Effect of 2 dosages of prepartum cholecalciferol injection on blood minerals, vitamin D metabolites, and milk production in multiparous dairy cows: A randomized clinical trial.

The objective of the present study was to evaluate the effect of 2 dosages of prepartum cholecalciferol injection on blood minerals, vitamin D metabolites, and milk production. Cows entering their second or greater lactation (n = 158) were randomly assigned to a control group (CON) or one of 2 treatment groups receiving either 6 × 106 IU (6VitD) or 12 × 106 IU (12VitD) cholecalciferol intramuscularly on d 275 ± 1.2 (SD) of gestation. Concentrations of serum total Ca (tCa), phosphate, and Mg were determined on 1, 2, 3, 5, 7, and 10 d in milk (DIM). For a subsample of 30 cows entering the third lactation (n = 10/group), these samples were analyzed for cholecalciferol, 25-hydroxycholecalciferol (25-OHD3), and 24,25-dihydroxycholecalciferol (24,25-[OH]2D3). In these cows, we also determined 1,25-dihydroxycholecalciferol (1,25-[OH]2D3), the biologically most active metabolite, on 1, 2, 3, and 5 DIM. Repeated measures ANOVA was performed to evaluate the effect of different dosages of cholecalciferol on blood minerals, vitamin D metabolites, and milk yield over the first 5 test days after calving. Binary outcomes such as retained placenta and metritis were analyzed using a chi-squared test. Although the 12VitD treatment increased tCa concentrations on 1, 2, and 3 DIM compared with CON, administration of 6VitD increased tCa concentrations only on 1 DIM. Compared with CON cows and 6VitD cows, 12VitD cows had greater serum phosphate concentration during the first 10 DIM. Furthermore, 6VitD cows had greater serum phosphate concentrations compared with CON cows. On the contrary, 12VitD cows had lower serum Mg concentrations during the first 10 DIM compared with CON and 6VitD cows. Cholecalciferol was increased by the treatment and decreased quickly until 10 DIM. In respect to 25-OHD3, the 6VitD treatment resulted in a 4.1-fold increase in comparison to the CON group, while a 6.5-fold increase was observed in 12VitD animals. The vitamin D metabolite 24,25-(OH)2D3 increased linearly with 25-OHD3 serum levels, resulting in the highest concentrations in the 12VitD group. An increase of 1,25-(OH)2D3 until 3 DIM was observed in all cows. However, this rise was most pronounced in the CON group. The incidence of retained placenta was 1.9%, 11.5%, and 29.6%, and that of metritis was 11.5%, 15.4%, and 31.5% for CON, 6VitD, and 12VitD cows, respectively. Although none of the treated cows exerted clinical signs of hypocalcemia, one cow in CON incurred clinical hypocalcemia. Cows of the 12VitD group had a lower milk yield over the first 5 monthly test days compared with the control and 6VitD group (42.2 ± 0.5, 42.0, ± 0.5 and 40.7 ± 0.5 kg for control cows, 6VitD cows and 12VitD cows, respectively). Although no negative side effects were observed in 6VitD cows, we do not recommend the general application of 6 × 106 IU cholecalciferol before calving as positive effects on calcium homeostasis were marginal and restricted to the first DIM. The present findings confirm that the application of 12 × 106 IU cholecalciferol negatively affected milk production on this farm.

Maternal cytokine status may prime the metabolic profile and increase risk of obesity in children.

BACKGROUND: The maternal inflammation status during pregnancy has been associated with metabolic imprinting and obesity development in the child. However, the influence of the maternal Th2 cytokines, interleukin-4 (IL4), IL5 and IL13, has not been studied so far. METHODS: We investigated the relationship between maternal innate (IL6, IL8, IL10 and tumor necrosis factor-α (TNFa)) and adaptive (interferon-γ, IL4, IL5 and IL13) blood cytokine levels at 34 weeks of gestation and children's overweight development until the age of 3 years in 407 children of the German longitudinal LINA (Lifestyle and Environmental Factors and their Influence on Newborns Allergy risk) cohort. Children's body weight and height were measured during the annual clinical visits or acquired from questionnaires. Body mass index (BMI) Z-scores were calculated according to the WHO reference data to adjust for child's age and gender. Cytokine secretion was stimulated with phytohemagglutinin or lipopolysaccharide and measured by cytometric bead assay. Furthermore, we assessed metabolic parameter in blood of 318 children at age 1 using the AbsoluteIDQ p180 Kit (Biocrates LIFE Science AG). RESULTS: Applying logistic regression models, we found that an increase of maternal IL4 and IL13 was associated with a decreased risk for overweight development in 1- and 2-year-old children. This effect was consistent up to the age of 3 years for IL13 and mainly concerns children without maternal history of atopy. Children's acylcarnitine concentrations at 1 year were positively correlated with maternal IL13 levels and inversely associated with the BMI Z-score at age 1. CONCLUSIONS: We were able to show for the first time that the maternal Th2 status may be linked inversely to early childhood overweight development accompanied by an altered metabolic profile of the fetus. However, our data do not support a direct mediating role of acylcarnitines on maternal IL13-induced weight development.

Effects of dietary fats rich in lauric and myristic acid on performance, intestinal morphology, gut microbes, and meat quality in broilers.

This study investigated the hypothesis that dietary fats rich in lauric (C12) and myristic acid (C14) increase broiler performance and that the underlying mechanism involves antimicrobial effects on gut bacteria and changes in gut morphology. One hundred eighty 1-day-old Cobb-500 broilers were allotted to 3 groups. All groups received a basal diet consisting of maize, wheat, soybean meal, and a fat source (4.5, 7.0, 7.6, and 8.0% of fat product in the diet during d 1 to 9, 10 to 17, 18 to 27, and 28 to 35, respectively) until 35 d of age. The diet of the control group contained a fat with 67% of oleic and linoleic acid and 1.4% of C12 and C14 of total fatty acids, that of the esterified lauric and myristic acid (ELA) group a fat with 33% of esterified C12 and C14 and that of the free lauric and myristic acid (FLA) group a fat with 31% of both esterified and free (1:1) C12 and C14 (6 replicates/treatment, 10 birds/replicate). Gain and feed consumption did not differ between groups, but feed:gain was lower in FLA group as compared to the control group (P < 0.05). Carcass weight, liver weight, triglyceride content of liver and muscle, and muscle cholesterol were similar between groups; however, breast muscle weight was higher in the FLA than in the control group (P < 0.05). The villus height:crypt depth ratio of the duodenal wall did not differ between groups, but in the jejunum, it was lower in the FLA group as compared to the control group (P < 0.05). DNA copy numbers of Lactobacillus, Bifidobacteria, Enterobacteria, Escherichia coli, and Campylobacter jejuni in jejunal digesta were similar among groups. The study shows that dietary fats rich in free C12 and C14 improved feed:gain and breast muscle yield, but the observed effects could not be conclusively explained based on the parameters measured. The decreased jejunal villi:crypt ratio may point to changes in gut protein or cell turnover.

Vitamin D is not linked to folate status and mRNA expression of intestinal proton-coupled folate transporter.

PURPOSE: In vitro studies discovered intestinal proton-coupled folate transporter (PCFT) as a vitamin D hormone-responsive gene. In vivo effects of vitamin D on PCFT and folate status are currently not available. METHODS: Three experiments were conducted. At first, vitamin D receptor knockout (VDR(-/-)) mice and corresponding wild-type (WT) mice were compared for their plasma and hepatic folate concentration and PCFT mRNA expression in intestinal mucosa. In a second experiment with rats, we analyzed the folate status of offspring in response to a maternal vitamin D-adequate (1,000 IU/kg) or vitamin D-deficient (0 IU/kg) diet that was fed for 11 weeks. Finally, the plasma folate concentration of healthy individuals was studied at baseline (in winter) and in response to an oral treatment for 8 weeks with 2,000 IU vitamin D3 per day or a placebo, respectively. RESULTS: Here, we show that folate status and intestinal PCFT mRNA abundance did not differ between the VDR(-/-) and the WT mice. No effect of vitamin D on folate status was also found in rat dams and their offspring, and plasma folate levels of individuals did not change in response to vitamin D. CONCLUSIONS: Current data from studies with model animals and humans provide no indication for a vitamin D effect on intestinal uptake and status of folate.

Maternal and newborn vitamin D status and its impact on food allergy development in the German LINA cohort study.

BACKGROUND: Vitamin D levels are known to be associated with atopic disease development; however, existing data are controversial. The aim of this study was to investigate whether corresponding maternal and cord blood vitamin D levels are associated with atopic outcomes in early infancy. METHODS: Within the LINA cohort study (Lifestyle and environmental factors and their Influence on Newborns Allergy risk), 25(OH)D was measured in blood samples of 378 mother-child pairs during pregnancy and at birth. Information about children's atopic manifestations during the first 2 years of life was obtained from questionnaires filled out by the parents during pregnancy and annually thereafter. Cord blood regulatory T cells (Treg) were detected by methylation-specific PCR using a Treg-specific demethylated region in the FOXP3 gene. RESULTS: The median maternal 25(OH)D(3) level was 22.19 ng/ml (IQR 14.40-31.19 ng/ml); the median cord blood 25(OH)D(3) 10.95 ng/ml (6.99-17.39 ng/ml). A high correlation was seen between maternal and cord blood 25(OH)D(3) levels, both showing a seasonal distribution. Maternal and cord blood 25(OH)D(3) was positively associated with children's risk for food allergy within the first 2 years. Further, higher maternal 25(OH)D(3) resulted in a higher risk for sensitization against food allergens at the age of two. Cord blood 25(OH)D(3) levels were negatively correlated with regulatory T cell numbers. CONCLUSION: Our study demonstrates that high vitamin D levels in pregnancy and at birth may contribute to a higher risk for food allergy and therefore argues against vitamin D supplement to protect against allergy.

Effects of fish oil and conjugated linoleic acids on carnitine homeostasis in laying hens.

1. The effects of n-3 polyunsaturated fatty acids (PUFA) and conjugated linoleic acids (CLA) on genes involved in carnitine homeostasis were compared in laying hens. Three groups of laying hens were fed on a control diet or a diet with either 3% of fish oil or CLA for 4 weeks. 2. Feed intake and egg production rate did not differ between the three groups. Diets with fish oil or CLA had only a weak effect on mRNA levels of PPARα target genes (ACO, CPT-I) in the liver and did not influence mRNA concentrations of the most important carnitine transporter OCTN2, enzymes of involved in carnitine synthesis (TMLD, TMABA-DH, BBD) or concentrations of carnitine in plasma, liver and total egg contents. 3. Hens fed the CLA diet had lower concentrations of free and total carnitine in egg yolk but higher concentrations of carnitine in albumen than control hens (P < 0·05), whereas the amount of free and total carnitine in whole egg did not differ. 4. In conclusion, the study showed that feeding fish oil or CLA causes only a weak activation of PPARα in tissues of laying hens that probably explained the lack of effect on carnitine homeostasis. The results contrast with those in humans and mice that show a significant effect of synthetic PPARα agonists on carnitine homeostasis in humans and mice.

Hypolipidaemic effects of potato protein and fish protein in pigs.

This study was performed to assess the effects of potato protein and fish protein on concentrations of lipids in plasma and lipoproteins and the expression of genes involved in lipid metabolism in pigs used as an animal model. Therefore, 27 young male pigs with an average body weight of 22 kg were fed diets supplemented with protein extracted from potatoes (containing 849 g protein/kg dry matter), Alaska Pollack fillet as a source of fish protein (containing 926 g crude protein/kg dry matter) or casein which was used as control, for 3 weeks. Diets were formulated to supply identical amounts of each protein to the pigs by the three protein sources, namely 116 g/day in first week and 150 g/day in the second and third week. Pigs fed potato protein had lower concentrations of cholesterol in plasma and LDL than pigs fed casein (p < 0.05); no effect was observed on concentrations of HDL cholesterol and triglycerides. Pigs fed fish protein had lower cholesterol concentrations in plasma, LDL and HDL, and lower triglyceride concentrations in triglyceride-rich lipoproteins than pigs fed casein (p < 0.05). mRNA concentrations of genes involved in bile acid synthesis and cholesterol uptake were higher in pigs fed fish protein than in pigs fed casein (p < 0.05); no effect on these genes was observed in pigs fed potato protein. Expression of genes involved in lipogenesis and fatty acid oxidation was not altered by fish protein. In conclusion, this study shows that fish protein and potato protein lower plasma cholesterol concentrations in pigs. The hypocholesterolaemic effect of fish protein might be in part caused by a stimulation of bile acid synthesis; the reason for the hypocholesterolaemic effect of potato protein requires further elucidation.

Dietary pea protein stimulates bile acid excretion and lowers hepatic cholesterol concentration in rats.

It has been shown that some dietary plant proteins beneficially influence lipid metabolism in animals. The effect of pea protein in this respect however has not yet been investigated. Therefore, we studied the effect of purified pea protein on the lipid metabolism in rats. Twenty-four rats received diets with either 200 g/kg of casein or purified pea protein for 16 days. Concentrations of triacylglycerols in liver, plasma and lipoproteins did not differ between both groups of rats. However, rats fed the pea protein diet had a lower concentration of total cholesterol in the liver and the very low density lipoproteins (VLDL) fraction than rats fed the casein diet (p < 0.05); cholesterol concentration in plasma, low density lipoproteins (LDL) and high density lipoproteins (HDL) did not differ between both groups. Rats fed pea protein moreover had an increased mRNA concentration of cholesterol-7alpha-hydroxylase in the liver and an increased amount of bile acids excreted via faeces compared with rats fed casein (p < 0.05). Concomitantly, mRNA concentrations of sterol regulatory element-binding protein (SREBP)-2 and its target genes 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and LDL receptor in the liver were increased in rats fed pea protein (p < 0.05). The data of this study suggests that pea protein stimulates formation and excretion of bile acids, which leads to a reduced hepatic cholesterol concentration and a reduced secretion of cholesterol via VLDL. An increased gene expression of SREBP-2 and its target genes HMG-CoA reductase and LDL receptor may be a means to compensate for the increased loss of cholesterol for bile acid synthesis.

Effects of clofibrate treatment in laying hens.

Expression of peroxisome proliferator-activated receptor-alpha (PPARalpha) has been shown in liver of chicks, but effects of its activation have not yet been investigated. In this study, laying hens were treated with clofibrate, a synthetic PPARalpha agonist, to investigate the effects of PPARalpha activation on liver lipid metabolism. Hens receiving a diet containing 5 g of clofibrate/kg had a lower food intake and higher liver mRNA concentrations of typical PPARalpha target genes (carnitine palmitoyltransferase 1A, acyl-coenzyme A oxidase, bifunctional enzyme, lipoprotein lipase) involved in hepatic mitochondrial and peroxisomal beta-oxidation and plasma triglyceride clearance than control hens that received the same diet without clofibrate (P<0.05). Hens treated with clofibrate also had lower mRNA concentrations of fatty acid synthase, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and low-density lipoprotein receptor, proteins involved in fatty acid biosynthesis and cholesterol biosynthesis and uptake, than hens fed the control diet (P<0.05). These changes in clofibrate-treated hens were accompanied by reduced liver triglyceride concentrations, strongly diminished very low density triglyceride and cholesterol concentrations (P<0.05), a disturbed maturation of egg follicles, a complete stop of egg production, and a markedly reduced plasma 17-beta-estradiol concentration (P<0.05). In conclusion, it is shown that clofibrate has complex effects on hepatic lipid metabolism in laying hens that mimic PPARalpha activation in mammals, affect maturation of egg follicles, and lead to a stop of egg production. Because clofibrate treatment strongly reduced food intake in the hens, some of these effects (i.e., egg production) may have been due to a low energy and nutrient intake.

Global Burden of Sugar-Related Dental Diseases in 168 Countries and Corresponding Health Care Costs.

Oral diseases such as dental caries, edentulism (tooth loss), periodontal disease (PD), and oral cancer currently constitute an increased major public health burden across the globe, with significant differences between countries. One of the main drivers of caries, edentulism, and PD is the excessive intake of sugars. Here, we aimed to quantify the global sugar-related dental health and cost burden in the year 2010. This study used a health-econometrical model to calculate the disease burden as well as the direct and indirect costs attributable to the intake of free sugars (mono- and disaccharides [MDS]). To this end, several databases from the Institute for Health Metrics and Evaluation (IHME), Organisation for Economic Co-operation and Development (OECD), Food and Agriculture Organization (FAO), and World Bank were used. In total, the corresponding disease burden in 168 countries and economic burden in 31 OECD countries were quantified. In 2010, the consumption of MDS was associated with a global dental disease burden of 4.1 million disability-adjusted life years (DALYs; 95% uncertainty interval [UI]: 2.1 to 7.4 million DALYs), with 2.7 million DALYs from MDS-related caries and 1.4 million DALYs from PD. In terms of economic costs, MDS-related dental diseases were associated with a global financial burden of 172 billion US dollars (USD; 95% UI: 91 to 295 billion USD), the largest share of which (151 billion USD) was incurred in OECD countries. Overall, 26.3% (95% UI: 13.3% to 47.5%) of the total global oral disease burden was attributed to the consumption of MDS. The present study emphasizes the need to further address the role of free sugars in oral health and nutrition policy. Although the largest share of the economic burden was accounted for by OECD countries, emerging economies should address this challenge early on in national public health policies if they are to avoid disease and the prospect of increased cost burdens.

Significantly enhanced lung metastasis and reduced organ NK cell functions in diet-induced obese rats.

BACKGROUND: Obesity was identified as a major risk factor for malignant diseases, but underlying mechanisms remain unclear. Natural killer (NK) cells, a pivotal aspect of innate immunity, are capable of identifying and killing virally infected and tumor cells. Previous studies have shown altered NK cell functions in obesity, and the current study aimed to investigate the relationship between altered NK cell functions and increased cancer risk in obesity. METHODS: To induce obesity male F344-rats received a high-fat diet (34% fat) or a control diet (4% fat). Thereafter, syngeneic mammary adenocarcinoma cells (MADB106) or a vehicle were intravenously (i.v.) injected. 15 min after injection, half of each group of rats were killed, lungs removed and immunohistochemically stained. Numbers of NK cells, MADB106 cells and NK cell-tumor cell interactions were quantified. Twenty-one days after tumor-cell injection the other half group of rats was killed and lung metastases were counted and relative mRNA concentrations of different NK cell receptors were determined. RESULTS: After short-term MADB106-challenge, DIO fed animals showed significantly decreased NK cell numbers in the blood and NK cell-tumor cell interactions in the lung as compared to their control littermates. Twenty-one days after MADB106 injection, the lungs of the DIO fed rats showed significantly more lung metastases compared to control animals, accompanied by reduced relative mRNA concentrations of the activating NK cell receptor NKG2D. CONCLUSIONS: We conclude that induction of obesity in F344-rats leads to reduced lung NK cell function against tumor cells and results in significantly enhanced lung metastasis as compared to lean animals. It can be hypothesized that obesity-induced altered NK cell functions play an important role in cancer growth and metastasis.

Estimation of the leucine and histidine requirements for piglets fed a low-protein diet.

Reduction of the CP content in the diets of piglets requires supplementation with crystalline essential amino acids (AA). Data on the leucine (Leu) and histidine (His) requirements of young pigs fed low-CP diets are limited and have primarily been obtained from nonlinear models. However, these models do not consider the possible decline in appetite and growth that can occur when pigs are fed excessive amounts of AA such as Leu. Therefore, two dose-response studies were conducted to estimate the standardised ileal digestible (SID) Leu : lysine (Lys) and His : Lys required to optimise the growth performance of young pigs. In both studies, the average daily gain (ADG), average daily feed intake (ADFI) and gain-to-feed ratio (G : F) were determined during a 6-week period. To ensure that the diets had sub-limiting Lys levels, a preliminary Lys dose-response study was conducted. In the Leu study, 60 35-day-old piglets of both sexes were randomly assigned to one of five treatments and fed a low-CP diet (15%) with SID Leu : Lys levels of 83%, 94%, 104%, 115% or 125%. The His study used 120 31-day-old piglets of both sexes, which were allotted to one of five treatments and fed a low-CP diet (14%) with SID His : Lys levels of 22%, 26%, 30%, 34% or 38%. Linear broken-line, curvilinear-plateau and quadratic-function models were used for estimations of SID Leu : Lys and SID His : Lys. The minimum SID Leu : Lys level needed to maximise ADG, ADFI and G : F was, on average, 101% based on the linear broken-line and curvilinear-plateau models. Using the quadratic-function model, the minimum SID Leu : Lys level needed to maximise ADG, ADFI and G : F was 108%. Data obtained from the quadratic-function analysis further showed that a ±10% deviation from the identified Leu requirement was accompanied by a small decline in the ADG (-3%). The minimum SID His : Lys level needed to maximise ADG, ADFI and G : F was 27% and 28% using the linear broken-line and curvilinear-plateau models, respectively, and 33% using the quadratic-function model. The preferred model to estimate the His requirement was the curvilinear-plateau model. However, a 10% reduction in the SID His : Lys level was associated with an 11% reduction in the ADG. In conclusion, the SID Leu : Lys level needed to maximise growth was 108% when using the quadratic-function model as the best-fitting model. The minimum SID His : Lys level required to optimise growth was 28% when using the curvilinear-plateau model as the best-fitting model.

High dietary levels of a conjugated linoleic acid mixture alter hepatic glycerophospholipid class profile and cholesterol-carrying serum lipoproteins of rats.

To investigate the body composition, hepatic lipids, and serum lipoproteins in response to graded levels of a conjugated linoleic acid (CLA) mixture added to a high linoleate diet, adult male Sprague-Dawley rats were randomly assigned into four dietary groups of 10 rats each and fed for 5 weeks controlled amounts of diets containing 0%, 1%, 3%, or 5% of a CLA mixture in exchange for sunflower oil. The various dietary lipid treatments did not significantly influence growth and body partitioning, although there was a trend toward decreased contents of extractable lipids in carcass (whole bled body without liver and gut) with increasing CLA. When carcass lipids of CLA-treated rats were extracted, a distinct accumulation of total CLA was observed. A dietary level of 1% CLA mixture exhibited only weak effects on hepatic glycerophospholipid levels. CLA levels of 3% and 5% caused distinct changes in phospholipid subclass distribution. These changes were reduced levels of lysophosphatidylethanolamine (LPE) and ethanolamine plasmalogen (EPL) and increased levels of phosphatidylcholine (PC). Further, a 5% level of CLA increased the hepatic concentration of phosphatidylserine (PS) compared with the other treatments. The incorporation of total CLA into individual phospholipids followed a dose-responsive manner. The extent of incorporation of CLA was not the same among the glycerophospholipid species analyzed, the order being cardiolipin > phosphatidylethanolamine and PC > LPE/EPL > phosphatidylinositol > PS. Further, CLA increased the proportions of n-3 fatty acids in the individual glycerophospholipids. High CLA diets containing 3% and 5% of a CLA mixture were associated with increased activity of catalase in the peroxisome-enriched cell fraction of liver and exhibited marked reductions of cholesterol in the low and high density lipoproteins relative to rats receiving no CLA.

Different degrees of moderate iron deficiency modulate lipid metabolism of rats.

Severe iron deficiency affects lipid metabolism. To investigate whether moderate iron depletion also alters lipid variables-including lipid levels in serum and liver, hepatic lipogenesis, and fatty acid composition indicative of an impaired desaturation-we carried out experiments with rats fed 9, 13, and 18 mg iron/kg diet over a total of 5 wk. The study also included three pair-fed control groups and an ad libitum control group, fed with 50 mg iron/kg diet. The iron-depleted rats were classified as iron-deficient on the basis of reduced serum iron, hemoglobin concentration, and hematocrit. All moderately iron-deficient rats had significantly lower cholesterol concentrations in liver and serum lipoproteins than their pair-fed controls. Rats with the lowest dietary iron supply had higher concentrations of hepatic phosphatidylcholine (PC) and phosphatidylethanolamine (PE), lower activities of glucose-6-phosphate dehydrogenase, malic enzyme and fatty acid synthase, and higher triacylglycerol concentrations in serum lipoproteins than the corresponding pair-fed control rats. Moderate iron deficiency also depressed the serum phospholipid level. Moreover, several consistent significant differences in fatty acid composition of hepatic PC and PE occurred within moderate iron deficiency, which indicate impaired desaturation by delta-9 and delta-6 desaturases of saturated and essential fatty acids. We conclude that lipid variables, including cholesterol in liver and serum lipoproteins as well as fatty acid desaturation, reflect the gradations of iron status best and can be used as an indicator of the degree of moderate iron deficiency.

Nickel deficiency alters nickel flux in rat everted intestinal sacs.

This study was conducted to determine nickel absorption in nickel-deficient rats. Jejunal segments obtained from dietary nickel-depleted (13 microg nickel/kg diet) and nickel-control (1 mg nickel/kg diet) adult rats from the first generation, and suckling pups from the second offspring were used. The nickel transfer across the intestinal epithelium and nickel uptake into the intestine were measured by use of everted jejunal sacs using a wide range of nickel concentrations administered on the luminal side (1.1 x 10(-8) M til 1.0 x 10(-4) M). Both the intestinal nickel transfer and nickel uptake were influenced by the dietary nickel supply in rat offspring, but not in the adult rats from the first generation. However, in nickel-deficient offspring, the nickel transfer across the small intestine was higher than in nickel-control offspring. This difference was greater using low intraluminal nickel concentrations than high nickel concentrations, and was significant at 1.1 x 10(-8) M, 6.1 x 10(-8) M, 5.1 x 10(-7) M, 1.0 x 10(-6) M, and 5.0 x 10(-6) M. Also, nickel uptake into the intestine was somewhat greater in nickel-deficient rat pups than in nickel-control pups, and significant using 1.1 x 10(-7) M and 1.0 x 10(-6) M nickel. A definite saturation type kinetic for the intestinal nickel absorption in relation to the intraluminal nickel concentration could not be observed.

Cobalt deficiency effects on trace elements, hormones and enzymes involved in energy metabolism of cattle.

This study was conducted to investigate the physiological consequences of long-term moderate cobalt deficiency in beef cattle, which have not hitherto been studied in detail. Cobalt deficiency was induced in cattle by feeding two groups of animals either a basal corn silage-based diet that was moderately low in cobalt (83 micrograms Co/kg), or the same diet supplemented with cobalt to a total of 200 micrograms per kg, for 43 weeks. Cobalt deficiency was induced, as judged by inappetance, diminished growth gain and a markedly reduced vitamin B12 status in serum and liver. The long-term cobalt deprivation which was primarily a combination of reduced feed intake and a tissue vitamin B12 deficiency did not show evidence of a significant dysfunction of energy metabolism. The activities of glucose-6-phosphate dehydrogenase and cytochrome oxidase in liver remained unaffected by cobalt deficiency, nor was there a significant change in serum glucose level of cattle on the cobalt-deprived diet. However, analysis of thyroid hormone status indicated a slight reduction of type I thyroxine monodeiodinase activity in liver accompanied by a significant reduction of the triiodothyronine level in serum. The diminished liver vitamin B12 level resulted in significantly reduced folate level in this tissue, reduced concentrations of heme-depending blood parameters. Moreover cobalt deficiency or rather vitamin B12 deficiency was accompanied by a dramatic accumulation of the trace elements iron and nickel in liver. These results indicate that long-term moderate cobalt deficiency may induce a number of physiological changes in cattle, but a follow-up study, which excluded different feed levels by including a pair-fed control group, will be necessary to actually obtain the single effect of cobalt deficiency in cattle.

Dietary thiamin supply during gestation effects thiamin status of lactating rats and their suckling offspring.

This investigation was designed to examine the effect of dietary thiamin supply during gestation on body thiamin status of lactating rats and their suckling offspring, and thiamin in milk from 1 to 13 days postpartum. Therefore, a study over two generations was conducted feeding 2, 6.7 and 20 mg/kg thiamin during gestation and 8 mg/kg thiamin during lactation. Rat dams receiving inadequate thiamin during gestation and their offspring were thiamin-deficient on the basis of reduced activity of transketolase in blood and erythrocytes, which did not reach completely the control level even two weeks postpartum. The thiamin intake during gestation influenced significantly the thiamin levels in tissues of the dams and their offspring. However, the observed dose-dependence remained only for the first days of lactation. The thiamin concentration in milk two days postpartum also reflected the nutritional thiamin status from the pregnant rats, in which the thiamin concentration raised continuously with the duration of the lactation cycle. The data indicate that an adequate thiamin supply during lactation can not completely compensate for an inadequate thiamin supply during gestation, and that necessitates a constant thiamin intake.

Precaecal digestibility of niacin and pantothenic acid from different foods.

This study was conducted to investigate the apparent precaecal digestibilities of niacin and pantothenic acid from human nutrient related foods including wheat, coarse whole-meal bread, boiled potatoes and boiled pork and beef. Therefore, pigs were subjected to an end-to-end ileo-rectal anastomosis, so digesta passed straight from ileum to rectum, eliminating endogenous vitamin synthesis. Excreted chyme was collected over 5-days periods, and concentrations of niacin, and pantothenic acid in the food and chyme samples were determined microbiologically. The intestinal bioavailability of niacin and pantothenic acid was affected differently by the food administered. The digestibility values of niacin deriving from the wheat-, potato- and the meat-based meals ranged from 59 to 69%. Wholemeal bread exerted a nutritionally important negative effect on the apparent intestinal availability of dietary niacin relative to the other foods, which averaged by 40%. Food-related differences of the pantothenic acid digestibility values were greater than that observed with niacin. The digestibility values of pantothenic acid from wheat, potatoes and the meat meals ranged between 65 and 81% and were of the order wheat diet > pork diet > potato diet > beef diet, although differences were not statistically significant. The digestibility of pantothenic acid from the coarse wholemeal bread diet was lower than 30%.

Effect of dietary methionine on plasma and liver cholesterol concentrations in rats and expression of hepatic genes involved in cholesterol metabolism.

Methionine has been shown to increase plasma cholesterol in animals. In the present study, mechanisms were investigated by which methionine could alter cholesterol metabolism. In the first experiment, forty growing rats were fed four casein-based diets differing in methionine content (2.6, 3.5, 4.5 or 6.0 g/kg) for 14 d. In the second experiment, isolated rat hepatocytes were incubated in media supplemented with 50, 100 or 200 micromol/l methionine. Dietary methionine tended to increase plasma homocysteine concentrations in the rats (P=0.058). A weak positive correlation between circulating homocysteine and plasma cholesterol was observed (R2 0.27, P<0.01). Rats fed 3.5 g/kg or more of methionine had higher concentrations of cholesterol in their plasma, in lipoprotein fractions of density (rho; kg/l) 1.0061.063, and in liver than rats fed 2.6 g/kg methionine. Rats fed 6 g/kg methionine had a higher hepatic expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol-7alpha-hydroxylase than rats fed less methionine. The phosphatidylcholine:phosphatidylethanolamine ratio in rat liver increased with rising dietary methionine concentration; the relative mRNA concentrations of phosphatidylethanolamine N-methyltransferase and cystathionine beta-synthase remained unaffected. Hepatocytes incubated in media supplemented with 100 or 200 micromol/l methionine had a higher cholesterol synthesis than hepatocytes incubated in a medium supplemented with 50 micromol/l methionine; the LDL uptake in hepatocytes was independent of the methionine concentration of the medium. In conclusion, the present study suggests that dietary methionine induces hypercholesterolaemia at least in part via an enhanced hepatic cholesterol synthesis.

Conjugated linoleic acids exhibit a strong fat-to-lean partitioning effect, reduce serum VLDL lipids and redistribute tissue lipids in food-restricted rats.

Effects of conjugated linoleic acids (CLA) on a series of metabolic events are expected to depend on the feeding regimen and levels of energy ingested. This study was the first examining the mode of action of CLA on body composition, tissue lipids, lipoproteins and hepatic enzymes in situations of enhanced fat store mobilization. Two groups of male growing Sprague-Dawley rats were fed for 3 wk a diet containing 0 (control group) or 3 g/100 g of a CLA mixture at the expense of sunflower oil, and were then subjected to a weight-loss feeding regimen for another 18 d. Rats fed the CLA-fortified diet gained 11% less weight than the control rats (P<0.05). Rats fed the high CLA diet had less body fat (1.47+/-0.16 vs. 1.07+/-0.09 g/100g, P<0.05) and a higher lean deposition (25.6+/-0.2 vs. 28.4+/-0.3 g/100 g, P<0.05) than control rats. CLA-fed rats had a 41% lower cholesterol concentration in liver than the control rats (P<0.05). Some differences in glycerophospholipid subclass profile of liver and erythrocyte membrane were observed; the hepatic concentrations of phosphatidylethanolamine (4.76+/-0.46 vs. 6.86+/-0.99 micromol/g, P = 0.07) and phosphatidylcholine (12.9+/-0.5 vs. 15.3+/-1.2 micromol/g, P = 0.09) tended to be greater and the level of phosphatidylcholine in erythrocyte membranes was significantly greater (1.40+/-0.12 vs. 1.83 +/-0.16 micromol/g, P<0.05) in the CLA-treated group than in the control group. The activities of catalase and ornithine decarboxylase in liver did not differ between the groups. Further, CLA-treated rats had significantly lower serum concentrations of VLDL lipids than control rats, whereas concentrations of LDL and HDL lipids were unaffected. The results indicate that a high dose of a CLA mixture is a strong repartitioning agent and a modulator of lipid metabolism under conditions of enhanced fat store mobilization in rats.