Consumption of fruits and vegetables has been investigated for their role in the prevention of many chronic conditions. Among the fruits, mango provides numerous bioactive compounds such as carotenoids, vitamin C and phenolic compounds, which have been shown to have antioxidant and anti-inflammatory properties. The present study examined the effects of dietary supplementation of freeze-dried mango pulp, in comparison with the hypolipidaemic drug, fenofibrate, and the hypoglycaemic drug, rosiglitazone, in reducing adiposity and alterations in glucose metabolism and lipid profile in mice fed a high-fat (HF) diet. Male C57BL/6J mice were randomly divided into six treatment groups (eight to nine/group): control (10 % energy from fat); HF (60 % energy from fat); HF+1 or 10 % freeze-dried mango (w/w); HF+fenofibrate (500 mg/kg diet); HF+rosiglitazone (50 mg/kg diet). After 8 weeks of treatment, mice receiving the HF diet had a higher percentage body fat (P = 0·0205) and epididymal fat mass (P = 0·0037) compared with the other treatment groups. Both doses of freeze-dried mango, similar to fenofibrate and rosiglitazone, prevented the increase in epididymal fat mass and the percentage of body fat. Freeze-dried mango supplementation at the 1 % dose improved glucose tolerance as shown by approximately 35 % lower blood glucose area under the curve compared with the HF group. Moreover, freeze-dried mango lowered insulin resistance, as indicated by the homeostasis model assessment of insulin resistance, to a similar extent as rosiglitazone and modulated NEFA. The present findings demonstrate that incorporation of freeze-dried mango in the diet of mice improved glucose tolerance and lipid profile and reduced adiposity associated with a HF diet.

The present study examines the effects of protein- and energy-type malnutrition in combination with Zn deficiency on the growth, serum insulin-like growth factor-1 (IGF-1), gastrocnemius muscle mass and fibre diameter of growing rats during a deficiency phase followed by nutritional rehabilitation. Rats (3-weeks old) were randomly assigned to baseline, or Zn-deficient (Z, < 1 mg Zn/kg), protein-deficient (P, 20 g protein/kg), combined Zn- and protein-deficient (ZP), energy-deficient (E, feed intake pair-fed to Z) or control (C, 30 mg Zn/kg and 170 g protein/kg) groups for a 3-week deficiency phase, followed by a 3-week repletion phase with the control diet. ATPase histochemical staining at pH 9·4 was used to differentiate type 1 and type 2 muscle fibres. After the deficiency phase, the ZP and P groups had lower body weight and smaller gastrocnemius muscle mass than the Z and E groups. Type 1 and 2 muscle fibre diameters (T1- and T2-MFD, respectively) were reduced in the ZP, P and Z groups compared with the E and C groups. Serum Zn was reduced in the ZP, P and Z groups, but serum IGF-1 was lowest in the Z and E groups. After the repletion phase, T1-MFD did not recover in the P and E groups nor T2-MFD in the P group, despite the P and E groups having a better recovery of body weight. In summary, previous protein deficiency, but not Zn deficiency, limited the recovery of both T1- and T2-MFD during nutritional repletion. The quality of skeletal muscle recovery in the malnourished groups was not associated with body weight, muscle mass, serum Zn or IGF-1 concentrations.

Ascorbic acid uptake is a key step in determining the overall bioactivity of this vitamin. Expression of Na-dependent vitamin C transporters (SVCT; SLC23A1 and SLC23A2) during long-term oxidative stress occurring in several chronic liver diseases may determine the antioxidant defence in this organ. In patients with hepatocellular cholestasis, primary biliary cirrhosis, haemochromatosis and non-alcoholic steatohepatitis, using real-time RT-PCR, an enhanced hepatic expression of both SLC23A1 and SLC23A2, but not other organic anions transporters, such as OATP1A2, OATP1B1 and OATP1B3, was found. To further investigate these findings, we used secondary biliary cirrhosis induced in rats by long-term biliary obstruction as a model of chronic liver disease accompanied by oxidative stress because of bile acid accumulation. In control rat liver, expression of Slc23a1 was low at birth, increased progressively up to adulthood and decreased in senescence, whereas expression of Slc23a2 did not change significantly after birth. In 8-week-old rats, immunohistochemistry and confocal microscopy studies revealed the expression in hepatocytes and bile duct cells of mainly Slc23a1, whereas both Slc23a1 and Slc23a2 were expressed in endothelial, stellate and Kupffer cells. In adult rats, when obstructive cholestasis was maintained for 8 weeks, a significant up-regulation of Slc23a2 accompanied by a down-regulation of Slc23a1 was found. In sum, there is a selective cell-type distribution of SVCT in the liver tissue, which, in addition to differential control in the expression of both isoforms, may play a role in the ability of different liver cell types to take up vitamin C under physiological and pathological conditions.

The aim of the present study was to investigate the association of PLIN1 11482G>A (rs894160) and PLIN1 13041A>G (rs2304795) polymorphisms with body composition, energy and substrate metabolism, and the metabolic response to a 12-week energy-restricted diet in obese women. The study comprised a total of seventy-eight obese (BMI 34·0 (sd 2·8) kg/m2) women (age 36·7 (sd 7) years). We measured weight, height and waist circumference before and after a 12-week controlled energy-restricted diet intervention. Body fat mass and lean mass were measured by dual-energy X-ray absorptiometry. RMR and lipid oxidation rate were measured by indirect calorimetry. We also analysed fasting plasma glucose, insulin, cholesterol and leptin. Women carrying the 11482A allele had a lower reduction in waist circumference than non-A allele carriers (3·2 (sd 0·5) v. 4·6 (sd 0·6) %, respectively, P = 0·047; P for gene–diet interaction = 0·064). Moreover, women with the 11482A allele had a higher decrease in lipid oxidation rate than non-A allele carriers (58·9 (sd 6·7) v. 31·3 (sd 8·2) %, respectively, P = 0·012; P for gene–diet interaction = 0·004). There was no interaction effect between the 13041A>G polymorphism and diet-induced changes on the outcome variables (all P>0·1). These results confirm and extend previous findings suggesting that the PLIN1 11482G>A polymorphism plays a modulating role on diet-induced changes in body fat and energy metabolism in obese women.

Data on body weight of pure-bred kittens (Maine Coon, Norwegian Forest Cat, Birman, Persian, Siamese/Oriental Shorthair Cat) from birth (n 245) to 12 weeks of age (n 135) were obtained from breeders. Absolute birth weight (in g) was higher in larger breeds than in smaller breeds, whereas relative birth weight (in % of mature female weight) tended to be higher in smaller breeds (Maine Coon 115 g, 2·3 %; Norwegian Forest Cat 106 g, 2·7 %; Birman 97 g, 2·8 %; Siamese 92 g, 2·8 %; Persian 82 g, 3·2 %). Relative birth weight was lower than that described in the literature for colony cats. Relative litter weight was highest in Norwegian Forest Cats (14·6 (sd 1·8) %; n 10) and lowest in Birmans (8·8 (sd 3·1) %, n 7; P < 0·05); the other breeds were in-between (11·9 (sd 2·0) %; n 19). Absolute growth was faster in larger breeds than in smaller breeds. In relation to expected mature weight, there was good agreement with data from colony cats but no clear-cut effect of breed size. There appeared to be a trend to an earlier onset of sexual dimorphism in larger breeds.

Epidemiological studies of dietary glycaemic index (GI) and glycaemic load (GL) in relation to diabetes risk have yielded inconsistent results. We aimed to examine the associations between dietary GI and GL and the risk of type 2 diabetes by conducting a meta-analysis of prospective cohort studies. Relevant studies were identified by a PubMed database search up to February 2011. Reference lists from retrieved articles were also reviewed. We included prospective cohort studies that reported risk estimates with 95 % CI for the associations between dietary GI and GL and the risk of type 2 diabetes. Either a fixed- or random-effects model was used to compute the summary relative risk (RR). We identified thirteen prospective cohort studies of dietary GI or GL related to diabetes risk. The summary RR of type 2 diabetes for the highest category of the GI compared with the lowest was 1·16 (95 % CI 1·06, 1·26; n 12), with moderate evidence of heterogeneity (P = 0·02, I2 = 50·8 %). For the GL, the summary RR was 1·20 (95 % CI 1·11, 1·30; n 12), with little evidence of heterogeneity (P = 0·10, I2 = 34·8 %). No evidence of publication bias was observed. In addition, the associations persisted and remained statistically significant in the sensitivity analyses. In conclusion, the present meta-analysis provides further evidence in support of significantly positive associations between dietary GI and GL and the risk of type 2 diabetes. Reducing the intake of high-GI foods may bring benefits in diabetes prevention.

A total of sixty surgically castrated male pigs (Large White × Landrace) weighing 31·2 (sd 4·3) kg were used in a randomised block experiment to examine the effect of added dietary inulin (0, 20, 40 and 80 g/kg) on the occurrence of swine dysentery (SD) and on fermentation characteristics in the large intestine after experimental challenge with the causative spirochaete Brachyspira hyodysenteriae. The pigs were allowed to adapt to the diets for 2 weeks before each pig was challenged orally four times with a broth culture containing B. hyodysenteriae on consecutive days. Increasing dietary levels of inulin linearly (P = 0·001) reduced the risk of pigs developing SD; however, eight out of fifteen pigs fed the diet with 80 g/kg inulin still developed the disease. The pH values in the caecum (P = 0·072) tended to decrease, and in the upper colon, the pH values did decrease (P = 0·047) linearly with increasing inulin levels in the diets, most probably due to a linear increase in the concentration of total volatile fatty acids in the caecum (P = 0·018), upper colon (P = 0·001) and lower colon (P = 0·013). In addition, there was a linear reduction in the proportion of the branched-chain fatty acids isobutyric acid and isovaleric acid in the caecum (P = 0·015 and 0·026) and upper colon (P = 0·011 and 0·013) with increasing levels of dietary inulin. In conclusion, the present study showed that a diet supplemented with a high level of inulin (80 g/kg) but not lower levels reduced the risk of pigs developing SD, possibly acting through a modification of the microbial fermentation patterns in the large intestine.

Autophagy, a catabolic process responsible for the degradation of cytosolic components and the preservation of cellular homeostasis in virtually all eukaryotic organisms, is up-regulated when nutrient supplies are limited. However, whether early weaning induces autophagy in infants is not completely clear. In the present study, we used piglets as the early-weaning model to examine the autophagic activity in different tissues in response to nutrient status. Western blot analysis demonstrated that microtubule-associated protein 1 light chain 3-II, a promising marker protein for macroautophagy, was expressed at a notably higher level at 12 and 24 h weaning treatments than without weaning treatment (P < 0·01), and that the p62 (sequestome 1; SQSTM1) expression level was significantly attenuated after weaning treatments (P < 0·01) in the liver, spleen and skeletal muscle tissues. In addition, autophagic vacuoles detected by transmission electron microscopy were dramatically accumulated in these tissues (P < 0·01). Together, these results indicate that autophagy induced by early weaning may be helpful for the physiological system, which controls the balance of energy and nutrients for basic cell functions in the piglet model.

Accumulation of muscle TAG content and modification of muscle phospholipid fatty acid pattern may have an impact on lipid metabolism, increasing the risk of developing diabetes. Some polyphenols have been reported to modulate lipid metabolism, in particular those issued from red grapes. The present study was designed to determine whether a grape polyphenol extract (PPE) modulates skeletal muscle TAG content and phospholipid fatty acid composition in high-fat–high-sucrose (HFHS) diet-fed rats. Muscle plasmalemmal and mitochondrial fatty acid transporters, GLUT4 and lipid metabolism pathways were also explored. The PPE decreased muscle TAG content in HFHS/PPE diet-fed rats compared with HFHS diet-fed rats and induced higher proportions of n-3 PUFA in phospholipids. The PPE significantly up-regulated GLUT4 mRNA expression. Gene and protein expression of muscle fatty acid transporter cluster of differentiation 36 (CD36) was increased in HFHS diet-fed rats but returned to control values in HFHS/PPE diet-fed rats. Carnitine palmitoyltransferase 1 protein expression was decreased with the PPE. Mitochondrial β-hydroxyacyl CoA dehydrogenase was increased in HFHS diet-fed rats and returned to control values with PPE supplementation. Lipogenesis, mitochondrial biogenesis and mitochondrial activity were not affected by the PPE. In conclusion, the PPE modulated membrane phospholipid fatty acid composition and decreased muscle TAG content in HFHS diet-fed rats. The PPE lowered CD36 gene and protein expression, probably decreasing fatty acid transport and lipid accumulation within skeletal muscle, and increased muscle GLUT4 expression. These effects of the PPE are in favour of a better insulin sensibility.

The present study was conducted to follow up on apparent differences in growth, relative organ sizes, cellular stress and immune function in Atlantic salmon fed feed containing GM Bacillus thuringiensis maize compared with feed containing the non-modified parental maize line. Gene expression profiling on the distal intestinal segment and liver was performed by microarray, and selected genes were followed up by quantitative PCR (qPCR). In the liver, qPCR revealed some differentially regulated genes, including up-regulation of gelsolin precursor, down-regulation of ferritin heavy subunit and a tendency towards down-regulation of metallothionein (MT)-B. This, combined with the up-regulation of anti-apoptotic protein NR13 and similar tendencies for ferritin heavy chain and MT-A and -B in the distal intestine, suggests changes in cellular stress/antioxidant status. This corresponds well with and strengthens previous findings in these fish. To exclude possible confounding factors, the maize ingredients were analysed for mycotoxins and metabolites. The GM maize contained 90 μg/kg of deoxynivalenol (DON), while the non-GM maize was below the detection limit. Differences were also observed in the metabolite profiles of the two maize varieties, some of which seemed connected to the mycotoxin level. The effects on salmon observed in the present and previous studies correspond relatively well with the effects of DON as reported in the literature for other production animals, but knowledge regarding effects and harmful dose levels in fish is scarce. Thus, it is difficult to conclude whether the observed effects are caused by the DON level or by some other aspect of the GM maize ingredient.

Thylakoid membranes, derived from chloroplasts, have previously been shown to retard fat digestion and lower blood glucose levels after oral intake. The purpose of the present study was to investigate the effect of thylakoid membranes on the passage of methyl-glucose, dextran and ovalbumin over rat intestine in vitro using Ussing chambers. The results show that thylakoids retard the passage of each of the test molecules in a dose-dependent way. The thylakoids appear to be attached on the mucosal surface and a mechanism is suggested that the thylakoids delay the passage of the test molecules by sterical hindrance. The present results indicate that thylakoid membranes may be useful both to control intestinal absorption of glucose and to enhance the barrier function of the intestine.

Cats are strict carnivores and in the wild rely on a diet solely based on animal tissues to meet their specific and unique nutritional requirements. Although the feeding ecology of cats in the wild has been well documented in the literature, there is no information on the precise nutrient profile to which the cat's metabolism has adapted. The present study aimed to derive the dietary nutrient profile of free-living cats. Studies reporting the feeding habits of cats in the wild were reviewed and data on the nutrient composition of the consumed prey items obtained from the literature. Fifty-five studies reported feeding strategy data of cats in the wild. After specific exclusion criteria, twenty-seven studies were used to derive thirty individual dietary nutrient profiles. The results show that feral cats are obligatory carnivores, with their daily energy intake from crude protein being 52 %, from crude fat 46 % and from N-free extract only 2 %. Minerals and trace elements are consumed in relatively high concentrations compared with recommended allowances determined using empirical methods. The calculated nutrient profile may be considered the nutrient intake to which the cat's metabolic system has adapted. The present study provides insight into the nutritive, as well as possible non-nutritive aspects of a natural diet of whole prey for cats and provides novel ways to further improve feline diets to increase health and longevity.

During diabetes, structural and functional changes in the alimentary tract are known to take place resulting in an increased absorption of intestinal glucose and alterations in the activities of brush-border disaccharidases. To elucidate the effect of administrating polysaccharide from Gynura divaricata (PGD) on disaccharidase activities, the specific activities of intestinal disaccharidases, namely sucrase, maltase and lactase, were measured in streptozotocin-induced diabetic rats. Normal control and diabetic rats were treated by oral administration with PGD. Specific activities of intestinal disaccharidases were increased significantly during diabetes, and amelioration of the activities of sucrase and maltase during diabetes was clearly visible by the treatment with PGD. However, the increased activity of lactase during diabetes mellitus was remarkably alleviated by the administration of PGD only in the duodenum. Meanwhile, oral sucrose tolerance tests demonstrated that PGD alleviated the hyperglycaemia during diabetes mellitus, resulting from the amelioration in the activities of intestinal disaccharidases. The present investigation suggests that PGD exerted an anti-diabetic effect partly via inhibiting the increased intestinal disaccharidase activities of diabetic rats. This beneficial influence of administration of PGD on intestinal disaccharidases clearly indicates their helpful role in the management of diabetes.

The aim of the present study was to examine the association of pre-pubertal dietary energy density (ED) with both age and body fatness at the start of the pubertal growth spurt (age at take-off, ATO). Analyses included 219 DOrtmund Nutritional and Anthropometric Longitudinally Designed Study participants with sufficient height measurements to estimate ATO who provided 3 d weighed dietary records at baseline, i.e. 2 and 3 years before ATO (mean age 6·9 (sd 1·2) years). Mean energy intakes and amounts of foods/drinks consumed at baseline were derived from the records. ED (kJ/g) was calculated based on (1) all foods and drinks (ED_all), (2) foods and energy-containing drinks (ED_energy), (3) foods and milk as a drink, but no other beverages (ED_milk) and (4) foods only, solid or liquid (ED_food). Using multiple regression analyses, the association between the ED variables and ATO was investigated. Furthermore, Z-scores of BMI and fat mass index (FMI) at ATO were considered as outcomes to reflect body fatness at puberty onset. The results showed that ED at baseline was not associated with ATO, regardless of the ED method used. For example, mean ATO in the lowest v. highest tertile of ED_food was 9·3 (95 % CI 9·0, 9·5) v. 9·4 (95 % CI 9·1, 9·7) years, Ptrend = 0·8 (adjusted for sex, maternal age, birth weight, dietary protein, dietary fibre, baseline BMI Z-score). Similarly, ED was not independently associated with BMI or FMI Z-score at ATO (Ptrend = 0·3–0·9). In conclusion, dietary ED in childhood did not influence timing or body fatness at ATO in this cohort of healthy, free-living children.

The present study examined, using rats as a model, the effects of sex and age of exposure to dietary soya components on serum total and soya-specific antibody content. In Expt 1, Sprague–Dawley rats at 50 d of age were fed diets containing 20 % casein or 20 % alcohol-washed soya protein isolate (SPI) with or without supplemental isoflavones (ISF, 250 mg/kg diet) for 70, 190 or 310 d. The offspring were fed the same diets as their parents. In Expt 2, juvenile Sprague–Dawley rats at 30 d of age were fed diets containing 20 % casein with or without supplemental ISF (50 mg/kg diet) or increasing amounts of alcohol-washed SPI (5, 10 or 20 %) for 90 d. Exposure of rats to dietary SPI before the age of 28 d increased serum total IgA and IgM, and induced the production of SPI-specific IgA, IgG, IgM and IgE antibodies. Feeding of juvenile or adult rats with SPI elevated serum total IgA in females, while the opposite occurred in males, and markedly stimulated the production of SPI-specific IgM in females and IgG in males. Our data suggest that the effects of soya proteins and ISF on the production of serum total and SPI-specific antibodies appear to be sex dependent and also related to the age of exposure to soya in rats. However, the physiological significance of these immune responses remains to be determined.

We have identified the effects of oligonol, a low-molecular polyphenol derived from lychee fruit, on oxidative stress and lipid metabolism in a type 2 diabetic model. Oligonol was orally administered at 10 or 20 mg per kg body weight per d for 8 weeks to db/db mice, and its effects were compared with those of the vehicle in db/db and m/m mice. Serum and hepatic biochemical factors, and protein and mRNA expression related to lipid metabolism were measured. In the oligonol-administered group, there were significant reductions of reactive oxygen species (ROS), lipid peroxidation, and the TAG and total cholesterol concentrations in both the serum and liver. Additionally, oligonol attenuated oxidative stress through the inhibition of advanced glycation endproduct formation and its receptor expression. Furthermore, augmented expressions of NF-κBp65 and inducible NO synthase were down-regulated to the levels of m/m mice in the group treated with oligonol at 20 mg/kg. Regarding lipid metabolism, lower hepatic lipid resulted from the down-regulation of sterol regulatory element-binding protein-1 and its target gene of lipogenic enzymes in the liver of db/db mice. The present results suggest that oligonol has protective effects against ROS-related inflammation and excess lipid deposition in the type 2 diabetic liver.

Short-chain fructo-oligosaccharides (FOS) are known to have beneficial effects on health. However, the effects of FOS on insulin resistance have not been fully clarified. We observed the effects of FOS feeding on insulin sensitivity and adipocytokine release from abdominal adipocytes in weaning rats. Male Sprague–Dawley rats, 3 weeks old, were divided into three groups and fed a sucrose-based American Institute of Nutrition (AIN)-93 growth diet (control), the control diet containing 5 % FOS for 5 weeks (FOS-5wk) or the control diet for 2 weeks followed by the 5 % FOS diet for 3 weeks (FOS-3wk). Tail blood was collected after fasting for 9 h on day 33 of feeding, and glucose and insulin levels were measured. On the last day, rats were anaesthetised and killed after the collection of aortic blood. Small- and large-intestinal mesenteric fat tissues were immediately excised, and the release of adiponectin, leptin and TNF-α was evaluated from the subsequently isolated adipocytes. The weight of the large-intestinal mesenteric fat, fasting blood insulin level and homeostatic model assessment for insulin resistance decreased in a time-dependent manner, and were much lower in the FOS-5wk group than in the control group. These values were correlated with aortic blood leptin levels. The secretion rate of leptin from the isolated mesenteric adipocytes in the small intestine, but not in the large intestine, was lower in the FOS-fed groups than in the control group. In conclusion, FOS feeding improved insulin sensitivity accompanied by the reduction in large-intestinal fat mass and leptin secretion from the mesenteric adipocytes of the small intestine.

The aim of the present study was to examine the effect of a single high-fat meal with different fat quality on circulating inflammatory markers and gene expression in peripheral blood mononuclear cells (PBMC) to elucidate the role of fat quality on postprandial inflammation. A postprandial study with fourteen healthy females consuming three test meals with different fat quality was performed. Test days were separated by 2 weeks. Fasting and postprandial blood samples at 3 and 6 h after intake were analysed. The test meal consisted of three cakes enriched with coconut fat (43 % energy as saturated fat and 1 % energy as α-linolenic acid (ALA)), linseed oil (14 % energy as ALA and 30 % energy as saturated fat) and cod liver oil (5 % energy as EPA and DHA and 5 % energy as ALA in addition to 31 % energy as saturated fat). In addition, ex vivo PBMC experiments were performed in eight healthy subjects investigating the effects of EPA and ALA on release and gene expression of inflammatory markers. The IL-8 mRNA level was significantly increased after intake of the cod liver oil cake at 6 h compared with fasting level, which was significantly different from the effect observed after the intake of linseed cake. In contrast, no effect was seen on circulating level of IL-8. In addition, ALA and EPA were shown to elicit different effects on the release and mRNA expression levels of inflammatory markers in PBMC cultured ex vivo, with EPA having the most prominent pro-inflammatory potential.

Waste from agricultural products represents a disposal liability, which needs to be addressed. Palm oil is the most widely traded edible oil globally, and its production generates 85 million tons of aqueous by-products annually. This aqueous stream is rich in phenolic antioxidants, which were investigated for their composition and potential in vitro biological activity. We have identified three isomers of caffeoylshikimic acid as major components of oil palm phenolics (OPP). The 2,2-diphenyl-1-picrylhydrazyl assay confirmed potent free radical scavenging activity. To test for possible cardioprotective effects of OPP, we carried out in vitro LDL oxidation studies as well as ex vivo aortic ring and mesenteric vascular bed relaxation measurements. We found that OPP inhibited the Cu-mediated oxidation of human LDL. OPP also promoted vascular relaxation in both isolated aortic rings and perfused mesenteric vascular beds pre-contracted with noradrenaline. To rule out developmental toxicity, we performed teratological studies on rats up to the third generation and did not find any congenital anomalies. Thus, these initial studies suggest that OPP is safe and may have a protective role against free radical damage, LDL oxidation and its attendant negative effects, as well as vascular constriction in mitigating atherosclerosis. Oil palm vegetation liquor thus represents a new source of phenolic bioactives.

dl-2-Hydroxy-(4-methylthio)butanoic acid (HMTBA) is a synthetic source of dietary methionine (Met) widely used in poultry nutrition. HMTBA is transported in the intestinal epithelium by the monocarboxylate transporter 1, after which its biological utilisation relies on its conversion to l-Met. This process involves stereospecific HMTBA oxidation to 2-keto-(4-methylthio)butanoic acid (KMB) and transamination to l-Met. In the present study, we examined HMTBA conversion to l-Met, further incorporation into cellular proteins and the regulation of both processes by HMTBA supplementation in differentiated intestinal Caco-2 cells. The results showed d- and l-HMTBA oxidation in the enterocytes, this process being up-regulated by HMTBA. The data also revealed that KMB transamination is not linked to a specific amino group donor. However, the branched-chain amino acid l-leucine is the preferred amino group donor. Furthermore, transamination was not affected by HMTBA availability. The incorporation of radioactivity from HMTBA into cellular proteins was not significantly different from that of l-Met and was not affected by HMTBA supplementation. In conclusion, the results reveal the capacity of Caco-2 cells to convert HMTBA to l-Met and the up-regulation of conversion by nutritional HMTBA supplementation, thus highlighting the contribution of the intestinal epithelium in the utilisation of HMTBA as a dietary source of Met.