched with TD controls and thirty-eight with DD controls. Fatty acid data were compared using paired t tests. In addition, blood fatty acids from treatment-naive autism subjects were compared with autism subjects who had consumed fish oil supplements by two-sample t tests. Relatively few differences were seen between erythrocyte fatty acids in autism and TD subjects although the former had an increased arachidonic acid (ARA):EPA ratio. This ratio was also increased in plasma samples from the same children. No changes in n-3 fatty acids or ARA:EPA ratio were seen when comparing autism with DD subjects but some SFA and MUFA were decreased in the DD subjects, most notably 24 : 0 and 24 : 1, which are essential components of axonal myelin sheaths. However, if multiple comparisons are taken into account, and a stricter level of significance applied, most of these values would not be significant. Autism subjects consuming fish oil showed reduced erythrocyte ARA, 22 : 4n-6, 22 : 5n-6 and total n-6 fatty acids and increased EPA, 22 : 5n-3, 22 : 6n-3 and total n-3 fatty acids along with reduced n-6:n-3 and ARA:EPA ratios. Collectively, the autism subjects did not have an underlying phospholipid disorder, based on erythrocyte fatty acid compositions, although the increased ARA:EPA ratio observed suggested that an imbalance of essential highly unsaturated fatty acids may be present in a cohort of autism subjects.

Human clinical trials have shown that fish oils reduce the risk of a variety of disorders including CVD. Despite this, results have been inconsistent. Fish oils are easily oxidised and some fish oils contain higher than recommended levels of oxidised products, but their effects have not been investigated. Recent evidence indicates that dietary oxidised fats can contribute to the development of atherosclerosis and thrombosis. This review summarises findings from cellular, animal and human trials that have examined the effects of oxidised lipids and their potential to affect health outcomes, and proposes that oxidised products in fish oils may attenuate their beneficial effects. More research is required to determine the magnitude of negative effects of fish oil on health outcomes in clinical trials.

The effects of an n-3 PUFA-enriched diet on cardiac cell membrane phospholipid fraction compositions and associated protein kinase-C (PKC) translocation modification have never been studied in higher mammals. This is of importance since membrane fatty acid composition has been shown to influence PKC signalling pathways. In the present study, we have tested whether the incorporation of n-3 PUFA in cardiac membrane phospholipids correlated with changes in the fatty acid composition of diacylglycerols (DAG) and led to a differential translocation of PKC isoforms. Two groups of five dogs were fed the standard diet supplemented with palm oil or fish oil for 8 weeks. Dogs fed a fish oil-enriched diet showed a preferential incorporation of EPA and, to a lesser extent, of DHA, at the expense of arachidonic acid, in the circulating TAG, plasma phospholipids, erythrocyte phospholipids and cardiomyocyte phospholipid fractions. Analysis of 1,2-DAG fatty acid composition also indicated a preferential enrichment of EPA compared with DHA. Associated with these results, a reduction in the expression of PKC-δ and PKC-ε isoforms in the particulate fractions was observed whereas no effect was seen for PKC-α and PKC-ζ. We conclude that a fish oil-enriched diet induces a modification in fatty acid composition of cardiac membrane phospholipids, associated with a differential translocation of PKC isoforms. These results can be explained by the production of structurally different DAG that may participate in some of the protective effects of n-3 PUFA against various chronic diseases.

Indian Asians living in the UK have a 50% higher CHD mortality rate compared with the indigenous Caucasian population, which cannot be attributed to traditional risk factors. Instead, features of the metabolic syndrome, including raised plasma triacylglycerol, reduced HDL-cholesterol (HDL-C) and an increased proportion of small dense LDL particles, together with insulin resistance and central obesity, are prevalent among this population. The present review examines evidence to support the hypothesis that an imbalance in dietary PUFA intake, specifically a higher intake of n-6 PUFA in combination with the lower intake of the long-chain (LC) n-3 PUFA, plays an important role in the prevalence of the metabolic syndrome observed in Indian Asians. Data are presented to illustrate the impact of manipulation of the background n-6 PUFA intake (moderate or high n-6 PUFA) and the subsequent response to supplementation with LC n-3 PUFA on blood lipids and insulin action in a group of Indian Asian volunteers. The results demonstrate that supplementation with LC n-3 PUFA had no impact on insulin action in those subjects consuming either the moderate- or high-n-6 PUFA diet. In the postprandial phase reductions in plasma triacylglycerol concentrations were greater in those consuming the high-n-6 PUFA background diet subsequent to fish oil supplementation. The present study concludes that, contrary to the central hypothesis, the prevalence of metabolic abnormalities in Indian Asians compared with Caucasians may not be attributable to differences in intakes of n-6 and n-3 PUFA.

Fish and fish oil-rich sources of long-chain n-3 fatty acids have been shown to be cardio-protective, through a multitude of different pathways including effects on arrythymias, endothelial function, inflammation and thrombosis, as well as modulation of both the fasting and postprandial blood lipid profile. To date the majority of studies have examined the impact of EPA and DHA fed simultaneously as fish or fish oil supplements. However, a number of recent studies have compared the relative biopotency of EPA v. DHA in relation to their effect on blood lipid levels. Although many beneficial effects of fish oils have been demonstrated, concern exists about the potential deleterious impact of EPA and DHA on LDL-cholesterol, with a highly-heterogenous response of this lipid fraction reported in the literature. Recent evidence suggests that apoE genotype may be in part responsible. In the present review the impact of EPA and DHA on cardiovascular risk and the blood lipoprotein profile will be considered, with a focus on the apoE gene locus as a possible determinant of lipid responsiveness to fish oil intervention.

Epidemiological evidence suggests that the diet influences CHD risk, although the protective effects of dietary intervention for patients in diseased states has gained less attention. Secondary care prevention strategies for patients often involves drug therapy that is expensive and can result in undesirable side effects. Therefore, it is potentially beneficial to utilise other strategies, such as diet, in the management of CHD. A systematic review was conducted to examine the effects of specific nutrients on progression of atherosclerosis, vascular function, haemostasis and inflammation in CHD patients. Results show substantial evidence for the efficacy of n–3 oils in reducing cardiovascular mortality and one mechanism may be related to the stabilisation of vulnerable atherosclerotic plaques, although the effects on progression of atherosclerosis, haemostatic activity and vascular inflammation remain equivocal. Promising data also exist for the efficacy of flavonoid-rich foods for improving endothelial function, although strong clinical endpoint evidence is lacking. The variation in the efficacy of certain nutrients in CHD patients may be explained by genetics, existing risk factors, psychosocial factors and methodological issues, although these are often not adequately taken into consideration. We conclude that there is a need to undertake more appropriately designed trials in specific clinical populations, controlling for additional lifestyle and risk factors, examining potential interactions with medications, and also establishing methods to increase compliance to dietary recommendations before specific nutrients can be widely prescribed for secondary prevention. Future research should also utilise techniques that provide a direct measure of atherosclerosis.

Six cannulated wether sheep weighing 57 (s.d. 4·3) kg were used to investigate the susceptibility of unprotected and protected n-3 polyunsaturated fatty acids from different sources to biohydrogenation in the rumen, their uptake into plasma and effects on ruminal metabolism. The sheep were assigned to one of six dietary treatments formulated to have a similar fatty acid content (60 g/kg DM) and containing: linseed oil (LO), linseed oil absorbed into vermiculite (VLO), formic acid-formaldehyde treated whole linseed (FLS), fish oil (FO), fat encapsulated fish oil (PFO) or a mixture of fish oil and marine algae (1: 1 on an oil basis; AF), in six periods of 28 days duration in a Latin-square design. Biohydrogenation of C20:5 (n-3) and C22:6 (n-3) was high in FO at approximately 870 g/kg, but reduced to 625 and 625 g/kg respectively for PFO, and 769 and 601 g/kg respectively for AF. Ruminal biohydrogenation of C18:3 (n-3) was similar across treatments based on linseed, averaging 860 g/kg, but C18:2 (n-6) was lower (P < 0·05) in animals given VLO or FLS at 792 and 837 g/kg respectively, compared with LO (907 g/kg). Duodenal flow of C18:1 trans in animals given any of the diets containing fish oil averaged 8·4 g/day compared with 2·8 g/day in animals given diets based on linseed (P < 0·001), whilst cis-9, trans-11 conjugated linoleic acid was not significantly different among treatments. Plasma C20:5 (n-3) and C22:6 (n-3) proportions were highest in animals given the AF diet (11·8 and 8·2 g per 100 g of the total fatty acids respectively) and lowest in animals given LO (2·8 and 2·7 g per 100 g of the total fatty acids respectively; P < 0·001). By contrast, plasma C18:3 (n-3) proportions were highest in animals given the LO or VLO diets at approximately 6·9 g per 100 g of the total fatty acids, and lowest in the AF treatment at 0·9 g per 100 g (P < 0·001). Duodenal non-ammonia-N flow was similar among treatments at 21·0 g/day except in animals given FLS which had the highest flow (25·9 g N per day; P < 0·01). Microbial N flow was also similar among treatments whilst microbial efficiency (g N per kg OM truly degraded in the rumen) was higher (P < 0·05) in animals given FLS than LO, FO or AF. By contrast, ruminal fibre digestion was higher (P < 0·05) in animals given LO or FO than those offered VLO, FLS, PFO or AF. In conclusion, compared with linseed oil, absorption of linseed oil into vermiculite improved duodenal flow but not plasma levels of C18:3 (n-3), whilst formic acid-formaldehyde treatment of linseed had little effect on protecting C18:3 (n-3) in the rumen, although duodenal non-ammonia nitrogen flow and microbial efficiency were improved. Compared with fish oil, the provision of marine algae or fat encapsulated fish oil resulted in a lower biohydrogenation of C22:6 (n-3) and C20:5 (n-3), and an increased duodenal flow and plasma concentration and offers the potential to favourably manipulate the n-3 fatty acid composition of sheep meat.

Duodenally and ruminally fistulated steers were offered grass silage and one of three concentrates at a ratio of 60: 40 (forage: concentrate on a dry-matter basis) : F0, F1 or F4 at 14 g/kg live weight. The concentrates were designed to be iso-lipid and to provide the same amount of sunflower oil but increasing amounts of fish oil : 0, 1 and 4 g per 100 g, respectively. Ruminal characteristics were measured along with fatty acid intakes and duodenal flows to determine the effect of fish oil on : ruminal pH, ammonia-N concentration, volatile fatty acid (VFA) concentration and polyunsaturated fatty acid (PUFA) metabolism. Fish oil had no significant effect on ruminal pH, ammonia-N concentration or the molar proportions of the major VFA, although total VFA concentration was significantly reduced at the highest level of fish oil inclusion. Fish oil significantly increased the flow of long chain PUFA, total conjugated linoleic acid and vaccenic acid to the duodenum and decreased the flow of stearic acid. Biohydrogenation, as determined by the net loss of fatty acid between the mouth and duodenum, of oleic and linolenic acid was not affected by fish oil inclusion and averaged 0·64 and 0·92, respectively. There was a small increase in the biohydrogenation of linoleic acid with increasing fish oil from 0·89 to 0·92 (P < 0·01) on F0 and F4, respectively. Biohydrogenation of the long chain PUFA C20 : 5(n-3) and C22 : 6(n-3) increased from 0·49 and 0·74 to 0·79 and 0·86 (P < 0·01), respectively when fish oil in the concentrate increased from 1 to 4 g per 100 g. The net effect of fish oil on lipid metabolism appears to inhibit the transition of vaccenic acid to stearic acid in the rumen resulting in a build up of this intermediate in the biohydrogenation pathway of C18 PUFA.

Two groups of six male goats were used to assess the effects of rumen-protected supplements offish oil on intake, digestibility and nitrogen (N) balance. The animals were offered a diet consisting of forage and concentrate, the latter fraction supplemented with 0 (control) or lOOg/kg of rumen-protected fish oil supplement (PFO), containing a high proportion of the n-3 series (whole diet contained 0 or 60 g PFO per kg dry matter). No significant differences (P > 0.05) were found between the two groups concerning live-weight gain, food intake, digestibility of DM, organic matter, N, neutral-detergent fibre and energy. In contrast, there were differences (P < 0.05) regarding the digestibility of fat and of acid-detergent fibre, which were higher among the animals given the PFO diet. With respect to the individual fatty acids, we observed higher digestibility (P < 0.05) of C14:0, C16:0, C18:0 and C20:0 among the animals given the PFO diet. The digestibility of C14:0, C18:0 and C20:0 was found to be negative among the animals given the control diet. No significant differences (P > 0-05) were found regarding digestibility of total C18:1. In contrast, the coefficients for C18:2 (n-6) and C18:3 (n-3) were higher (P < 0.05) among the non-supplemented animals. The intake and faecal flow values of C18:0 suggest that the mono- and polyunsaturated fatty acids with 18 atoms of carbon may, in both cases, undergo partial hydrogenation, which would be greater among the control group. The utilization of C20:5 (n-3) and, especially, of C22 : 6 (n-3), which were consumed only by the animals given the PFO diet, was estimated at 1-000. The PFO diet also produced lower levels ofurinary-N excretion (P < 0.05), giving rise to higher N balances (P < 0.05).

High doses of n–3 PUFA found in fish oils can reduce the circulating concentration of triacylglycerol (TG), which may contribute to the positive impact of these fatty acids on the risk of CVD. The present study aimed to establish the differential impact of EPA and docosahexaenoic (DHA) on plasma lipids and apo in adults. Forty-two normolipidaemic adult subjects completed a double-blind placebo controlled parallel study, receiving an EPA-rich oil (4·8 g EPA/d), DHA-rich oil (4·9 g DHA/d) or olive oil as control, for a period of 4 weeks. No effects of treatment on total cholesterol, LDL-cholesterol or HDL-cholesterol were evident. There was a significant 22 % reduction in TG level relative to the control value following the DHA treatment (P=0·032), with the 15 % decrease in the EPA group failing to reach significance (P=0·258). There were no significant inter-group differences in response to treatment for plasma apoA1, -C3 or -E levels, although a significant 15 % within-group increase in apoE was evident in the EPA (P=0·006) and DHA (P=0·003) groups. In addition, a within-group decrease in the apoA1:HDL-cholesterol ratio was observed in the DHA group, suggesting a positive impact of DHA on HDL particle size. The DHA intervention resulted in a significant increase in the proportion of EPA P=0·000 and DHA P=0·000 in plasma phospholipids, whilst significant increases in EPA P=0·000 and docosapentaenoic acid P=0·002, but not DHA P=0·193, were evident following EPA supplementation (P>0·05). Our present results indicate that DHA may be more efficacious than EPA in improving the plasma lipid profile.

The UK Food Standards Agency convened a group of expert scientists to review current research investigating the effect of dietary lipids on vascular function. The workshop highlighted the need for intervention studies to be sufficiently powered for these measures and that they should be corroborated with other, more validated, risk factors for CVD. Work presented at the workshop suggested a beneficial effect of long-chain n-3 PUFA and a detrimental effect of trans fatty acids. The workshop also considered the importance of the choice of study population in dietary intervention studies and that ‘at risk’ subgroups within the general population may be more appropriate than subjects that are unrepresentatively healthy.

The UK Food Standards Agency convened a group of expert scientists to review current research investigating whether n-3 polyunsaturated fatty acids (PUFA) from plant oils (α-linolenic acid; ALA) were as beneficial to cardiovascular health as the n-3 PUFA from the marine oils, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The workshop also aimed to establish priorities for future research. Dietary intake of ALA has been associated with a beneficial effect on CHD; however, the results from studies investigating the effects of ALA supplementation on CHD risk factors have proved equivocal. The studies presented as part of the present workshop suggested little, if any, benefit of ALA, relative to linoleic acid, on risk factors for cardiovascular disease; the effects observed with fish-oil supplementation were not replicated by ALA supplementation. There is a need, therefore, to first prove the efficacy of ALA supplementation on cardiovascular disease, before further investigating effects on cardiovascular risk factors. The workshop considered that a beneficial effect of ALA on the secondary prevention of CHD still needed to be established, and there was no reason to look further at existing CHD risk factors in relation to ALA supplementation. The workshop also highlighted the possibility of feeding livestock ALA-rich oils to provide a means of increasing the dietary intake in human consumers of EPA and DHA.

Although there have been a number of studies of effects of diet and hormones on lipoprotein lipase (EC 3.1.1.34; LPL) activity and levels of LPL mRNA (Raynolds et al. 1990), there have been no studies which have investigated effects of different dietary fatty acids on LPL gene expression. In the present study male Wistar Albino rats were pair-fed diets containing 50 g fat/kg of different fatty acid composition for 2 weeks. The diets fed were (1) a mixed oil (450 g saturated fatty acids, 420 g monounsaturated fatty acids, 130 g polyunsaturated fatty acids/kg; n 8), (2) maize oil (n 8), or (3) fish oil (n 8). Animals were killed, RNA was extracted from liver and perirenal and epididymal fat pads, and analysed by ‘Northern methodology’. Samples were hybridized to a human cDNA probe for LPL (Gotoda et al. 1989). Two transcripts were identified in epididymai and perirenal adipose tissue which were approximately 3·7 and 1·7 kb in size. The results suggested that (1) fish oil-fed animals had significantly greater production of LPL mRNA in epididymai adipose tissue compared with maize oil-fed animals (P < 0·05), (2) maize oil-fed animals had significantly greater production of LPL mRNA in perirenal fat compared with the other dietary groups (P < 0·05), (3) expression in the liver was not significant. Rats fed on a fish oil diet had significantly reduced plasma triacylglycerol concentrations compared with the mixed-oil group (P < 0·05), but there were no significant differences in plasma cholesterol. The differences in LPL could not be explained directly by the changes in plasma immunoreactive-insulin and glucose-dependent insulinotrophic polypeptide levels in the three groups.