Antioxidant requirements have neither been defined for endurance nor been defined for ultra-endurance athletes. To verify whether an acute bout of ultra-endurance exercise modifies the need for nutritive antioxidants, we aimed (1) to investigate the changes of endogenous and exogenous antioxidants in response to an Ironman triathlon; (2) to particularise the relevance of antioxidant responses to the indices of oxidatively damaged blood lipids, blood cell compounds and lymphocyte DNA and (3) to examine whether potential time-points of increased susceptibility to oxidative damage are associated with alterations in the antioxidant status. Blood that was collected from forty-two well-trained male athletes 2 d pre-race, immediately post-race, and 1, 5 and 19 d later was sampled. The key findings of the present study are as follows: (1) Immediately post-race, vitamin C, α-tocopherol, and levels of the Trolox equivalent antioxidant capacity, the ferric reducing ability of plasma and the oxygen radical absorbance capacity (ORAC) assays increased significantly. Exercise-induced changes in the plasma antioxidant capacity were associated with changes in uric acid, bilirubin and vitamin C. (2) Significant inverse correlations between ORAC levels and indices of oxidatively damaged DNA immediately and 1 d post-race suggest a protective role of the acute antioxidant responses in DNA stability. (3) Significant decreases in carotenoids and γ-tocopherol 1 d post-race indicate that the antioxidant intake during the first 24 h of recovery following an acute ultra-endurance exercise requires specific attention. Furthermore, the present study illustrates the importance of a diversified and well-balanced diet to maintain a physiological antioxidant status in ultra-endurance athletes in reference to recommendations.

Different diets have distinct impacts on glucose homoeostasis, for which insulin sensitivity (IS) after a meal (postprandial IS) is highly relevant. Postprandial IS depends upon hepatic parasympathetic activation and glutathione content elevation. We tested the hypothesis that postprandial IS is compromised in high-fat diet (HFD)-induced obesity. Sprague–Dawley rats were fed a standard diet (STD, n 10), 1-week HFD (n 9) or 4-week HFD (n 8). IS was tested in postprandial state using the rapid IS test (RIST) before and after the blockade of the parasympathetic nerves (atropine, 1 mg/kg); parasympathetic-dependent IS was obtained from the difference between control and post-atropine RIST. Fasting IS was also assessed in the STD-fed rats (n 4) and 4-week HFD-fed rats (n 3) using the RIST. Whole-body fat and regional fat pads were heavier in the 1-week HFD-fed rats (79·8 (se 7·9) and 23·7 (se 1·0) g, respectively) or 4-week HFD-fed rats (106·5 (se 6·1) and 30·1 (se 1·4) g, respectively) than in the STD-fed rats (32·5 (se 3·7) and 13·7 (se 1·0) g, respectively; P < 0·001). Fasted-state IS was similar between the groups studied. Postprandial IS was higher in the STD-fed rats (185·8 (se 5·6) mg glucose/kg body weight (bw)) than in both the 1-week HFD-fed rats (108·8 (se 2·9) mg glucose/kg bw; P < 0·001) and 4-week HFD-fed rats (69·3 (se 2·6) mg glucose/kg bw; P < 0·001). Parasympathetic-dependent IS was impaired in both HFD-fed groups (STD, 108·9 (se 3·9) mg glucose/kg bw; 1-week HFD, 38·6 (se 4·2) mg glucose/kg bw; 4-week HFD, 5·4 (se 1·7) mg glucose/kg bw; P < 0·001). Total (postprandial) and parasympathetic-dependent IS correlated negatively with whole-body fat (R2 0·81 and 0·87) and regional adiposity (R2 0·85 and 0·79). In conclusion, fat accumulation induced by HFD is associated with postprandial insulin resistance, but not with fasting insulin resistance. HFD-associated postprandial insulin resistance is largely mediated by impairment of parasympathetic-dependent insulin action, which correlates with adiposity.

Mucositis resulting from cancer chemotherapy is a serious disorder of the alimentary tract. Emu oil has demonstrated anti-inflammatory properties in animal models of arthritis and wound healing; however, its effects on the intestine remain unknown. We investigated emu oil for its potential to decrease the severity of mucositis in a rat model. Female Dark Agouti rats (110–150 g) were orogastrically gavaged with emu oil (0·5 or 1 ml) or water (1 ml) for 5 d before intraperitoneal injection of 5-fluorouracil (5-FU, 150 mg/kg) or saline (control), and this was continued up to the day of sacrifice (48, 72 and 96 h post 5-FU administration). Histological (villus height, crypt depth (CD) and disease severity score) and biochemical (myeloperoxidase (MPO) activity) parameters were determined in intestinal tissues collected at sacrifice. Sucrase activity in vivo was quantified by the sucrose breath test. Activated neutrophil activity (MPO) in the ileum was significantly decreased by emu oil (0·5 ml, 451 (sem 168) U/g and 1 ml, 503 (sem 213) U/g) compared with 5-FU-treated controls (1724 (sem 431) U/g) 96 h post 5-FU administration. There were also significant increases in CD (152 (sem 8) μm) in the ileum of rats that receivied 1 ml emu oil at 96 h compared with 5-FU-treated controls (CD (106 (sem 12) μm)). Emu oil did not affect sucrase activity. Emu oil decreased acute ileal inflammation, and improved mucosal architecture in the intestine during recovery from chemotherapy in rats. Further studies investigating the potential benefits of emu oil as a nutritional supplement for the treatment of intestinal disorders are indicated.

Na+/glucose co-transporter 1 (SGLT1) transports dietary sugars from the lumen of the intestine into enterocytes. Regulation of this protein is essential for the provision of glucose to the body and, thus, is important for maintenance of glucose homeostasis. We have assessed expression of SGLT1 at mRNA, protein and functional levels in the intestinal tissue of 28 d old piglets weaned onto isoenergetic diets with differing concentrations of digestible carbohydrate (CHO). We show that expression of SGLT1 remains constant when piglets are fed up to 40 % CHO-containing diets. However, there is a significant increase in SGLT1 expression when the CHO content of the diet is>50 %. Morphometric analyses indicate that the increased expression is not due to a trophic effect. It has been proposed that in rat intestine, in response to a high-CHO diet, GLUT2 (the classical basolateral membrane monosaccharide transporter) is translocated to the luminal membrane of enterocytes to absorb excess dietary glucose. We show, using immunohistochemistry and Western blotting with antibodies raised to amino acids in different epitopes of GLUT2, that under all dietary conditions, low to high CHO, GLUT2 is expressed on the basolateral membrane of pig enterocytes. Furthermore, functional studies indicate that there is no uptake of 2-deoxy-d-glucopyranoside, a specific substrate of Na+-independent glucose transporters into brush-border membrane vesicles isolated from the intestines of piglets either maintained on low- or high-CHO diets. Thus, SGLT1 is the major route for absorption of dietary sugars across the luminal membrane of swine enterocytes.

Consumption of grape seed extract (GSE) is widely marketed as a dietary supplement and is considered safe for human health. Nevertheless, the analytical composition of GSE from different grape cultivars, growing in special agronomic constraints, differs greatly in flavan-3-ols content. The major concern with GSE studies is a lack of availability of uniformly standardised preparations, which raises an important question whether different GSE samples have comparable activity and trigger the same mechanisms of action on a given biological system. Therefore, it is tempting to speculate that GSE, obtained from different cultivars, could exert differentiated anticancer effects. The focus of the present study is to determine the selective biological efficacy of GSE obtained from three different sources on the human colon cancer cell line Caco-2. Irrespective of its source, high doses of GSE induced a significant inhibition on Caco-2 cell growth. Moreover, apoptosis was enhanced through both caspase-dependent and caspase-independent mechanisms, leading to an early apoptosis-inducing factor release and, further, to a dramatic increase in caspase 7 and 3 activity. However, a significant difference in apoptotic rates induced by the three grape sources clearly emerged when treating cancer cells with low and intermediate GSE concentrations (25 and 50 μg/ml).

Flax oil feeding has been proposed to have beneficial effects on the outcome of the metabolic syndrome due to the high n-3 fatty acid content of flax oil; however, the mechanisms of its action remain largely unknown. We investigated the effects of flax oil feeding on hyperlipidaemia, hyperglycaemia, hepatic steatosis and oxidative stress in the spontaneously hypertensive (SHR)/NDmcr-cp rats, a genetic model of the metabolic syndrome. Hepatic gene expression of PPAR-α, PPAR-γ and sterol-regulatory element-binding protein-1c was also assessed in order to investigate the possible underlying mechanisms. Obese and lean SHR/NDmcr-cp rats were fed high-fat diets enriched with either lard or flax oil for a period of 4 weeks. Obese rats exhibited higher body weight, liver weight and mesenteric fat-, epididymal fat- and renal fat-pad weights, and also TAG and cholesterol concentrations in serum and VLDL, LDL and HDL fractions, when compared with the lean rats (P < 0·001), irrespective of the diets. Concentrations of fasting serum insulin and urinary thiobarbituric acid reactive substances were lower in flax oil-fed obese (FO) rats compared with the lard-fed obese (LO) rats (P < 0·01). Flax oil feeding also revealed a significant reduction in hepatic TAG and cholesterol concentrations in obese rats compared with the LO rats (P < 0·05). In addition, FO rats exhibited significantly higher hepatic mRNA expression of PPAR-γ, which negatively correlated (r − 0·98, P < 0·05) with their hepatic lipid levels. These findings suggest that flax oil feeding may activate PPAR-γ-dependent pathways to alter the hepatic lipid metabolism and to increase insulin sensitivity in the obese SHR/NDmcr-cp rats.

There are insufficient data to provide conclusive evidence on the health effects of most flavonoid subclasses. Future research of polyphenol bioactivity requires a more complete understanding of their intake, bioavailability and metabolism. The following summarises the limitations of polyphenol research as described across various reviews throughout the literature and presents the key requirements for future research. These include establishing the effects of processing, bioavailability and metabolism, developing physiologically appropriate in vitro models, standard methods of analysis and appropriate clinical biomarkers. The future of flavonoid research will undoubtedly depend upon the resolve of these issues, and although the field has shown continuous progress for many years, progress will likely slow if these challenges are not met.

We sought to determine whether postcaesarean treatment with whey peptides (WP) affects the healing of skin and uterine incision in rats during puerperium. Forty-eight rats were randomly divided into two groups. After a caesarean section, twenty-four rats were intragastrically administered WP, while others were administered a control vehicle. On days 7, 14 and 21 after delivery, the serum total protein/albumin concentration, skin tensile strength, uterine bursting pressure, skin/uterine hydroxyproline (Hyp) concentration and histological characteristics of the scar were measured in eight rats in each group. In the WP group, the albumin concentration, skin tensile strength, uterine bursting pressure and Hyp concentration in the skin increased significantly on days 21, 7, 14 and 21, respectively. Low neutrophil count and smaller scar width in the skin incision were found in the WP group on day 7. Postcaesarean treatment with WP promoted significant wound healing in the skin incision, and had a significant wound healing potential in the uterus.

N balance and postprandial acylcarnitine profile following intestinal fermentation of oligofructose and inulin were investigated in healthy cats. Two diets were tested in a crossover design: a commercial high-protein cat food supplemented with 4 % DM oligofructose and inulin (spectrum: degree of polymerisation (DP) 2–10: 60 (se 5) % DM; DP>10: 28 (se 5) % DM) as high-fermentable fibre (HFF) diet, and the same commercial diet supplemented with 4 % DM cellulose as low-fermentable fibre diet. Eight adult cats were randomly allotted to each of the two diets at intervals of 4 weeks. At the end of each testing period, faeces and urine were collected over a 5-d period, and blood samples were obtained before and at the selected time points postprandially. No differences were found for N intake, N digestibility and faecal N excretion, whereas urinary N excretion was lower when the HFF diet was fed (P = 0·044). N balance was positive in all the cats, and tended to be increased when the HFF diet was fed (P = 0·079). Propionylcarnitine concentrations (P = 0·015) and their area under the curve (AUC) (P = 0·013) were increased when the HFF diet was fed, revealing a more pronounced production and absorption of propionate. Yet, methylmalonylcarnitine concentrations and concurrent AUC were not elevated when the HFF diet was fed, indicating reduced amino acid catabolism. 3-Hydroxy-3-methylglutarylcarnitine concentrations (P = 0·026) and their AUC (P = 0·028) were also reduced when the HFF diet was fed, implying diminished use of branched-chain amino acids as well. In healthy cats, oligofructose and inulin added to a high-protein diet were suggested to reduce postprandial amino acid-induced gluconeogenesis by substitution with propionate.

The aim of the present study was to investigate the cataract preventive effect of dietary histidine regimes in adult Atlantic salmon (Salmo salar L.) in seawater, both through manipulating the dietary histidine level and feeding period. Mean body weight of individually tagged Atlantic salmon at the start of the experiment was 1662 (sd 333) g. Low prevalence of mild cataracts were recorded in the beginning of June. Three fishmeal and fish oil-based extruded diets (crude protein: 375 g/kg and fat: 342 g/kg), differing only in histidine content (low (L): 9·3, medium (M): 12·8 and high (H): 17·2 g histidine/kg diets), were fed to duplicate net pens in seawater. The experimental period was divided into three seasons (June–July; July–September; September–October), each starting and ending with individual cataract examination, assessment of somatic data, and sampling of lens and muscle tissues for analysis of histidine and histidine derivatives. In July and September, a part of the population fed L- and H-histidine feeds were transferred (crossed over) to respective series of replicate net pens fed L-, M- and H-histidine diets (i.e. eleven experimental feeding groups at trial conclusion). The fish doubled their body weight from June to October, with no systematic effects on weight gain of dietary histidine feeding regimes. Development of severe cataracts was observed between July and September. The cataract severity was directly related to the dietary histidine level fed during the first and second periods. Feeding histidine-supplemented diets (M or H) in the first period from June to July mitigated later cataract outbreaks. The status of selected free imidazoles in muscle and lens tissues reflected the dietary histidine feeding regimes, relative to both feed concentration and feeding duration. The study shows the risk for cataract development for adult Atlantic salmon, 1 year after the transfer of salmon smolts from freshwater to seawater, which to a major extent can be prevented by histidine supplementation just before and during the early phase of cataract development.

Although the flavonol quercetin is used as a supplement in commercial dog food, data on quercetin bioavailability in dogs are not available. Thus, we investigated quercetin bioavailability (measured as area under the concentration–time curve) in nine adult beagle dogs at an oral dose of 10 mg/kg body weight (b.w.). The major fraction (>80 %) of flavonols circulating in blood plasma were conjugated metabolites of quercetin. The absolute bioavailability of quercetin (i.e. the fraction that reaches the systemic circulation) was only about 4 %. We also compared the oral bioavailability between the aglycone quercetin and its more often used glucorhamnoside (rutin) and 3-O-glucoside (isoquercitrin) at an equimolar dose of 30 μmol/kg b.w. (corresponding to 10 mg quercetin/kg). Quercetin and isoquercitrin were mainly absorbed in the small intestine with isoquercitrin being one and a half times more bioavailable than quercetin. Maximal plasma concentration after isoquercitrin treatment was 0·89 (sem 0·07) μmol/l. Although quercetin absorption from rutin was delayed, relative bioavailability was not lower than from the aglycone itself. The latter observation is in clear contrast to findings in human subjects, pigs or rats and might indicate that rutin is a better source of quercetin in dogs than in other species. However, potential in vivo quercetin effects beyond the gastrointestinal tract are limited by the intensive metabolism as well as by the rather low bioavailability of this flavonol.

Dietary fish oil modulates skeletal muscle membrane fatty acid composition. Similar changes in heart membrane composition modulate myocardial oxygen consumption and enhance mechanical performance. The rat in vivo autologous perfused hindlimb was used to investigate the influence of membrane composition on skeletal muscle function. Male Wistar rats were fed either saturated fat (SF), n-6 PUFA (linoleic acid rich) or n-3 PUFA (fish oil) diets for 8 weeks. Hindlimb skeletal muscle perfused using the animal's own blood was stimulated via the sciatic nerve (1 Hz, 6-12 V, 0·05 ms) to contract in repeated 10 min bouts. The n-3 PUFA diet markedly increased 22 : 6n-3 DHA, total n-3 PUFA and decreased the n-6:n-3 PUFA ratio (P < 0·05) in red and white skeletal muscle membranes. There was no difference in initial twitch tension but the n-3 PUFA group maintained greater twitch tension within all contraction bouts and recovered better during rest to produce greater twitch tension throughout the final contraction bout (P < 0·05). Hindlimb oxygen consumption during contraction was significantly lower in the n-3 PUFA group compared with the SF group, producing a significantly higher O2 efficiency index compared with both SF and n-6 PUFA groups (P < 0·05). Resting oxygen consumption was increased in recovery in the SF group (P < 0·05) but did not change in the n-3 PUFA group. Membrane incorporation of n-3 PUFA DHA following fish oil feeding was associated with increased efficiency of muscle O2 consumption and promoted resistance to muscle fatigue.

The beneficial influences of xylo-oligosaccharides (XOS) obtained from alkali-pretreated corncob and fructo-oligosaccharides (FOS) obtained from cane sugar were evaluated in experimental diabetes. These oligosaccharides were supplemented at 10 % (w/w) in the basal diet of streptozotocin-induced diabetic Wistar rats, while the control rats were fed with a basal diet for a period of 6 weeks. Both the oligosaccharides exerted favourable influences in diabetic rats by significantly improving body weight and reducing hyperglycaemia and cholesterol. The characteristic diabetic complications such as severe glucosuria, proteinuria and advanced glycation end products in renal tissue, diabetic nephropathy, and blood creatinine and urea concentrations were notably reduced. Besides, these oligosaccharide supplementations significantly increased the activity of antioxidant enzymes – catalase and glutathione reductase – in the blood of diabetic rats. Supplementation of XOS and FOS resulted in a significant increase in the bifidobacteria and lactobacilli population in the caecum. The present study indicates that XOS and FOS have an ameliorating influence on metabolic abnormalities associated with diabetes, besides conferring an optimal milieu of lactobacilli and bifidobacteria, thus suggesting their potential health benefit in diabetics.

The increase in VLDL TAG concentration after ingestion of a high-fructose diet is more pronounced in men than in pre-menopausal women. We hypothesised that this may be due to a lower fructose-induced stimulation of de novo lipogenesis (DNL) in pre-menopausal women. To evaluate this hypothesis, nine healthy male and nine healthy female subjects were studied after ingestion of oral loads of fructose enriched with 13C6 fructose. Incorporation of 13C into breath CO2, plasma glucose and plasma VLDL palmitate was monitored to evaluate total fructose oxidation, gluconeogenesis and hepatic DNL, respectively. Substrate oxidation was assessed by indirect calorimetry. After 13C fructose ingestion, 44·0 (sd 3·2) % of labelled carbons were recovered in plasma glucose in males v. 41·9 (sd 2·3) % in females (NS), and 42·9 (sd 3·7) % of labelled carbons were recovered in breath CO2 in males v. 43·0 (sd 4·5) % in females (NS), indicating similar gluconeogenesis from fructose and total fructose oxidation in males and females. The area under the curve for 13C VLDL palmitate tracer-to-tracee ratio was four times lower in females (P < 0·05), indicating a lower DNL. Furthermore, lipid oxidation was significantly suppressed in males (by 16·4 (sd 5·2), P < 0·05), but it was not suppressed in females ( − 1·3 (sd 4·7) %). These results support the hypothesis that females may be protected against fructose-induced hypertriglyceridaemia because of a lower stimulation of DNL and a lower suppression of lipid oxidation.

Inconsistent results exist from human and animal studies for Se and methionine (Met) regarding their influence on homocysteine (HCys) and cholesterol (Chol) metabolism. To elucidate these contradictions, sixty-four weanling albino rats were divided into eight groups of 8, and were fed diets containing four different Se levels (15, 50, 150 and 450 μg/kg) either in combination with the recommended Met level of 3 g/kg (C15, C50, C150 and C450) or with an increased Met concentration of 15 g/kg (M15, M50, M150 and M450) for 8 weeks. Plasma HCys was twofold higher in the Se-supplemented C groups than in group C15. Met addition also doubled plasma HCys compared with the respective C groups. In contrast, the expression of the key enzymes of glutathione biosynthesis in the liver was significantly lowered by Se and in particular by Met. Liver Chol concentration was significantly higher in all the Se-supplemented C and M groups than in groups C15 and M15. Plasma Chol was, however, lowered. The uninfluenced expression of sterol-regulatory element-binding protein 2 and of hydroxymethyl-glutaryl-CoA reductase, the increased LDL receptor expression and the reduced expression of the hepatobiliary Chol exporter ATP-binding-cassette-transporter 8 (ABCG8) by Se and/or Met explain these findings. We conclude that the elevation of plasma HCys in rats by Se and Met results from a higher export into plasma. The fact that Se in particular combined with Met increases liver Chol but reduces plasma Chol should be addressed in future investigations focussing on the regulation of ABCG8, which is also selectively involved in the reverse transport of phytosterols in the small intestine.

A growing body of evidence supports the therapeutic effects of blueberry in neurodegenerative disorders. Biotransformation of blueberry juice by Serratia vaccinii bacteria increases its phenolic content and antioxidant activity. In neuronal cell culture, biotransformed blueberry juice (BJ) significantly increased the activity of antioxidant enzymes, namely catalase and superoxide dismutase. Moreover, BJ protected neurons against H2O2-induced cell death in a dose-dependent manner. This associated with the upregulation of mitogen-activated protein kinase (MAPK) family enzymes p38 and c-Jun N-terminal kinase (JNK) activation, as well as with the protection of extracellular signal-regulated kinase (ERK1/2) and MAPK/ERK kinase (MEK1/2) activity loss induced by H2O2. The present studies demonstrate that BJ can protect neurons against oxidative stress possibly by increasing antioxidant enzyme activities and activating p38- and JNK-dependent survival pathways while blocking MEK1/2- and ERK1/2-mediated cell death. Thus, BJ may represent a novel approach to prevent and to treat neurodegenerative disorders, and it may represent a source of novel therapeutic agents against these diseases.

There is strong epidemiological evidence that more physical activity is associated with reduced risk of colon cancer, but the amount or type of activity necessary to invoke this protection is disputed, and the mechanism that is responsible has not been elucidated. The present study compared the effects of two contrasting exercise regimens on intestinal tumourigenesis in Min mice, and investigated two novel mechanistic factors: colonic butyrate and sleep. From 5 weeks of age, Min mice were exercised by running on a treadmill (TR; ≤ 21 m/min, 30–60 min/d, 5 d/week, ≤ 12 weeks). Additional groups of mice were provided with an exercise wheel (WH) or no exercise (CON). Mice had free access to a Western-style, high-fat diet. WH mice ran 3·97 km (females) and 1·92 km (males) daily (P = 0·002). There were no differences in body weight gain or body composition between treatment groups. Treadmill running reduced the numbers of larger ( ≥ 2 mm diameter) tumours (P = 0·042), and tended to reduce tumour multiplicity in the colon (P = 0·049). TR mice had a higher molar proportion of butyrate in colonic digesta than CON mice (P = 0·030), and when treatment groups were combined, there was a weak negative correlation (r − 0·174, P = 0·061) between butyrate molar proportion and total tumour number. In a subset of animals in which non-exercise physical activity was monitored, there were strong positive correlations between sleep duration and both tumour multiplicity (P < 0·001) and tumour burden (P = 0·001). More studies of the effects of sleep and of colonic butyrate in mediating the effects of physical activity on intestinal tumourigenesis are warranted.

EPA or fish oil supplementation has been suggested as treatments for the prevention of type 2 diabetes mellitus (T2DM) due to their lipid-lowering and potential insulin-sensitising effects. We investigated the effects of supplementation with EPA (1 g/kg body weight per d) or fish oil (3 g/kg body weight per d) on the age of onset of T2DM and circulating glucose, insulin, lipids, leptin and adiponectin in UC Davis (UCD)-T2DM rats. Animals were divided into three groups starting at 1 month of age: control, EPA and fish oil. All the animals were followed until diabetes onset or for up to 12 months of age. Monthly fasting blood samples were collected for the measurement of glucose, lipids, hormones and C-reactive protein (CRP). Neither EPA nor fish oil delayed the onset of T2DM or altered fasting plasma glucose, insulin, CRP, adiponectin or leptin concentrations. The groups did not differ in energy intake or body weight. Fish oil treatment lowered fasting plasma TAG concentrations by 39 (sd 7) % (P < 0·001) and EPA lowered fasting plasma NEFA concentrations by 23 (sd 5) % (P < 0·05) at 4 months of age compared with the control group. EPA and fish oil lowered fasting plasma cholesterol concentrations at 4 months of age by 19 (sd 4) and 22 (sd 4) % compared with the control group, respectively (both P < 0·01). In conclusion, EPA and fish oil supplementation lowers circulating lipid concentrations, but does not delay the onset of T2DM in UCD-T2DM rats.

We have demonstrated previously that both acute and chronic oral administration of adenosine have novel functions such as anti-hypertensive effects and improved hyperlipidaemia in stroke-prone spontaneously hypertensive rats (SHRSP) fed a normal diet. The purpose of the present study was to investigate the effect of adenosine administration on metabolic syndrome-related parameters in SHRSP fed a high-fat diet. Six-week-old rats were divided into three groups, and were administered either water (control) or adenosine (10 or 100 mg/l) for 8 weeks. During this period, the rats had free access to a high-fat diet based on AIN-93M. The results showed that hypertension, plasma lipid, NO, insulin, glucose and urinary 8-hydroxy-2′-deoxyguanosine levels improved significantly in both adenosine groups. The mRNA expression levels of genes involved in anti-oxidative activity and adenosine receptors were also altered in the adenosine groups. Administration of adenosine also increased plasma adiponectin levels, accompanied by upregulation of mRNA expression level of adiponectin and adiponectin receptor 1 in perirenal fat and adiponectin receptor 2 in the liver. In conclusion, oral administration of adenosine is effective for improving metabolic syndrome-related parameters in SHRSP, and accordingly it may prevent the progression of the metabolic syndrome.