In the present study, we investigated nutritional status and health-related factors in a multistage cluster sample of 3119 Thai urban and rural children aged 0·5–12·9 years. In a subsample, blood samples were collected for the measurement of Hb, transferrin receptor, vitamin A and vitamin D concentrations. The prevalence of stunting and underweight was higher in rural children than in urban children, whereas the wasting rate was similar in both rural and urban areas. Among children aged 3·0–5·9 years, the prevalence of overweight was significantly higher in urban areas than in rural areas and so was the obesity rate in children aged 6·0–12·9 years. Protein intakes of all age groups were relatively high in both the areas. Intakes of Ca, Fe, Zn and vitamin C were significantly higher in urban areas than in rural areas. The prevalence of anaemia in rural areas was twice as high as that in urban areas, particularly in infants and young children. However, the prevalence of Fe-deficiency anaemia was similar in both urban and rural areas. While the prevalence of vitamin A deficiency (by serum retinol cut-off < 0·7 μmol/l) seemed to be very low, vitamin A insufficiency (by serum retinol cut-off < 1·05 μmol/l) was more prevalent (29·4–31·7 %) in both the areas. The prevalence of vitamin D insufficiency ranged between 27·7 and 45·6 % among the children. The present study indicates that the double burden of malnutrition is still a major public health problem in Thailand. Further studies need to explore the associated risk factors for these nutrient deficiencies. Effective strategies and actions are needed to tackle the nutritional problems in Thai children.

We have observed a stiffening of the gastric wall in mice following oral administration of viscous methyl cellulose (MC) solution as a vehicle for food chemicals, an effect which has not previously been reported. To further investigate this effect, young male ICR mice (n 48) were divided into four groups (one control and three experimental groups) of twelve mice each. Experimental groups I, II and III were administered 0·2 ml of 0·5 % (w/v) MC viscous solution/d via a stomach tube for 2, 3 and 4 weeks, respectively. Stomachs were collected following 12 h fasting. The weight of the stomach and mucosa of seven mice per group was measured, and the mucosa was used for the measurement of 8-oxo-2′-deoxyguanosine (8-oxodG). Stomach tissue slices from the remaining five mice per group were stained with haematoxylin and eosin to measure mucosal thickness, and were immunostained with an HIK1083 antibody to determine the number of gastric gland mucous cells. The mucosal thickness of the groups administered the MC solution for 3 and 4 weeks, and the size of the HIK1083-immunostained area of the groups administered the MC solution for 2, 3 and 4 weeks were significantly increased (P< 0·01) compared with those of the control group. The amount of 8-oxodG was not significantly affected. These results indicate that oral administration of viscous MC solution leads to the thickening of the gastric mucosa, which may be related to an increase in the number of gland mucous cells.

We previously demonstrated that the chronic consumption of a high-fat diet (HFD) promotes lung and liver metastases of 4T1 mammary carcinoma cells in obesity-resistant BALB/c mice. To examine early transcriptional responses to tumour progression in the liver and lungs of HFD-fed mice, 4-week-old female BALB/c mice were divided into four groups: sham-injected, control diet (CD)-fed; sham-injected, HFD-fed (SH); 4T1 cell-injected, CD-fed (TC); 4T1 cell-injected, HFD-fed (TH). Following 16 weeks of either a CD or HFD, 4T1 cells were injected into the mammary fat pads of mice in the TC and TH groups and all mice were continuously fed identical diets. At 14 d post-injection, RNA was isolated from hepatic and pulmonary tissues for microarray analysis of mRNA expression. Functional annotation and core network analyses were conducted for the TH/SH Unique gene set. Inflammation in hepatic tissues and cell mitosis in pulmonary tissues were the most significant biological functions in the TH/SH Unique gene set. The biological core networks of the hepatic TH/SH Unique gene set were characterised as those genes involved in the activation of acute inflammatory responses (Orm1, Lbp, Hp and Cfb), disordered lipid metabolism and deregulated cell cycle progression. Networks of the pulmonary Unique gene set displayed the deregulation of cell cycle progression (Cdc20, Cdk1 and Bub1b). These HFD-influenced alterations may have led to favourable conditions for the formation of both pro-inflammatory and pro-mitotic microenvironments in the target organs that promote immune cell infiltration and differentiation, as well as the infiltration and proliferation of metastatic tumour cells.

The present randomised parallel study assessed the impact of adding MUFA to a dietary portfolio of cholesterol-lowering foods on the intravascular kinetics of apoAI- and apoB-containing lipoproteins in subjects with dyslipidaemia. A sample of sixteen men and postmenopausal women consumed a run-in stabilisation diet for 4 weeks. Subjects were then randomly assigned to an experimental dietary portfolio either high or low in MUFA for another 4 weeks. MUFA substituted 13·0 % of total energy from carbohydrate (CHO) in the high-MUFA dietary portfolio. Lipoprotein kinetics were assessed after the run-in and portfolio diets using a primed, constant infusion of [2H3]leucine and multicompartmental modelling. The high-MUFA dietary portfolio resulted in higher apoAI pool size (PS) compared with the low-MUFA dietary portfolio (15·9 % between-diet difference, P= 0·03). This difference appeared to be mainly attributable to a reduction in apoAI fractional catabolic rate (FCR) after the high-MUFA diet ( − 5·6 %, P= 0·02 v. pre-diet values), with no significant change in production rate. The high-MUFA dietary portfolio tended to reduce LDL apoB100 PS compared with the low-MUFA dietary portfolio ( − 28·5 % between-diet difference, P= 0·09), predominantly through an increase in LDL apoB100 FCR (23·2 % between-diet difference, P= 0·04). These data suggest that adding MUFA to a dietary portfolio of cholesterol-lowering foods provides the added advantage of raising HDL primarily through a reduction in HDL clearance rate. Replacing CHO with MUFA in a dietary portfolio may also lead to reductions in LDL apoB100 concentrations primarily by increasing LDL clearance rate, thus potentiating further the well-known cholesterol-lowering effect of this diet.

Intestinal amino acid (AA) transport is critical for the supply of AA to other tissues. Few studies regarding AA intestinal transport systems during the period from postnatal intense development of piglets until weaning are available. In the present study, we measured the intestinal expression of b0,+AT according to developmental stage using the suckling Huanjiang piglet model, and documented the effect of intra-uterine growth restriction (IUGR) on such expression using real-time PCR and Western blot analysis. Suckling piglets that recovered after IUGR and those with normal body weights (NBW) were used after birth or at 7, 14 and 21 d of age. Blood samples were used for the measurement of plasma AA concentrations, and the jejunum was collected for the measurement of b0,+AT expression. In NBW piglets, b0,+AT expression was markedly decreased from days 0 to 21 (P< 0·01) and remained at a low level during all the suckling periods. In IUGR piglets, there was a marked decrease in b0,+AT expression at birth, which remained lower, when compared with NBW piglets, during the suckling period. These results coincided with decreased plasma arginine concentration at birth and decreased lysine concentration in 21-d-old piglets (P< 0·05). It is concluded that the high expression of b0,+AT at birth decreases during the suckling period, and that IUGR is associated with decreased expression of this apical AA transporter. The possible causal relationship between decreased b0,+AT expression and lower body weight of IUGR piglets in the suckling period is discussed.

Cognitive dysfunction syndrome is a major disease affecting old cats and is the consequence of severe and irreversible loss of brain cells and brain atrophy. The present study focused on the hypothesis that the optimal strategy for promoting successful brain ageing is to target risk factors associated with brain ageing and dementia. We used a nutritional strategy involving supplementation with a blend of nutrients (antioxidants, arginine, B vitamins and fish oil) to test this hypothesis. Middle-aged and old cats between 5·5 and 8·7 years of age were assigned to cognitively equivalent control or treatment groups based on prior cognitive experience and performance on baseline cognitive tests. The cats in the treatment group were maintained on a diet supplemented with the nutrient blend and the cats in the control group were maintained on the identical base diet without the additional supplementation. After an initial wash-in period, all cats were tested on a battery of cognitive test protocols. The cats fed the test diet showed significantly better performance on three of four test protocols: a protocol assessing egocentric learning, a protocol assessing discrimination and reversal learning and a protocol focused on acquisition of a spatial memory task. The results support the hypothesis that brain function of middle-aged and old cats can be improved by the nutrient blend that was selected to minimise or eliminate the risk factors associated with brain ageing and dementia.

Lactose malabsorption is associated with rapid production of high levels of osmotic compounds, such as organic acids and SCFA in the colon, suspected to contribute to the onset of lactose intolerance. Adult rats are lactase deficient and the present study was conducted to evaluate in vivo the metabolic consequences of acute lactose ingestion, including host–microbiota interactions. Rats received diets of 25 % sucrose (S25 control group) or 25 % lactose (L25 experimental group). SCFA and lactic acid were quantified in intestinal contents and portal blood. Expression of SCFA transporter genes was quantified in the colonic mucosa. Carbohydrate oxidation (Cox) and lipid oxidation (Lox) were computed by indirect calorimetry. Measurements were performed over a maximum of 13 h. Time, diet and time × diet variables had significant effects on SCFA concentration in the caecum (P< 0·001, P= 0·004 and P= 0·007, respectively) and the portal blood (P< 0·001, P= 0·04 and P< 0·001, respectively). Concomitantly, expression of sodium monocarboxylate significantly increased in the colonic mucosa of the L25 group (P= 0·003 at t= 6 h and P< 0·05 at t= 8 h). During 5 h after the meal, the L25 group's changes in metabolic parameters (Cox, Lox) were significantly lower than those of the S25 group (P= 0·02). However, after 5 h, L25 Cox became greater than S25 (P= 0·004). Thus, enhanced production and absorption of SCFA support the metabolic changes observed in calorimetry. These results underline the consequences of acute lactose malabsorption and measured compensations occurring in the host's metabolism, presumably through the microbiota fermentations and microbiota–host interactions.

In the present study, we hypothesised whether in vitro digestion of salmon oil would release different amounts of PUFA depending on the origin of the lipolytic enzymes used. For this purpose, in vitro digestion of salmon oil (SO) was performed using human duodenal juice (HDJ) or a commercial enzyme preparation consisting of porcine pancreatin and bile (PB). The lipolytic effect was determined by measuring the release of fatty acids (FA) using solid-phase extraction and GC–flame ionisation detection, withdrawing samples every 20 min during digestion. The amount of FA released indicated that a plateau was reached after 80 min with approximately similar amounts of FA detected using both HDJ and PB (379 (sd 18) and 352 (sd 23) mg/g SO, respectively). However, the release of 18 : 2, EPA (20 : 5) and DHA (22 : 6) was significantly different during in vitro digestion. At 80 min, HDJ and PB released 43 and 33 % of 18 : 2, 14 and 9 % of EPA and 11 and 9 % of DHA, respectively. Both enzyme preparations released approximately the same amounts of the other FA analysed. The effect of the addition of bile salts (BS) was significantly different in the two enzyme systems, where porcine pancreatin highly responded to the increase in BS concentration, in contrast to HDJ.

Glutamate is linked to the glycolytic process, particularly when co-ingested with carbohydrate, but its effects on glucose metabolism are poorly characterised. The present study aimed to (1) specifically examine the effects of carbohydrate administration on circulating glutamate concentrations and (2) investigate the effect of increased glutamate availability, independent of carbohydrate ingestion, on glucose metabolism. A total of nine participants underwent four trials: (1) glutamate supplement+carbohydrate drink (GLU+CHO); (2) glutamate supplement+placebo drink (GLU); (3) placebo supplement+carbohydrate drink (CHO); (4) placebo supplement+placebo drink (CON). Following a fasting blood sample, participants ingested monosodium l-glutamate (MSG; 150 mg/kg body weight) or placebo capsules at each trial followed by a 75 g carbohydrate or a non-energy placebo drink 30 min later. Blood samples were taken at 0, 10, 20, 30, 40, 50, 60, 75, 90, 105 and 120 min. Plasma glutamate concentrations were significantly elevated relative to baseline during the GLU (approximately 10-fold) and GLU+CHO trials (approximately 6-fold). The glucose response to a carbohydrate load was blunted when glutamate was increased in the circulation (peak serum glucose: 5·50 (se 0·54) mmol/l during the GLU+CHO trial v. 7·69 (se 0·53) mmol/l during the CHO trial, P< 0·05). On average, c-peptide results revealed that insulin secretion did not differ between the GLU+CHO and CHO trials; however, four participants demonstrated increased insulin secretion during the GLU+CHO trial and five participants demonstrated decreased insulin secretion under the same conditions. In conclusion, when administration is staggered, MSG and carbohydrate supplementation can be used to manipulate plasma glutamate; however, future studies should control for this dichotomous insulin response.

The exact mechanisms of the relationship between obesity and cardiovascular events are not yet fully understood; however, oxidative stress may be involved. Thus, the aim of the present study was to evaluate the effects of resveratrol and fish oil on catecholamine-induced mortality in obese rats. To begin with, rats were divided into five groups: (1) lean, (2) obese, (3) obese supplemented with resveratrol, (4) obese supplemented with fish oil and (5) obese supplemented with resveratrol and fish oil (n 18 rats per group), for 2 months. After supplementation, the groups were subdivided as with (n 10) and without (n 8) cardiovascular catecholaminergic stress after isoproterenol (60 mg/kg) injection. At 24 h later, the survival rate was analysed. The obese group showed lower survival rates (10 %) when compared with the lean group (70 %). On the other hand, resveratrol (50 %) and fish oil (40 %) increased the survival rate of obese rats (χ2 test, P= 0·019). Biochemical analyses of the myocardium and aorta revealed that obese rats had higher levels of superoxide and oxidative damage to lipids and protein. This was associated with reduced superoxide dismutase and glutathione peroxidase activity in both the myocardium and aorta. The supplementation increased antioxidant enzyme activities and reduced oxidative damage. We also evaluated the nuclear factor-erythroid 2 p45-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 antioxidant pathway. Nrf2 protein levels that were reduced in obese rats were increased by the antioxidant treatment. Taken together, these results showed that resveratrol and fish oil reduce catecholamine-induced mortality in obese rats, partly through the reduction of oxidative stress.

In the present study, quadruplicate groups of juvenile Atlantic salmon (Salmo salar) were fed plant protein-based diets with increasing arginine inclusions (range 28·8–37·4 g/kg DM) to investigate whether arginine supplementation affects growth and lipid accumulation through an elevated polyamine turnover. Dietary lysine was held at a constant concentration, just below the requirement. All other amino acids were balanced and equal in the diets. Arginine supplementation increased protein and fat accretion, without affecting the hepatosomatic or visceralsomatic indices. Dietary arginine correlated with putrescine in the liver (R 0·78, P= 0·01) and with ornithine in the muscle, liver and plasma (P= 0·0002, 0·003 and 0·0002, respectively). The mRNA of ornithine decarboxylase, the enzyme producing putrescine, was up-regulated in the white adipose tissue of fish fed the high-arginine inclusion compared with those fed the low-arginine diet. Concomitantly, spermidine/spermine-(N1)-acetyltransferase, the rate-limiting enzyme for polyamine turnover that consumes acetyl-CoA, showed an increased activity in the liver of fish fed the arginine-supplemented diets. In addition, lower acetyl-CoA concentrations were observed in the liver of fish fed the high-arginine diet, while ATP, which is used in the process of synthesising spermidine and spermine, did not show a similar trend. Gene expression of the rate-limiting enzyme for β-oxidation of long-chain fatty acids, carnitine palmitoyl transferase-1, was up-regulated in the liver of fish fed the high-arginine diet. Taken together, the data support that increased dietary arginine activates polyamine turnover and β-oxidation in the liver of juvenile Atlantic salmon and may act to improve the metabolic status of the fish.

Barley β-glucan (BG) has been shown to reduce glycaemic response (GR) in some studies. It is hypothesised that this reduction may be a function of its physical properties that delay gastric emptying (GE). The effect of these changes in GR and GE on diet-induced thermogenesis (DIT) is not known. The aim of the present study was to assess the effect of BG of different molecular weights and purities on GR, GE and DIT in healthy subjects. This was a randomised, single-blind, repeated-measures design where fifteen healthy subjects were tested on three occasions following an overnight fast. Following the baseline measurements, the volunteers were fed a soup containing high-molecular-weight BG (HBG), a soup containing low-molecular-weight BG (LBG) or a control soup with no BG (CHO). Following the consumption of the breakfast, GR was measured using finger-prick blood samples, GE was determined using the 13C-octanoic acid breath test and DIT was measured using indirect calorimetry. There was a difference in GR AUC between the soups after 60 min but not after 120 min. The CHO and LBG meals had a greater GR than the HBG meal. There were differences in all GE time points, with the HBG meal having the slowest GE time. There was a correlation between the GR and the initial GE times. There were differences in total DIT between the three test meals with the HBG meal having the lowest DIT. The present study indicates that HBG has the ability to delay GE due to increased viscosity, resulting in a decreased GR and DIT.

A total of sixteen lambs were divided into two groups and fed two different diets. Of these, eight lambs were fed a control diet (C) and eight lambs were fed the C diet supplemented with quebracho tannins (C+T). The objective of the present study was to assess whether dietary quebracho tannins can improve the antioxidant capacity of lamb liver and plasma and if such improvement is due to a direct transfer of phenolic compounds or their metabolites, to the animal tissues. Feed, liver and plasma samples were purified by solid-phase extraction (SPE) and analysed by liquid chromatography–MS for phenolic compounds. Profisitinidin compounds were identified in the C+T diet. However, no phenolic compounds were found in lamb tissues. The liver and the plasma from lambs fed the C+T diet displayed a greater antioxidant capacity than tissues from lambs fed the C diet, but only when samples were not purified with SPE. Profisetinidin tannins from quebracho seem not to be degraded or absorbed in the gastrointestinal tract. However, they induced antioxidant effects in animal tissues.

The present study evaluated the antihypertrophic potential of the ethanolic extract of Boerhaavia diffusa (BDE), a well-known edible cardiotonic plant reported in Ayurveda against angiotensin II-induced hypertrophy in H9c2 cardiac myoblast cells. Markers of hypertrophy such as cell size, protein content and the concentrations of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) were analysed for the confirmation of hypertrophy induction. Angiotensin II (100 nm) caused an increase in cell volume (69·26 (sd 1·21) %), protein content (48·48 (sd 1·64) %), ANP (81·90 (sd 1·22) %) and BNP (108·57 (sd 1·47) %). BDE treatment significantly reduced cell volume, protein content and the concentrations of ANP and BNP (P≤ 0·05) in H9c2 cells. The activity of various antioxidant enzymes and the concentration of reduced glutathione, which was lowered due to hypertrophy, were increased in BDE-treated cells. The BDE treatment also reduced intracellular reactive oxygen species generation, lipid peroxidation and protein carbonyls in cells. In addition, the expression patterns of NF-κβ and transforming growth factor β1 were found to be increased during hypertrophy, and their expressions were reduced on BDE treatment. In vitro chemical assays showed that BDE inhibits angiotensin-converting enzyme and xanthine oxidase in a dose-dependent manner with an estimated 50 % effective concentration (EC50) value of 166·12 (sd 2·42) and 60·05 (sd 1·54) μg/ml, respectively. The overall results clearly indicate the therapeutic potential of B. diffusa against cardiac hypertrophy, in addition to its nutritional qualities.

Essential oil components from turmeric (Curcuma longa L.) are documented for neuroprotective, anti-cancer, anti-thrombotic and antioxidant effects. The present study aimed to investigate the disease-modifying potential of curcuma oil (C. oil), a lipophilic component from C. longa L., in hyperlipidaemic hamsters. Male golden Syrian hamsters were fed a chow or high-cholesterol (HC) and fat-rich diet with or without C. oil (30, 100 and 300 mg/kg) for 28 d. In HC diet-fed hamsters, C. oil significantly reduced plasma total cholesterol, LDL-cholesterol and TAG, and increased HDL-cholesterol when compared with the HC group. Similar group comparisons showed that C. oil treatment reduced hepatic cholesterol and oxidative stress, and improved liver function. Hyperlipidaemia-induced platelet activation, vascular dysfunction and repressed eNOS mRNA expression were restored by the C. oil treatment. Furthermore, aortic cholesterol accumulation and CD68 expression were also reduced in the C. oil-treated group. The effect of C. oil at 300 mg/kg was comparable with the standard drug ezetimibe. Delving into the probable anti-hyperlipidaemic mechanism at the transcript level, the C. oil-treated groups fed the chow and HC diets were compared with the chow diet-fed group. The C. oil treatment significantly increased the hepatic expression of PPARα, LXRα, CYP7A1, ABCA1, ABCG5, ABCG8 and LPL accompanied by reduced SREBP-2 and HMGCR expression. C. oil also enhanced ABCA1, ABCG5 and ABCG8 expression and suppressed NPC1L1 expression in the jejunum. In the present study, C. oil demonstrated an anti-hyperlipidaemic effect and reduced lipid-induced oxidative stress, platelet activation and vascular dysfunction. The anti-hyperlipidaemic effect exhibited by C. oil seems to be mediated by the modulation of PPARα, LXRα and associated genes involved in lipid metabolism and transport.

Host factors influencing the absorption and excretion of Si are poorly understood, although previous murine and human studies have suggested that age, sex and oestrogen status may affect Si metabolism and thus function. Here, serum and urine samples were collected from twenty-six healthy adults at baseline and over a 6 h period following ingestion of 17·4 mg Si (orthosilicic acid) and analysed by inductively coupled plasma optical emission spectrometry. Fasting baseline serum and urinary Si concentrations were marginally higher in older adults (51–66 years old) compared with young adults (20–47 years old); however, there was no difference in the absorption of Si into serum (overall profile, rate of Si appearance, peak concentration and time to peak) between the different adult groups. The rate of elimination of Si from serum did not significantly differ with age or sex, although serum concentration at 6 h was higher in older adults and significantly correlated with age (r 0·5; P= 0·01). There were, however, no significant differences in the excretion of Si into urine (a proxy for overall uptake) between the groups, averaging approximately 45 %. Oestradiol levels did not correlate with any of the above measures of Si. Thus, overall, host age and sex did not appear to markedly influence Si absorption or excretion in human adults and no correlations were found with serum oestradiol status. The marginally higher baseline and 6 h post-dose Si levels in older adults may reflect modestly impaired renal function and/or the loss of Si from connective tissues with ageing.

A considerable number of epidemiological investigations and intervention studies have supported an association between the intake of flavanol- and proanthocyanidin-containing foods and a decreased risk of metabolic diseases. Nonetheless, less is know about the capacity of tissues to accumulate flavanols and/or their metabolites. The main objective of the present study was to determine (n 20) plasma bioavailability and disposition in the liver, muscle, brown adipose tissue (BAT) and white adipose tissues (mesenteric and perirenal) in rats after a long-term consumption of three doses of grape seed phenolic extract (5, 25 and 50 mg/kg body weight) for 21 d in order to determine whether there is a dose–response relationship. Glucuronidated conjugates (total glucuronidated conjugates: C5mg/kg 1·9; C25mg/kg 6·4; C50mg/kg 27·7 μmol/l plasma) followed by methyl glucuronidated conjugates (total methyl glucuronidated conjugates: C5mg/kg 1·98; C25mg/kg 4·48; C50mg/kg 12·5 μmol/l plasma) were the main flavanol metabolites quantified in plasma, also detecting a dimer in its free form (C25mg/kg 0·74; C50mg/kg 0·79 μmol/l plasma). Each of the studied organs has a particular behaviour of accumulation and response to the assayed grape seed extract doses, with an exponential bioavailability–dose relationship in BAT, in which flavanols could play an important role in the reduction or prevention of obesity, modulating the functionality of that tissue.

The benefits of iodine supplements during pregnancy remain controversial in areas with a mild-to-moderate iodine deficiency. The aim of the present study was to determine the effect of improving iodine intakes, with iodised salt (IS) or iodine supplements, in pregnant Spanish women. A total of 131 pregnant women in their first trimester were randomly assigned to three groups: (1) IS in cooking and at the table, (2) 200 μg potassium iodide (KI)/d or (3) 300 μg KI/d. No differences were found in thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3) or thyroid volume (TV) between the three groups. Regardless of the group in which women were included, those who had been taking IS for at least 1 year before becoming pregnant had a significantly lower TV in the third trimester (P= 0·01) and a significantly higher urinary iodine in the first (173·7 (sd 81·8) v. 113·8 (sd 79·6) μg/l, P= 0·001) and third trimesters (206·3 (sd 91·2) v. 160·4 (sd 87·7) μg/l, P= 0·03). Also, no differences were seen in TSH, FT4 or FT3. Children's neurological development was not significantly associated with the consumption of IS for at least 1 year before becoming pregnant and no differences were found according to the treatment group. In conclusion, in pregnant women with insufficient iodine intake, the intake of IS before becoming pregnant was associated with a better maternal thyroid function. The form of iodide intake was not associated with maternal thyroid function or children's neurological development.

The incidence of metabolic syndrome components including obesity, lipid deregulation, insulin resistance (IR) and non-alcoholic fatty liver disease is increasing rapidly in wealthy societies. The present study was designed to determine the effect of different nutritional lipid patterns (quantity and quality) on lipid utilisation and oxidative stress in the liver and muscle of rats in an integrated fashion. A total of forty-eight Wistar male rats were fed for 12 weeks with a mixed, lard or fish-oil diet, containing either 50 or 300 g lipid/kg. Rats developed liver steatosis associated with moderate liver injury when fed the 30 % lipid diets, in spite of the absence of overt obesity or IR, except when fed the lard 30 % lipid diet. The intake of the 30 % lipid diets decreased hepatic lipogenesis and mitochondriogenesis and increased lipid peroxidation and protein oxidation. Surprisingly, muscle lipid content was not modified whatever the administered diet. The intake of the 30 % lipid diets increased the muscle protein expression of fatty acid (FA) translocase/cluster of differentiation 36 (FAT/CD36), PPARγ co-activator 1α (PGC-1α) and muscle carnitine palmitoyltransferase 1 (m-CPT1), reflecting increased FA transport in the muscle associated with increased oxidative metabolism. The lard 30 % lipid diet led to IR without modifying the muscle lipid content. The fish-oil 30 % lipid diet failed to prevent the development of hepatic steatosis and made the tissues more prone to oxidation. Overall, the present study suggests that the FA composition of muscle is more important than lipid accumulation itself in the modulation of insulin sensitivity, and indicates that precaution should be taken when advising an unphysiologically high (pharmacological) supplementation with long-chain n-3 PUFA.

Leucine and leptin play important roles in regulating protein synthesis and degradation in skeletal muscles in vitro and in vivo. However, the objective of the present study was to determine whether leptin and leucine function synergistically in regulating protein metabolism of skeletal muscles. In the in vitro experiment, C2C12 myotubes were cultured for 2 h in the presence of 5 mm-leucine and/or 50 ng/ml of leptin. In the in vivo experiment, C57BL/6 and ob/ob mice were randomly assigned to be fed a non-purified diet supplemented with 3 % l-leucine or 2·04 % l-alanine (isonitrogenous control) for 14 d. Ob/ob mice were injected intraperitoneally with sterile PBS or recombinant mouse leptin (0·1 μg/g body weight) for 14 d. In C57BL/6 mice, dietary leucine supplementation increased (P< 0·05) plasma leptin, leptin receptor expression and protein synthesis in skeletal muscles, but reduced (P< 0·05) plasma urea and protein degradation in skeletal muscles. Dietary leucine supplementation and leptin injection increased the relative weight of the gastrocnemius and soleus muscles in ob/ob mice. Moreover, leucine and leptin treatments stimulated (P< 0·05) protein synthesis and inhibited (P< 0·05) protein degradation in C2C12 myotubes and skeletal muscles of ob/ob mice. There were interactions (P< 0·05) between the leucine and leptin treatments with regard to protein metabolism in C2C12 myotubes and soleus muscles of ob/ob mice but not in the gastrocnemius muscles of ob/ob mice. Collectively, these results suggest that leptin and leucine synergistically regulate protein metabolism in skeletal muscles both in vitro and in vivo.