Carotenoids have been shown to have potential beneficial effects on human health which has led to an increasing interest in the study of their bioavailability. A Caco-2 cell model, as previously described, was employed to examine the percentage transfer of the carotenoids α-carotene, β-carotene, lycopene, astaxanthin, β-cryptoxanthin, lutein and zeaxanthin through an intact, highly differentiated Caco-2 cell monolayer at a range of different amounts. Our results show that astaxanthin, a carotenoid with powerful antioxidant capacity, had the highest percentage transfer overall. We examined the cellular uptake and secretion of lutein and zeaxanthin to compare two structurally similar carotenoids. Both were efficiently transported through the monolayer with a range between 5·1 (sem 1·2) % to 20·2 (sem 3·3) % and 5·5 (sem 2·5) % to 13·4 (sem 4) % for lutein and zeaxanthin, respectively. These carotenoids were compared to each other at each added amount and no significant difference was observed between the two xanthophylls. The carotene carotenoids α-carotene, β-carotene and lycopene and the xanthophyll β-cryptoxanthin were also examined and had lower uptake and secretion values when compared to lutein, zeaxanthin and astaxanthin. The xanthophyll β-cryptoxanthin was also not significantly different when compared to the carotene carotenoids. Data generated from this study compares well with in vivo bioavailability studies. Furthermore, the model provides comparative data on the relative absorption and transfer of seven different carotenoids. Our data indicate that lower amounts of carotenoids were absorbed and transferred more efficiently than higher amounts suggesting a saturation effect at higher exposure.

Microminerals including copper and iron are essential to immunity and health in human beings. The development of powerful tools in analytical cell biology and molecular genetics has facilitated efforts to identify specific cellular and molecular functions of trace elements in the maturation, activation and functions of host defence mechanisms. Selected recent reports about the role of copper and iron nutrition on immune functions are critically analysed here. Effects of trace element supplementation on infectious morbidity are also reviewed. While micromineral deficiencies, in general, may have widespread effects on nearly all components of immune response, these effects can be reversed by supplementation. However, the conflicting effects of iron deficiency and iron supplementation in vitro on the defensive systems reveals the urgent need for further additional information on the in vivo situation. In the elderly, vaccination against respiratory infections is likely to protect only 30–70 % of the population. However, it may be possible to modulate immune function and ultimately reduce the severity of infections through micronutrient supplementation. Thus, microminerals contribute to the maintenance of the balance between immunity and health in humans.

One aim of the EC Framework V project, ’Rumen-up’ (QLK5-CT-2001-00 992), was to find plants or plant extracts that would inhibit the nutritionally wasteful degradation of protein in the rumen. A total of 500 samples were screened in vitro using 14C-labelled casein in a 30-min incubation with ruminal digesta. Eight were selected for further investigation using a batch fermentation system and soya protein and bovine serum albumin as proteolysis substrates; proteolysis was monitored over 12 h by the disappearance of soluble protein and the production of branched SCFA and NH3. Freeze-dried, ground foliage of Peltiphyllum peltatum, Helianthemum canum, Arbutus unedo, Arctostaphylos uva-ursi and Knautia arvensis inhibited proteolysis (P < 0·05), while Daucus carota, Clematis vitalba and Erica arborea had little effect. Inhibition by the first four samples appeared to be caused by the formation of insoluble tannin–protein complexes. The samples were rich in phenolics and inhibition was reversed by polyethyleneglycol. In contrast, K. arvensis contained low concentrations of phenolics and no tannins, had no effect in the 30-min assay, yet inhibited the degradation rate of soluble protein (by 14 %, P < 0·0001) and the production of branched SCFA (by 17 %, P < 0·05) without precipitating protein in the 12-h batch fermentation. The effects showed some resemblance to those obtained in parallel incubations containing 3 μm-monensin, suggesting that K. arvensis may be a plant-derived feed additive that can suppress growth and activity of key proteolytic ruminal micro-organisms in a manner similar to that already well known for monensin.

This study assessed the impact of reduced dietary protein during specific periods of fetal life upon muscle fibre development in young rats. Pregnant rats were fed a control or low-protein (LP) diet at early (days 0–7 gestation, LPEarly), mid (days 8–14, LPMid), late (days 15–22, LPLate) or throughout gestation (days 0–22, LPAll). The muscle fibre number and composition in soleus and gastrocnemius muscles of the offspring were studied at 4 weeks of age. In the soleus muscle, both the total number and density of fast fibres were reduced in LPMid females (P = 0·004 for both, Diet × Sex × Fibre type interactions), while both the total number and density of glycolytic (non-oxidative) fibres were reduced in LPEarly, LPMid and LPLate (but not LPAll) offspring compared with controls (P < 0·001 for both, Diet × Fibre type interaction). In the gastrocnemius muscle, only the density of oxidative fibres was reduced in LPMid compared with control offspring (P = 0·019, Diet × Fibre type interaction), with the density of slow fibres being increased in LPAll males compared with control (P = 0·024, Diet × Sex × Fibre type interaction). There were little or no effects of maternal diet on fibre type diameters in the two muscles. In conclusion, a maternal low-protein diet mainly during mid-pregnancy reduced muscle fibre number and density in 4-week-old rats, but there were muscle-specific differences in the fibre types affected.

Adequate intakes of micronutrients are required for the immune system to function efficiently. Micronutrient deficiency suppresses immunity by affecting innate, T cell mediated and adaptive antibody responses, leading to dysregulation of the balanced host response. This situation increases susceptibility to infections, with increased morbidity and mortality. In turn, infections aggravate micronutrient deficiencies by reducing nutrient intake, increasing losses, and interfering with utilization by altering metabolic pathways. Insufficient intake of micronutrients occurs in people with eating disorders, in smokers (active and passive), in individuals with chronic alcohol abuse, in certain diseases, during pregnancy and lactation, and in the elderly. This paper summarises the roles of selected vitamins and trace elements in immune function. Micronutrients contribute to the body's natural defences on three levels by supporting physical barriers (skin/mucosa), cellular immunity and antibody production. Vitamins A, C, E and the trace element zinc assist in enhancing the skin barrier function. The vitamins A, B6, B12, C, D, E and folic acid and the trace elements iron, zinc, copper and selenium work in synergy to support the protective activities of the immune cells. Finally, all these micronutrients, with the exception of vitamin C and iron, are essential for antibody production. Overall, inadequate intake and status of these vitamins and trace elements may lead to suppressed immunity, which predisposes to infections and aggravates malnutrition. Therefore, supplementation with these selected micronutrients can support the body's natural defence system by enhancing all three levels of immunity.

We examined the antioxidant effects of polyphenol/anthocyanin-rich potato (Solanum tuberosum cv. Shadow-Queen) flakes in male rats fed a high-cholesterol diet. The rats were served either a high-cholesterol (0·5 % cholesterol plus 0·125 % sodium cholate) diet, or a high-cholesterol diet containing a mixture of 243 g α-maize starch/kg supplemented with one of the following (per kg diet): 300 g medium purple potato (Shadow-Queen), 300 g white potato (Solanum tuberosum cv. Toyoshiro) or 300 g dark purple sweet potato (Ipomoea batatas cv. Ayamurasaki) flakes for 28 d. We analysed thiobarbituric acid reactive substance (TBARS) levels in the serum and liver, and antioxidant enzyme activities in the liver. At this dosage, TBARS levels in the serum and liver of the Shadow-Queen and Ayamurasaki groups were significantly lower than those in the control and Toyoshiro groups. The serum urate levels in all the flake groups were significantly lower than that in the control group. The hepatic glutathione levels in the Shadow-Queen and Ayamurasaki groups were significantly higher than in the control and Toyoshiro groups. The activities of hepatic glutathione reductase and glutathione S-transferase in the Shadow-Queen and Ayamurasaki groups were significantly greater than those in the control group. These results show that modulation of antioxidant enzymes and oxidative status in the serum and liver by the purple potato flake diet (Shadow-Queen) containing polyphenols/anthocyanins may play an important role in the protection against adverse effects related to oxidative damage in rats fed a high-cholesterol diet.

Miglitol, a 1-deoxynojirimycin derivative, is an α-glucosidase inhibitor. In the present study, the effects of acute (single-dose) and chronic (8-week) oral administration of miglitol in Goto-Kakizaki (GK) rats, an animal model of type 2 diabetes, were investigated. Dose-dependent decreases in incremental blood glucose concentrations integrated over a period of 2 h (ΔAUC0–2 h) for values of blood glucose after sucrose-loading in miglitol-treated GK rats were observed following an acute oral administration of miglitol (1, 3 or 10 mg/kg body weight). At 10 mg/kg, the ΔAUC0–2 h of blood glucose was decreased by 45 % compared with the control group. Following the oral administration of miglitol in a dietary mixture (10 mg, 20 mg or 40 mg miglitol/100 g control diet) for 8 weeks, the ratio of HbA1c at 8 weeks compared with 0 weeks in GK rats treated with 40 mg miglitol/100 g control diet miglitol was significantly decreased compared with control GK rats without changes in body weight. In oral glucose tolerance testing, miglitol caused a slight decrease in the ΔAUC0–2 h of plasma glucose concentration. In addition, miglitol treatment slightly inhibited the reduction in β-cell mass, and lessened the irregular contours and fibrosis of the islets in GK rats. These results indicate that miglitol ameliorates the hyperglycaemic state of GK rats and the impaired function of the pancreatic islets, as well as preventing the degeneration of islets in GK rats.

Anthocyanins are natural dietary pigments with a wide array of biological properties that are possibly involved in the prevention of various diseases. These properties depend on their absorption and metabolism in the body. In the present study we first examined the gastric and intestinal absorption of pelargonidin 3-glucoside (Pg 3-glc) using rat in situ models. A high proportion of Pg 3-glc was rapidly absorbed from both the stomach (23 %) and small intestine (24 %). Its metabolism was further studied by feeding rats during 8 d with a diet enriched in freeze-dried strawberries. Only low amounts of total anthocyanins were recovered in 24 h urine (0·163 (sem 0·013) % of ingested anthocyanins; n 8). Strawberry anthocyanins were analysed in urine by HPLC-electrospray ionisation-tandem MS. Similar proportions of intact glycosides (about 53 %) and glucuronidated metabolites (about 47 %) were found. Pg 3-glc was thus glucuronidated to a larger extent than cyanidin 3-glucoside. These results highlight the influence of the aglycone structure on anthocyanin metabolism.

Zn deficiency reduces food intake and growth rate in rodents. To determine the relationship between Zn deficiency and the regulation of food intake, we evaluated leptin gene expression in epididymal white adipose tissue (eWAT), and hypothalamic corticotropin-releasing hormone (hCRH) and hypothalamic neuropeptide Y (hNPY) of rats Zn-deficient only to show reduced food intake and growth rate but not food intake cycling. Growing male Sprague-Dawley rats (240 g) were randomly assigned to one of four dietary groups: Zn-adequate (ZA; 30 mg/kg diet), Zn-deficient (ZD; 3 mg/kg diet), pair-fed with ZD (PF; 30 mg/kg diet) and Zn-sufficient (ZS; 50 mg/kg diet) (n 8), and were fed for 3 weeks. Food intake and body weight were measured, as were blood mononuclear cells and pancreas Zn levels. eWAT leptin, hCRH and hNPY mRNA levels were determined. Food intake was decreased by about 10 % in ZD and PF rats compared to ZA and ZS rats. Growth and eWAT leptin mRNA levels were unaffected in PF rats but were significantly (P < 0·05) decreased in ZD rats. However, hNPY showed a tendency to increase, and hCRH significantly (P < 0·05) decreased, in both ZD and PF rats. These results suggest that while leptin gene expression may be directly affected by Zn, hNPY and hCRH are likely responding to reduced food intake caused by Zn deficiency.

Digestibility is the result of two competing processes: digestion and digesta transit. To develop or parameterise mechanistic models of digestion, both processes have to be quantified. The aim of this study was to determine the effect of insoluble dietary fibre on the transit in the gastrointestinal tract of pigs. Six barrows (33 kg initial body weight and fitted with two simple T-cannulas at the proximal duodenum and distal ileum) were used in a double 3 × 3 Latin square design. Pigs were offered diets differing in total dietary fibre content (170, 220 and 270 g/kg DM) at 4 h intervals. A single meal marked with YbO2 and Cr-EDTA was used to determine the kinetics of markers concentrations of the solid and liquid phases, respectively. The mean retention time (MRT), calculated by the method of the moments, averaged 1, 4 and 38 h in the stomach, small intestine and large intestine, respectively. Increasing the insoluble fibre content in the diet had no effect on MRT in the stomach and decreased the MRT of both phases in the small intestine (P < 0·05). In the large intestine, increasing the insoluble fibre content decreased the MRT of the liquid phase (P = 0·02) and tended to decrease the MRT of the solid phase (P = 0·06). Transit of the solid phase in the large intestine was 4–8 h slower than transit of the liquid phase. Analysis of marker excretion curves indicated that the small and large intestine should be represented mathematically to have both a tubular (propulsion) and compartmental (mixing) structure.

CVD is associated with a cellular inflammatory/immune response. n-3 PUFA and moderate aerobic exercise independently alter cytokine production and leucocyte function. There is limited evidence for the combined effect of these treatments on immune function, particularly in patients with risk factors for CVD. We hypothesised that exercise would enhance the anti-inflammatory effects of n-3 PUFA. In a randomised, placebo-controlled study, fifty volunteers were allocated double-blind to consume either sunflower oil (6 g/d, placebo) or DHA-rich fish oil (6 g/d; about 2 g n-3 PUFA; 1·6 g DHA /d) for 12 weeks. Volunteers were further randomised to undertake regular exercise (walking 3 d/week for 45 min at 75 % of maximum heart rate) or maintain their usual physical activity for 12 weeks. Immune functions were assessed in blood taken initially and after 12 weeks. There was no effect on cytokine production by T cells and monocytes. Superoxide anion production from stimulated blood neutrophils was decreased by fish oil (19·5 (sem 8·5) %, P = 0·016) but not by exercise, and this change was negatively correlated with the incorporation of DHA into erythrocytes (r–0·385, P = 0·047). Participation in regular exercise maintained neutrophil bactericidal activity, which decreased in non-exercising subjects (2·9 (sem 0·7) %, P = 0·013). Neutrophil chemotaxis and adherence were not significantly affected by exercise, oil, or the combination of the two. Thus the combination of moderate exercise and fish-oil supplementation, which reduces cardiovascular risk, may also help to counteract inflammation.

Increased partitioning of amino acids (AA) from skeletal muscle to the intestine and immune system during parasitic infection may be the cause of poor growth in parasitised animals. The effect of an established Trichostrongylus colubriformis infection (6000 L3 T. colubriformis larvae for 6 d (n 5) or kept as parasite-free controls (n 6)) on AA fluxes across the mesenteric-drained viscera, portal-drained viscera (PDV), liver, total splanchnic tissues (TSP) and hindquarters were determined in lambs fed fresh Sulla (Hedysarum coronarium; 800 g DM/d) 48 d post-infection. The lambs were infused with ρ-aminohippuric acid (PAH; 723 mg/h) into the mesenteric vein for 8 h to measure TSP plasma flow. Concurrently, indocyanine green (ICG; 14·6 mg/h) was infused into the abdominal aorta to measure plasma flow across the hindquarters. Blood was continuously collected from the mesenteric, portal and hepatic veins, vena cava and the mesenteric artery and plasma harvested. PAH, ICG, AA, metabolite and insulin concentrations were measured. Intestinal worm burdens on day 48 post-infection were higher in the infected lambs (P < 0·05). Plasma flows across the tissue beds were unaffected by parasitic infection (P>0·10). There was a 28 % reduction in the release of AA from the PDV of infected lambs (P < 0·05). The uptakes of most AA were similar in the liver; however, there was increased uptake (P < 0·10) of AA by the TSP of infected lambs. Despite this reduction in AA availability at the liver, there was no effect of parasitic infection on AA uptake across the hindquarters (P < 0·05).

Taurine has been shown to be tissue protective in many models of oxidant-induced injury. However, its protective role against retinal damage induced by photochemical stress is less well known. The purpose of the present study was to investigate whether dietary taurine reduced retinal photochemical damage in Sprague–Dawley rats and to further explore the underlying molecular mechanisms of this action. Twenty rats fed AIN-93 formulation and maintained in the dark for 48 h were used as controls (n 20). Another forty rats were randomly divided into two groups and then treated with (n 20) or without 4 % taurine (n 20) for 15 d respectively. After treatment, these two groups were exposed to fluorescent light (3000 ± 200 lux and 25°C), and the protective effects of dietary taurine were then evaluated. The present results showed that dietary taurine effectively prevented retinal photochemical damage as assessed by changes of morphology. Also, the supplementation caused an increase of taurine in the retina, a decrease of malondialdehyde (P < 0·01), and elevation of superoxide dismutase (P < 0·01) and glutathione peroxidase activities in the retina (P < 0·01). Moreover, dietary taurine inhibited activator protein-1 (AP-1) (c-fos/c-jun subunits) expression (P < 0·05), up regulated NF-κB (p65) expression (P < 0·05), and decreased caspase-1 expression (P < 0·05) so as to reduce the apoptosis of photoreceptors in the retina (P < 0·05). These results suggest that dietary taurine reduced retinal damage produced by photochemical stress via antioxidant and anti-AP-1–NF-κB–caspase-1 apoptotic mechanisms in rats.

Previously we have reported that maternal malnutrition during lactation programmes body weight and thyroid function in the adult offspring. In the present study we evaluated the effect of maternal protein restriction during lactation upon body composition and hormones related to glucose homeostasis in adult rats. During lactation, Wistar lactating rats and their pups were divided into two experimental groups: control (fed a normal diet; 23 % protein) and protein-restricted (PR; fed a diet containing 8 % protein). At weaning, offspring received a normal diet until they were 180 d old. Body weight (BW) and food intake were monitored. Serum, adrenal glands, visceral fat mass (VFM) and carcasses were collected. PR rats showed lower BW ( − 13 %; P < 0·05), VFM ( − 33 %; P < 0·05), total body fat ( − 33 %; P < 0·05), serum glucose ( − 7 %; P < 0·05), serum insulin ( − 26 %, P < 0·05), homeostasis model assessment index ( − 20 %), but higher total adrenal catecholamine content (+90 %; P < 0·05) and serum corticosterone concentration (+51 %; P < 0·05). No change was observed in food intake, protein mass or total body water. The lower BW of PR rats is due to a reduction of white fat tissue, probably caused by an increase in lipolysis or impairment of lipogenesis; both effects could be related to higher catecholaminergic status, as well as to hypoinsulinaemia. To conclude, changes in key hormones which control intermediary metabolism are programmed by maternal protein restriction during lactation, resulting in BW alterations in adult rats.

There are nationwide folic acid (FA) fortification programmes of staple foods established or under consideration in order to prevent neural tube defects. Universal FA fortification still remains controversial because of the concern that additional FA in the diets of population groups (e.g. children and elderly) not initially targeted for fortification may suffer adverse effects. However, dietary surveys regarding folate generally deal with adults and little is known about the consumption and long-term effects of fortified food and supplements in growing individuals. Recent reports from our laboratory show several effects of high-dose folate supplementation in rats. In the present work, we studied the effect of FA on the methionine cycle in weanling (3-week-old) male rats after 4 weeks of supplementation with 40 mg FA/kg diet v. control (1 mg FA/kg diet). FA supplementation resulted in a reduction of homocysteine and creatinine concentrations v. control group. FA supplementation did not alter S-adenosylmethionine/S-adenosylhomocysteine ratio, DNA methylation, enzymatic activities or concentrations of vitamins involved in the nutritional regulation of the methionine cycle, except for folate. FA supplementation of 40 mg/kg did not lead to hepatic or renal damage. In conclusion, there were no apparent adverse effects on one-carbon metabolism after FA supplementation in the studied conditions.

Vitamins have traditionally been considered as food components that are required in the normal diet to prevent deficiencies. However, a newer concept of the function of vitamins in nutrition has taken them beyond simply prevention of deficiency symptoms. This concept considers that many vitamins, when taken in relatively larges doses, have important functions beyond preventing deficiencies. Linus Pauling was instrumental in putting forward this concept, particularly for vitamin C. Thus, relatively high intakes of vitamins, and in particular vitamins C and E which are antioxidants, are considered to be healthy for the human population. This may be true in some special situations such as, for instance, the prevention of Alzheimer's disease progression. However, recent epidemiological evidence has not supported the claim that antioxidant vitamins increase well-being and prolong life span. In fact, vitamin supplementation may be even detrimental and reduce life span. A new concept that we would like to put forward is that nutrients up-regulate the endogenous antioxidant defences. This is particularly true in the case of phytoestrogens for example, which bind to oestrogen receptors and eventually up-regulate the expression of antioxidant genes. In this review we discuss the pros and cons of antioxidant vitamin supplementation and also the possibility that the ingestion of some nutrients may be very effective in increasing antioxidant defences by up-regulating the activity of antioxidant enzymes which are normally present in the cell.

Oxidised frying oil (OFO) and fish oil have been shown to be peroxisome proliferator-activated receptor (PPAR)α activators and their ingestion results in pleotropic peroxisome proliferator responses in rats. To examine the effect of dietary OFO on adiposity, four groups of weanling Sprague–Dawley rats were fed isoenergetically with, respectively, a low fat basal diet containing 5 g/100 g of fresh soybean oil (LSB) or a high fat diet containing 20 g/100 g of fresh soybean oil (HSB), OFO (HO) or fish oil (HF). The tissue mass, cell size and lipid/DNA ratio in the retroperitoneal fat pad and serum leptin levels were lowest in the HO group (P < 0·05), indicating that dietary OFO has a greater anti-adipogenic action than dietary fish oil. However, a tendency to hyperglycaemia was observed in the HO group (P = 0·0528). To examine the effect of dietary OFO on glucose tolerance, three groups of rats and three groups of mice were fed, respectively, the LSB, HSB or HO diet, and an oral glucose tolerance test was performed. After oral glucose load, the area under the curve for blood glucose (AUCglu) over 2 h was significantly higher, and that for serum insulin (AUCins) over 90 min was significantly lower, in the HO group than in the other two groups (P < 0·05). These results demonstrate that, in rats and mice, a high OFO diet is less adipogenic, but induces glucose intolerance.

The improved effects of dietary chickpeas on visceral adiposity, dyslipidaemia and insulin resistance were examined. Rats were fed a normal-fat diet (NFD), a high-fat diet (HFD) or a high-fat plus chickpea diet (HFD+CP) for 8 months. The epididymal fat pad weight v. total body weight of rats was higher in the HFD group (0·032 (sd 0·0042) g/g) than in the NFD group (0·015 (sd 0·0064) g/g) and smaller in the HFD+CP group (0·023 (sd 0·0072) g/g) compared with the HFD group (P < 0·05). Chickpea treatment also induced a favourable plasma lipid profile reflecting decreased TAG, LDL-cholesterol (LDL-C) and LDL-C:HDL-cholesterol levels (P < 0·05). HFD-fed rats had higher TAG concentration in muscle and liver, whereas the addition of chickpeas to the HFD drastically lowered TAG concentration (muscle, 39 %; liver, 23 %). The activities of lipoprotein lipase (LPL) in epididymal adipose tissue and hepatic TAG lipase in liver recorded a 40 and 23 % increase respectively in HFD rats compared with those in NFD rats; dietary chickpeas completely normalised the levels. Furthermore, chickpea-treated obese rats also showed a markedly lower leptin and LPL mRNA content in epididymal adipose tissue. An insulin tolerance test, oral glucose tolerance test and insulin-releasing test showed that chickpeas significantly improved insulin resistance, and prevented postprandial hyperglycaemia and hyperinsulinaemia induced by the chronic HFD. The present findings provide a rational basis for the consumption of chickpeas as a functional food ingredient, which may be beneficial for correcting dyslipidaemia and preventing diabetes.

Subjects with obesity and elevated fasting blood glucose are at high risk of developing type 2 diabetes which may be reduced by a dietary intervention leading to an improvement of insulin resistance. We investigated the potential of a whole-grain based dietary product (WG) with reduced starch content derived from double-fermented wheat during a hypo-energetic diet to positively influence body weight, fasting blood glucose, insulin resistance and lipids in comparison to a nutrient-dense meal replacement product (MR) in a randomized two-way cross-over study with two 4-week treatment periods separated by a 2-week wash-out. Subjects replaced at least two daily meals with WG and MR, respectively, targeting for a consumption of 200 g of either product per day. Total daily energy intake was limited to 7120 kJ. Thirty-one subjects (BMI 33·9 (sd 2·7) kg/m2, fasting blood glucose 6·3 (sd 0·8) mmol/l) completed the study. In both treatment groups body weight ( − 2·5 (sd 2·0) v. − 3·2 (sd 1·6) kg for WG v. MR), fasting blood glucose ( − 0·4 (sd 0·3) v. − 0·5 (sd 0·5) mmol/l), total cholesterol ( − 0·5 (sd 0·5) v. − 0·6 (sd 0·5) mmol/l), TAG ( − 0·3 (sd 0·9) v. − 0·3 (sd 1·2) mmol/l) and homeostasis model assessment (HOMA) insulin resistance score ( − 0·7 (sd 0·8) v. − 1·1 (sd 1·7) μU/ml ×  mmol/l) improved (P < 0·05) with no significant differences between the treatments. After statistical adjustment for the amount of body weight lost, however, the comparison between both groups revealed that fasting serum insulin (P = 0·031) and HOMA insulin resistance score (P = 0·049) improved better with WG than with MR. We conclude that WG favourably influences metabolic risk factors for type 2 diabetes independent from the amount of body weight lost during a hypo-energetic diet.

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.