In areas where iodized salt is not available, oral iodized oil is often used to correct I deficiency despite a lack of consensus on the optimal dose or duration of effect, particularly in children, a main target group. Annual doses ranging from 400 to 1000 mg have been advocated for school-age children. Because lower doses of iodized oil have been shown to be effective in treating I deficiency in adults, the aim of this study was to evaluate the efficacy and safety of a low dose of oral iodized oil in goitrous I-deficient children. Goitrous children (n 104, mean age 8·4 years, range 6–12 years, 47 % female) received 0·4 ml oral iodized poppyseed-oil containing 200 mg I. Baseline measurements included I in spot urines (UI), serum thyroxine (T4), whole blood thyroid-stimulating hormone (TSH), and thyroid-gland volume using ultrasound. At 1, 5, 10, 15, 30 and 50 weeks post-intervention, UI, TSH and T4 were measured. At 10, 15, 30 and 50 weeks, thyroid-gland volume was remeasured. At 30 and 50 weeks the mean percentage change in thyroid volume from baseline was -35 % and -41 % respectively. The goitre rate fell to 38 % at 30 weeks and 17 % at 50 weeks. No child showed signs of I-induced hypo- or hyperthyroidism. UI remained significantly increased above baseline for the entire year (P < 0·001); the median UI at 50 weeks was 97 μg/l, at the World Health Organization cut-off value (100 μg/l) for I-deficiency disorders risk. In this group of goitrous children, an oral dose of 200 mg I as Lipiodol (Guerbert, Roissy CdG Cedex, France) was safe and effective for treating goitre and maintaining normal I status for at least 1 year.

The possibility of achieving blood-lipid-lowering characteristics of pig fat by increasing the content of unsaturated fat in pig feed was evaluated. Three pig feeding regimens were applied: basal feed (no added fat or vitamin E), basal feed + rapeseed oil (60 g/kg feed), and basal feed + rapeseed oil (60 g/kg) + vitamin E (200 mg/kg). Meat and meat products from the three pig groups were incorporated into diets providing 86 g pig fat/10 MJ. The diets were served to twelve healthy human male subjects for 3 weeks each in a randomised crossover design. The diets prepared from pigs fed rapeseed oil had a lower content of saturated fatty acids (approximately 9 v. 11 % of energy) and a higher content of polyunsaturated fatty acids (approximately 6 v. 4 % of energy) than the diet prepared from pigs fed the basal feed. Diets based on fat from pigs fed the rapeseed oil resulted in significantly lower (approximately 4 %, P = 0·019) total serum cholesterol concentration compared with the diet from pigs fed the basal feed. No differences were observed in LDL-, HDL- or VLDL-cholesterol, or in triacylglycerol or VLDL-triacylglycerol concentrations. Addition of vitamin E to the pig feed resulted in only a minor increase in vitamin E content in the human subjects' diet and the vitamin E content was low in all three pig diets. Plasma vitamin E concentration in the human subjects at the end of the period with diets from pigs fed rapeseed oil without vitamin E was significantly lower (P = 0·04) than in the other two diet periods. In conclusion, an increased content of rapeseed oil in pig feed changes the fatty acid composition of the pig fat in a way that has a potential to reduce blood cholesterol concentrations in human subjects. However, intake of pig fat with a higher content of unsaturated fatty acids needs to be matched by a higher dietary intake of vitamin E.

No sensitive functional index is currently available to assess Cu status in healthy human populations. This study evaluated the effect of Cu supplementation on putative indices of Cu status in twelve women and twelve men, aged between 22 and 45 years, who participated in a double-blind placebo controlled crossover study. The study consisted of three 6-week supplementation regimens of 3 mg CuSO4, 3 mg Cu-glycine chelate and 6 mg Cu-glycine chelate, each separated by placebo periods of equal length. Women had significantly higher caeruloplasmin oxidase activity (P < 0·001), caeruloplasmin protein concentration (P < 0·05), and serum diamine oxidase activity (P < 0·01) at baseline than men. Erythrocyte and leucocyte superoxide dismutase activity, leucocyte cytochrome c oxidase activity, and erythrocyte glutathione peroxidase activity did not respond to Cu supplementation. Platelet cytochrome c oxidase activity was significantly higher (P < 0·01), after supplementation with 6 mg Cu-glycine chelate in the total group and in women but did not change in men. Caeruloplasmin oxidase activity was significantly higher (P < 0·05), in men after supplementation with 3 mg Cu-glycine chelate, while caeruloplasmin protein concentration was significantly lower in men after supplementation with 6 mg Cu-glycine chelate (P < 0·05). Serum diamine oxidase activity was significantly higher after all supplementation regimens in the total group and in both men and women (P < 0·01). These results indicate that serum diamine oxidase activity is sensitive to changes in dietary Cu intakes and may also have the potential to evaluate changes in Cu status in healthy adult human subjects.

The effect of abomasal infusion of glucose (120 kJ/d per kg body weight (BW)0·75, 758 mmol/d) on urea production, plasma alanine-N flux rate and the conversion of alanine-N to urea was studied in sheep offered a low-N diet at limited energy intake (500 kJ/d per kg BW0·75), based on hay and grass pellets. Glucose provision reduced urinary N (P = 0·040) and urea (P = 0·009) elimination but this was offset by poorer N digestibility. Urea-N production was significantly reduced (822 v. 619 mmol/d, P = 0·024) by glucose while plasma alanine-N flux rate was elevated (295 v. 342 mmol/d, P = 0·011). The quantity of urea-N derived from alanine tended to be decreased by glucose (127 v. 95 mmol/d) but the fraction of urea production from alanine was unaltered (15 %). Plasma urea and alanine concentrations (plus those of the branched chain amino acids) decreased in response to exogenous glucose, an effect probably related to enhanced anabolic usage of amino acids and lowered urea production.

Recently we have shown the susceptibility of Fe-deficient rat intestine to oxidative damage during Fe repletion. The role of dietary antioxidants like ascorbic acid, α-tocopherol and a combination of both in counteracting the oxidative stress was tested in this study. Five groups of thirteen weanling WKY female rats were fed with an Fe-deficient diet for a period of 5 weeks. Another set of thirteen rats received an Fe-sufficient diet and served as the control group (Con). Oral administration of either vehicle (D), 8 mg Fe alone (D+) or in the presence of 24 mg ascorbic acid (D+ + C), 40 mg α-tocopherol (D+ + E) or a combination of both (D+ + C + E) per d for 15 d was carried out in Fe-depleted rats. The impact of this treatment protocol on Fe status, oxidative stress and antioxidant status at the site of Fe absorption was assessed. It was observed that though the indicators of Fe status were normalised on Fe supplementation, the oxidative stress as reflected by the levels of both thiobarbituric-acid reactive substances (TBARS) and protein carbonyls were significantly greater in D+ and D+ + C compared to D+ + E, D+ + C + E and Con groups. The mucosal cell DNA damage was seen in D+, D+ + C and D+ + E groups on electrophoresis. Functional integrity as assessed by the activities of alkaline phosphatase and lys-ala-dipeptidyl aminopeptidase were normalized in all the groups treated with the antioxidant(s). There were significant positive alterations in some of the endogenous antiperoxidative systems and in serum caeruloplasmin activity in D+ + E and D+ + C + E groups. Paradoxically, serum ascorbate levels were significantly lower in D+ + C than in D+ + E and D+ + C + E groups. This could be due to the protection offered by α-tocopherol in the presence of Fe. It is concluded that supplementation of α-tocopherol alone or in combination with ascorbic acid protects the gastrointestinal tract of Fe-deficient rats against Fe-mediated oxidative damage during Fe repletion. However, ascorbic acid alone does not protect the gastrointestinal tract against Fe-induced oxidative stress.

We examined the effect of dietary fats rich in n-3 polyunsaturated fatty acids (PUFA) on mRNA levels in white and brown adipose tissues in rats. Four groups of rats were fed on a low-fat diet (20 g safflower oil/kg) or a high-fat diet (200 g/kg) containing safflower oil, which is rich in n-6 PUFA (linoleic acid), or perilla (α-linolenic acid) or fish oil (eicosapentaenoic and docosahexaenoic acids), both of which are rich in n-3 PUFA, for 21 d. Energy intake was higher in rats fed on a high-safflower-oil diet than in those fed on low-fat or high-fish-oil diet, but no other significant differences were detected among the groups. Perirenal white adipose tissue weight was higher and epididymal white adipose tissue weight tended to be higher in rats fed on a high-safflower-oil diet than in those fed on a low-fat diet. However, high-fat diets rich in n-3 PUFA, compared to a low-fat diet, did not increase the white adipose tissue mass. High-fat diets relative to a low-fat diet increased brown adipose tissue uncoupling protein 1 mRNA level. The increases were greater with fats rich in n-3 PUFA than with n-6 PUFA. A high-safflower-oil diet, compared to a low-fat diet, doubled the leptin mRNA level in white adipose tissue. However, high-fat diets rich in n-3 PUFA failed to increase it. Compared to a low-fat diet, high-fat diets down-regulated the glucose transporter 4 mRNA level in white adipose tissue. However, the decreases were attenuated with high-fat diets rich in n-3 PUFA. It is suggested that the alterations in gene expression in adipose tissue contribute to the physiological activities of n-3 PUFA in preventing body fat accumulation and in regulating glucose metabolism in rats.

Development of muscle is critically dependent on several hormones which in turn are regulated by nutritional status. We therefore determined the impact of mild postnatal undernutrition on key markers of myofibre function: type I slow myosin heavy chain (MyHC) isoform, myosin ATPase, succinate dehydrogenase and α-glycerophosphate dehydrogenase. In situ hybridization, immunocytochemistry and enzyme histochemistry were used to assess functionally distinct muscles from 6-week-old pigs which had been fed an optimal (6 % (60 g food/kg body weight per d)) or low (2 % (20 g food/kg per d)) intake for 3 weeks, and kept at 26°C. Nutritional status had striking muscle-specific influences on contractile and metabolic properties of myofibres, and especially on myosin isoform expression. A low food intake upregulated slow MyHC mRNA and protein levels in rhomboideus by 53 % (P < 0·01) and 18 % (P < 0·05) respectively; effects in longissimus dorsi, soleus and diaphragm were not significant. The oxidative capacity of all muscles increased on the low intake, albeit to varying extents: longissimus dorsi (55 %), rhomboideus (30 %), soleus (21 %), diaphragm (7 %). Proportions of slow oxidative fibres increased at the expense of fast glycolytic fibres. These novel findings suggest a critical role for postnatal nutrition in regulating myosin gene expression and muscle phenotype. They have important implications for optimal development of human infants: on a low intake, energetic efficiency will increase and the integrated response to many metabolic and growth hormones will alter, since both are dependent on myofibre type. Mechanisms underlying these changes probably involve complex interactions between hormones acting as nutritional signals and differential effects on their cell membrane receptors or nuclear receptors.

There is a wealth of epidemiological information on antioxidants and their possible prevention of disease progression but very little of the research on antioxidants has involved intervention studies. In this study, the potential protective effect of vitamin C or E supplementation in vivo against endogenous and H2O2-induced DNA damage levels in lymphocytes was assessed. The supplementation involved fourteen healthy male and female non-smokers mean age 25·53 (SD 1·82) years, who were asked to supplement an otherwise unchanged diet with 1000 mg vitamin C daily for 42 d or 800 mg vitamin E daily for 42 d. DNA damage in H2O2-treated peripheral blood lymphocytes (PBL) and untreated PBL before and after supplementation, and during a 6-week washout period was assessed using an ELISA. At each sampling time-point, the red cell concentrate activities of superoxide dismutase, catalase and glutathione peroxidase were also determined. Supplementation with vitamin C or vitamin E decreased significantly H2O2-induced DNA damage in PBL, but had no effect on endogenous levels of DNA damage. The activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were suppressed during the supplementation period. These supplementation regimens may be used to limit the possible adverse effects of reactive oxygen species (including those produced during the course of an immune response) on lymphocytes in vivo, and so help to maintain their functional capacity.

A large number of studies in recent years have investigated the effects of hyperlipidaemias and diabetes on cholesteryl ester transfer protein (CETP) on neutral lipid transfer activity and plasma lipids. There has been an ongoing debate as to whether CETP is pro- or anti-atherogenic as it provides a mechanism for the transfer of cholesterol from the cardioprotective HDL subfraction to the potentially atherogenic LDL subfraction. This study was designed to investigate whether there was significant variability of CETP mass and activity in a large normolipidaemic population and whether there is an association between CETP and plasma lipoprotein composition. The presence of a known polymorphism of CETP gene (Taq 1B) was investigated to see if there was any association between this polymorphism and CETP mass and activity, and plasma lipids. There was significant (P < 0·0001) increase in CETP mass and activity in plasma postprandially at 6 h. Using multiple stepwise regression analysis there was significant association with fasting CETP mass and activity (β = 0·055; P = 0·002) and triacylglycerol-rich lipoprotein (β = 0·013; P = 0·005) and postprandial CETP mass (β = 0·254; P = 0·007). Repeated-measures analysis showed a strong association between the absence of Taq 1B polymorphism and low CETP mass and elevated HDL- and HDL2-cholesterol and HDL-phospholipid concentrations than did those who were homozygous or heterozygous for the presence of the restriction site.

Effects of dietary protein and S-containing amino acids on oxidative damage were investigated in rat liver. After feeding rats for 3 weeks from weaning, lower GSH levels and higher metallothionein (MT) levels were found in the liver of rats fed on a 10 % soyabean-protein-isolate (SPI)-based diet than those fed on a 10 % casein-based diet. After injection of N-nitrosodimethylamine (NDMA) at 20 mg/kg body weight, increases in lipid peroxide, determined as thiobarbituric-acid reactive substances (TBARS), and γ-glutamyltransferase (GGT) activity in the liver were observed in the 10 % SPI diet group. By supplementing the 10 % SPI diet with 0·3 % cystine or methionine, GSH levels were increased, while MT levels were decreased, and elevation in TBARS levels after NDMA injection was diminished. On the other hand, increase in GGT activity could be prevented only by methionine supplement. On a 20 % SPI or casein diet, TBARS concentration and GGT activity were not altered after NDMA injection with concomitant increase in GSH levels and decrease in MT levels. These results indicate that sufficient amounts of methionine and cystine in a diet are important to protect the liver from oxidative damage after NDMA administration, and GSH plays a primary role in the cellular protective function when compared with MT.

The objective of this investigation was to compare the acute effects of exercise and diet manipulations on energy intake, between dietary restrained and unrestrained females. Comparisons of two studies using an identical 2 × 2 repeated-measures design (level of activity (rest or exercise) and lunch type (high-fat or low-fat)) including thirteen dietary unrestrained and twelve restrained females were performed. Energy expenditure during the rest session was estimated and the energy cost of exercise was measured by indirect calorimetry. Relative energy intake was calculated by subtracting the energy expenditure of the exercise session from the energy intake of the test meal. Post-meal hedonic ratings were completed after lunch. Energy intake and relative energy intake increased during high-fat conditions compared with the low-fat, independently of exercise (P < 0·001). There was a positive relationship between dietary restraint scores and energy intake or relative energy intake in the rest conditions only (r 0·54, P < 0·01). The decrease of relative energy intake between the rest and exercise conditions was higher in restrained than in unrestrained eaters (P < 0·01). These results confirm that a high-fat diet reversed the energy deficit due to exercise. There was no energy compensation in response to an acute bout of exercise during the following meal. In restrained eaters, exercise was more effective in creating an energy deficit than in unrestrained eaters. Exercise may help restrained eaters to maintain control over appetite.

A double-blind randomized crossover study was performed with nineteen normal-weight men to investigate the effect on subsequent ad libitum food intake of replacing 29 g sucrose with 29 g D-TAGATOSE AS SWEETENER TO A BREAKFAST MEAL. d-Tagatose is a malabsorbed stereoisomer of fructose with potential application as a bulk sweetener. Food intake was measured at lunch offered 4 h after the breakfast meal, during the afternoon with access to abundant snacks, and finally at a supper buffet 9 h after the breakfast. Energy intake at lunch and during the snacking period was similar after ingesting the two sugars, while it was 15 % lower after ingesting d-tagatose than with sucrose at supper (P < 0·05). Gastrointestinal factors such as the osmotic effects of unabsorbed d-tagatose causing distension of the gut might have mediated the acute appetite-suppressing effect. The present paper also refers to data from a preceding study in which we observed an increased self-reported energy intake after ingestion of d-tagatose compared with sucrose which, in fact, suggests a relative hyperphagic effect of d-tagatose. However, self-reported food intake may be biased by selective under-reporting and this subsequent study with a more controlled assessment of food intake was therefore conducted. This present study did not support any hyperphagic effect of d-tagatose, but rather suggests that d-tagatose may contribute to a reduced energy intake.

Ten pairs of normal men were overfed by 5 MJ/d for 21 d with either a carbohydrate-rich or a fat-rich diet (C- and F-group). The two subjects in each pair were requested to follow each other throughout the day to ensure similar physical activity and were otherwise allowed to maintain normal daily life. The increase in body weight, fat free mass and fat mass showed great variation, the mean increases being 1·5 kg, 0·6 kg and 0·9 kg respectively. No significant differences between the C- and F-group were observed. Heat production during sleep did not change during overfeeding. The RQ during sleep was 0·86 and 0·78 in the C- and F-group respectively. The accumulated faecal loss of energy, DM, carbohydrate and protein was significantly higher in the C- compared with the F-group (30, 44, 69 and 51 % higher respectively), whereas the fat loss was the same in the two groups. N balance was not different between the C- and F-group and was positive. Fractional contribution from hepatic de novo lipogenesis, as measured by mass isotopomer distribution analysis after administration of [1-13C]acetate, was 0·20 and 0·03 in the C-group and the F-group respectively. Absolute hepatic de novo lipogenesis in the C-group was on average 211 g per 21 d. Whole-body de novo lipogenesis, as obtained by the difference between fat mass increase and dietary fat available for storage, was positive in six of the ten subjects in the C-group (mean 332 (SEM 191) g per 21 d). The change in plasma leptin concentration was positively correlated with the change in fat mass. Thus, fat storage during overfeeding of isoenergetic amounts of diets rich in carbohydrate or in fat was not significantly different, and carbohydrates seemed to be converted to fat by both hepatic and extrahepatic lipogenesis.

To investigate the nutritional status of the population of the UK during the Second World War, nutritional surveys were commissioned in 1941. These included surveys of two groups of pregnant women: the first comprised 120 working-class women who were studied in the spring of 1942, and a second group of 253 women in 1944. Both groups were followed up until after delivery. Detailed biochemical assessments were performed on each subject. Our statistical analysis of the haematological data showed that nearly 25 % of women from the 1942 group were deficient in protein, over 60 % were deficient in Fe and vitamin A, and over 70 % had severe vitamin C deficiency. The findings were reported to the Ministries of Health and Food who instigated a food supplementation policy at the end of 1942 that entitled pregnant women in the UK to extra rations of fruit, dairy produce and to a supply of cod-liver-oil tablets. A second group of 253 pregnant women were studied 15 months later which enabled the effects of this programme to be investigated. Supplementation reduced the proportion of women with vitamin A concentrations below the normal range from 63 % to 38 %, and vitamin C from 78 % to 20 %, but protein and Fe concentrations were not increased but actually declined. These findings continued to exert an influence over government food policy for pregnant women until the abolition of rationing in 1954.