Metallothionein-null mice absorb less Zn from an egg-white diet, but a similar amount from solutions, although with altered intertissue Zn distribution

The influence of metallothionein (MT) on Zn transfer into non-gut tissues was investigated in MT-null (MT-/-) and normal (MT+/+) mice 4 h after oral gavage of aqueous 65ZnSO4solution at doses of 154, 385, 770 and 1540 nmol Zn per mouse. Zn transfer was not significantly different between MT+/+ and MT-/- mice and was directly proportional to the oral dose (slope = 0.127, r = 0.991; 0. 146, r = 0.994, respectively). Blood 65Zn and plasma Zn concentrations increased progressively in MT-/- mice at doses >154 nmol Zn, reaching levels of 2.4% of oral dose and 60 micromol/L, respectively, at the 1540 nmol Zn dose. The corresponding values for MT+/+ mice were approximately half, 1.0% and 29 micromol/L. Intergenotypic differences were found in tissue distribution of 65Zn within the body; MT-/- mice had higher 65Zn levels in muscle, skin, heart and brain, whereas MT+/+ mice retained progressively more Zn in the liver, in conjunction with a linear increase in hepatic MT up to the highest Zn dose. MT induction in the small intestine reached its maximum at an oral dose of 385 nmol Zn and did not differ at higher doses. Absorption of a 770 nmol 65Zn dose from a solid egg-white diet was only one fourth (MT+/+) and one eighth (MT-/-) of the Zn absorption from the same dose of 65Zn in aqueous solution. MT+/+ mice had greater (P < 0.05) Zn absorption from the egg-white diet than did MT-/- mice, indicating that gut MT confers an absorptive advantage, but only when Zn is incorporated into solid food.     

Zn-depleted mice absorb more of an intragastric Zn solution by a metallothionein-enhanced process than do Zn-replete mice

The influence of metallothionein (MT)(2) on Zn absorption was investigated in MT-null (MT-/-) and normal (MT+/+) mice fed Zn-depleted (ZnD) diets for 7 d and compared with those fed Zn-replete (ZnR) diets in a previous study. Mice were starved for 20 h, then administered an oral gavage of aqueous (65)ZnSO(4) solution at doses of 154, 770 or 1540 nmol of Zn, and the amount transferred into nongut tissues was determined 4 h later. (65)Zn transfer did not differ between genotypes in ZnR mice. However ZnD MT+/+ mice had a 30-40% greater transfer from the 154 and 770 Zn doses compared to ZnR MT+/+ mice. This was not observed in MT-/- mice. In MT+/+ mice, Zn depletion enhanced the induction of MT by Zn in the intestine and pancreas. (65)Zn uptakes in the liver and pancreas were greater in MT+/+ than MT-/- mice, and this was greater (50%) at the 154 and 770 doses in mice fed ZnD diets. Plasma Zn concentrations were raised to a similar extent in ZnR and ZnD MT-/- mice. ZnR MT+/+ mice had significantly lower plasma Zn levels than MT-/-mice; this difference was less marked in the ZnD mice. We conclude that a MT-facilitated enhancement in Zn absorption occurs in response to dietary Zn deficiency.     

Development of a compartmental model of zinc kinetics in mice

To investigate zinc (Zn) kinetics in mice, tracer ((65)Zn) was administered orally to 9-wk-old female mice in the fed state and tracer and Zn concentration were measured in 21 tissues over the following 8 d. Data were analyzed by compartmental modeling using WinSAAM. A published model for Zn kinetics in rats was modified to fit the data from mice and to calculate transfer rates and pool sizes of Zn. Parallel studies were performed in mice lacking genes for metallothionein (MT), MT-I and MT-II (MT-/-), to quantify differences in Zn kinetics in the absence of these proteins in vivo. We confirmed that tracer time course in most tissues was similar in wild-type mice and those lacking MT, except for the pancreas of MT-/-, which retained less tracer. By fitting tissue and intestinal data simultaneously, we found that intestinal tracer could be explained by unabsorbed isotope and loss of Zn from pancreas went through plasma. Differences in pancreatic data in MT-/- were explained by Zn turning over twice as fast in this tissue (4 h) compared with wild type (9 h). These kinetic studies provide parameter values for normal, fed mice that can be used to assess Zn kinetics in abnormal conditions, as demonstrated by the higher turnover of Zn in the pancreas of MT knockout mice.     

Pharmacokinetics of enterolignans in healthy men and women consuming a single dose of secoisolariciresinol diglucoside

High concentrations of enterolignans in plasma are associated with a lower risk of acute coronary events. However, little is known about the absorption and excretion of enterolignans. The pharmacokinetic parameters and urinary excretion of enterodiol and enterolactone were evaluated after consumption of their purified plant precursor, secoisolariciresinol diglucoside (SDG). Twelve healthy volunteers ingested a single dose of purified SDG (1.31 micromol/kg body wt). Enterolignans appeared in plasma 8-10 h after ingestion of the purified SDG. Enterodiol reached its maximum plasma concentration 14.8 +/- 5.1 h (mean +/- SD) after ingestion of SDG, whereas enterolactone reached its maximum 19.7 +/- 6.2 h after ingestion. The mean elimination half-life of enterodiol (4.4 +/- 1.3 h) was shorter than that of enterolactone (12.6 +/- 5.6 h). The mean area under the curve of enterolactone (1762 +/- 1117 nmol/L . h) was twice as large as that of enterodiol (966 +/- 639 nmol/L . h). The mean residence time for enterodiol was 20.6 +/- 5.9 h and that for enterolactone was 35.8 +/- 10.6 h. Within 3 d, up to 40% of the ingested SDG was excreted as enterolignans via urine, with the majority (58%) as enterolactone. In conclusion, a substantial part of enterolignans becomes available in the blood circulation and is subsequently excreted. The measured mean residence times and elimination half-lives indicate that enterolignans accumulate in plasma when consumed 2-3 times a day and reach steady state. Therefore, plasma enterolignan concentrations are expected to be good biomarkers of dietary lignan exposure and can be used to evaluate the effects of lignans.     

Copper deficiency does not lead to taurine deficiency in rats

Copper deficiency has been reported to cause a decrease in urinary taurine excretion in rats. We determined whether Cu deficiency would decrease taurine status and the hepatic activities of cysteine dioxygenase (CDO) and/or cysteine sulfinic acid decarboxylase (CSAD) in rats. Ten weanling male rats were assigned to either a Cu-adequate (+Cu) or Cu-deficient (-Cu) group. All rats consumed a Cu-deficient purified diet and water ad-libitum for 16 wk. The water for the (+Cu) group contained 20 mg Cu/L as CuSO(4). At wk 16, the groups differed (P < 0.05) in the following variables (means +/- SEM, -Cu vs. +Cu): body weight (BW), 375 +/- 19 vs. 418 +/- 2.9 g; food intake, 16.2 +/- 0.7 vs. 18.5 +/- 0.4 g/d; hematocrit, 0.294 +/- 0.027 vs. 0.436 +/- 0.027; hemoglobin, 95.2 +/- 9 vs 134 +/- 10 g/L; liver Cu, 8.7 +/- 2.0 vs. 65.9 +/- 2.5 nmol/g; plasma Cu, 0.38 +/- 0.09 vs. 13.4 +/- 0.61 micromol/L; plasma ceruloplasmin activity, 1.75 +/- 1.0 vs. 67.9 +/- 8.4 IU; relative heart weight, 0.56 +/- 0.04 vs. 0.35 +/- 0.02% BW; relative liver weight, 4.06 +/- 0.23 vs. 3.37 +/- 0.06% BW; and liver CSAD activity, 18.8 +/- 1.37 vs. 13.5 +/- 1.11 nmol x min(-1) x mg protein(-1). The groups did not differ at wk 16 in: plasma taurine, 249 +/- 14 vs. 298 +/- 63 micromol/L; whole blood taurine, 386 +/- 32 vs. 390 +/- 25 micromol/L; urinary taurine excretion, 82.5 +/- 15 vs. 52.0 +/- 8.3 micromol/d; liver taurine, 2.6 +/- 0.7 vs. 2.8 +/- 0.4 micromol/g; liver total glutathione, 6.9 +/- 0.48 vs. 6.3 +/- 0.40 micromol/g; liver cyst(e)ine, 96 +/- 7.1 vs. 99 +/- 5.3 nmol/g and liver CDO activity, 2.19 +/- 0.33 vs. 2.74 +/- 0.21 nmol x min(-1) x mg protein(-1). These findings support the conclusion that Cu deficiency does not affect body taurine status.     

Effect of zinc supplementation on protein metabolism in late-middle-aged men: The Zenith study

OBJECTIVE: Zinc (Zn) is an essential trace element that is a potent enhancer of protein metabolism due to its numerous roles in metabolic processes. Protein turnover decreases with age. We determined whether a Zn supplementation, which increases serum Zn concentration and Zn exchangeable pool mass, modifies whole-body protein turnover and albumin and fibrinogen synthesis rates in late-middle-aged men. METHODS: Three groups of 16 healthy subjects 55-70 y of age participated in a randomized, doubled-blinded, placebo-controlled intervention. Each group received 0, 15, or 30 mg/d of supplemental Zn for 6 mo. At the end of the supplementation period, each subject received an intravenous infusion of L-[1-13C] leucine to quantify whole-body leucine fluxes and synthesis rates of albumin and fibrinogen. RESULTS: In the placebo group, mean +/- SEM whole-body leucine fluxes to protein synthesis, to oxidation, and from protein degradation were 1.46 +/- 0.05, 0.40 +/- 0.01, and 1.73 +/- 0.06 micromol.kg(-1).min(-1), respectively. Zn supplementation did not significantly change whole-body leucine fluxes. In the placebo group, plasma concentration and fractional rate of protein synthesis were 45 +/- 1 g/L and 8.2 +/- 0.6%/d for albumin and 3.6 +/- 0.2 g/L and 16.7 +/- 1.3%/d for fibrinogen, respectively. Zn supplementation did not significantly change these parameters or the absolute rates of synthesis of these proteins. CONCLUSION: Increasing Zn supply does not modify whole-body protein metabolism and synthesis rates of albumin and fibrinogen in late-middle-aged men.     

Rapid gut transit time and slow fecal isoflavone disappearance phenotype are associated with greater genistein bioavailability in women

The bioavailability of soybean isoflavones varies widely among individuals due to many factors, including activities of gut microflora. To characterize factors that affect fecal isoflavone disappearance phenotype and isoflavone bioavailability in women, 35 Asian and 33 Caucasian women, 18-43 y of age, provided fecal samples for anaerobic incubation with isoflavones in vitro at two times 5 mo apart (Phases I and II). Diet, physical activity and health history were investigated at these times. A single dose of soymilk powder [1.2 mg (4.57 micromol) total isoflavone/kg body] was given to all subjects with breakfast in phase II. Daidzein and genistein from fecal incubations, urine and fecal samples were measured by reverse-phase HPLC. Three significantly different daidzein and two genistein disappearance phenotypes were identified from fecal isoflavone incubations. More Asians than Caucasians were identified within the high daidzein disappearance phenotype. Caucasians and Asians differed significantly in daily intake of red meat (0.3 +/- 0.1 vs. 1.0 +/- 0.1 servings/d), dairy foods (2.9 +/- 0.2 vs. 1.2 +/- 0.2 servings/d) and insoluble dietary fiber (3.6 +/- 0.3 vs. 1.4 +/- 0.3 g). BMI, maximal oxygen uptake (VO(2 max)) and physical activity level were significantly greater in Caucasians than in Asians. Asian subjects of the low genistein disappearance phenotype had more rapid gut transit time (GTT) and greater isoflavone bioavailability as reflected in urinary genistein excretion than did Asians of the high genistein disappearance phenotype (GTT, 40 +/- 8 vs. 63 +/- 5 h; 11.0 +/- 2.7 vs. 4.0 +/- 1.7% of ingested genistein excreted in urine). Caucasians of both genistein disappearance phenotypes had longer GTT than did Asian subjects (84 +/- 5 vs. 56 +/- 6 h) and resembled Asians of the high genistein disappearance phenotype in genistein bioavailability. Relatively rapid GTT coupled with a low fecal isoflavone disappearance phenotype as occurred in Asian but not Caucasian subjects produced greater genistein bioavailability, as reflected in urinary genistein excretion.     

Potential antioxidant effects of zinc and chromium supplementation in people with type 2 diabetes mellitus.

OBJECTIVE: To determine the effects of combined zinc (Zn) and chromium (Cr) supplementation on oxidative stress and glucose homeostasis of people with type 2 diabetes. DESIGN: Tunisian adult subjects with HbA1C > 7.5% were supplemented for 6 months with 30 mg/d of Zn as Zn gluconate or 400 microg/d of Cr as Cr pidolate or combined Zn/Cr supplementation or placebo. The effects of supplementation on plasma zinc (Zn), copper (Cu), selenium (Se), urinary Zn, Cr, plasma thiobarbituric acid reactive substances (TBARS), Cu-Zn superoxide dismutase (SOD) and Se glutathione peroxidase (GPx) in red blood cells, blood lipids and lipoproteins, HbA1C and fasting glucose were measured at the beginning of the study and after six months. RESULTS: At the beginning of the study, more than 30% of the subjects may have been Zn deficient with plasma Zn values less than 10.7 mircomol/L, whereas levels of plasma Cu, Se and antioxidant RBC enzyme activities were in the normal ranges. Following supplementation, there were significant decreases of plasma TBARS in the Cr (13.6%), Zn (13.6%) and Zn/Cr (18.2%) groups with no significant changes in the placebo group. The value for the TBARS of the control healthy Tunisian subjects was 2.08 +/- 0.04 micromol/L and that of the Tunisian subjects with diabetes was 3.32 +/- 0.05 micromol/L. This difference of 1.24 micromol/L between the control group and the subjects with diabetes was reduced from 36% to 50% in the three supplemented groups. Supplementation did not modify significantly HbAIC nor glucose homeostasis. No adverse effects of Zn supplementation were observed on Cu status. HDL cholesterol nor interactions in Zn or Cr. CONCLUSIONS: These data suggest the potential beneficial antioxidant effects of the individual and combined supplementation of Zn and Cr in people with type 2 DM. These results are particularly important in light of the deleterious consequences of oxidative stress in people with diabetes.     

Increased rat mammary tissue vitamin A associated with increased vitamin A intake during lactation is maintained after lactation

Although increases in dietary vitamin A increase milk vitamin A, little is known about effects of vitamin A intake on mammary tissue vitamin A levels during and after the reproductive cycle. First, we measured vitamin A concentrations in milk, mammary tissue and liver of lactating rats fed 0, 4, or 50 micromol of vitamin A/kg diet during pregnancy and through d 12 of lactation. Liver vitamin A concentration was significantly affected by diet in lactating females and pups 12 d after parturition. Milk vitamin A concentrations were significantly higher (7.1 +/- 2.2 micromol/L, n = 8) in dams fed 50 micromol/kg than in those fed 0 or 4 micromol/kg (1.9 +/- 0.3, n = 5 and 2.9 +/- 0.7 micromol/L, n = 7; P < 0.001), as were mammary tissue vitamin A concentrations (5.1 +/- 1.1 versus 2.2 +/- 0.4 and 2.4 +/- 0.6 nmol/g; P < 0.001). Next, we maintained female rats on 50 or 10 micromol vitamin A/kg diet during pregnancy and lactation and then on 4 micromol/kg diet after pups were weaned on d 21. On d 21, mammary tissue vitamin A concentrations were 3.14 +/- 0.75 versus 1.52 +/- 0.21 nmol/g in dams fed 50 versus 10 micromol/kg (n = 4/group; P < 0.001). Mammary tissue vitamin A concentrations were not significantly affected by time from 7 to 49 d after lactation and averaged 8.5 +/- 0.4 and 4.9 +/- 0.8 nmol/g on d 49 in dams fed 50 versus 10 micromol/kg (n = 4; P < 0.001). We conclude that diet-induced differences in rat mammary tissue vitamin A developed during pregnancy and lactation are maintained for > or =7 wk after lactation.     

Dietary folate intake, blood folate status, and urinary folate catabolite excretion in Korean women of childbearing age

This study assessed folate intake, folate concentrations in plasma and erythrocytes, plasma total homocysteine (tHcy) concentrations, and urinary excretion of folate metabolites in Korean women of childbearing age. A total of 36 women voluntarily participated in this study. Precise dietary intake for 3 consecutive days was determined by weighing all foods consumed, and folate intake was calculated with a computer-aided dietary analysis system. Folate concentrations in plasma and erythrocytes were determined via microbiological methods and in plasma by HPLC. Urine excreted over the same period of time was collected and assayed for folate catabolites, para-aminobenzoylglutamate (pABG) and para-acetamidobenzoylglutamate (ApABG) by reverse-phase HPLC after affinity chromatography. The mean folate intake was 206.9+/-90.8 mug DFE/d, and the mean concentrations in plasma and erythrocytes were 10.5+/-3.7 and 249.9+/-77.8 ng/mL, respectively. Erythrocyte folate concentration was low in 2.8% of the subjects (<140 ng/mL) and was marginal in 5.5% (140-156 ng/mL). The mean plasma tHcy concentration was 12.7+/-0.2 nmol/mL, and 11% of the subjects evidenced hyperhomocysteinemia (>/=15 nmol/mL). The mean urinary excretion levels of pABG and ApABG were 10.7+/-3.8 and 89.1+/-19.5 nmol/d, respectively. The means of folate reserve and folate turnover rate were 26.2+/-11.6 and 10.5+/-3.9, respectively. We noted positive relationships between folate intake and the folate concentrations in plasma and erythrocytes, as well as the urinary excretions of ApABG and total folate catabolites. In addition, the erythrocytic folate concentrations were positively associated with the urinary excretions of ApABG and total folate catabolites. In conclusion, the folate status of Korean women of childbearing age was marginally deficient with inadequate concentrations of erythrocyte folate and elevated plasma tHcy, largely due to insufficient folate intake. The marginally deficient folate status was confirmed by the low excretion of folate catabolites in urine.     

Piperine enhances the bioavailability of the tea polyphenol (-)-epigallocatechin-3-gallate in mice

(-)-Epigallocatechin-3-gallate (EGCG), from green tea (Camellia sinensis), has demonstrated chemopreventive activity in animal models of carcinogenesis. Previously, we reported the bioavailability of EGCG in rats (1.6%) and mice (26.5%). Here, we report that cotreatment with a second dietary component, piperine (from black pepper), enhanced the bioavailability of EGCG in mice. Intragastric coadministration of 163.8 micromol/kg EGCG and 70.2 micromol/kg piperine to male CF-1 mice increased the plasma C(max) and area under the curve (AUC) by 1.3-fold compared to mice treated with EGCG only. Piperine appeared to increase EGCG bioavailability by inhibiting glucuronidation and gastrointestinal transit. Piperine (100 micromol/L) inhibited EGCG glucuronidation in mouse small intestine (by 40%) but not in hepatic microsomes. Piperine (20 micromol/L) also inhibited production of EGCG-3"-glucuronide in human HT-29 colon adenocarcinoma cells. Small intestinal EGCG levels in CF-1 mice following treatment with EGCG alone had a C(max) = 37.50 +/- 22.50 nmol/g at 60 min that then decreased to 5.14 +/- 1.65 nmol/g at 90 min; however, cotreatment with piperine resulted in a C(max) = 31.60 +/- 15.08 nmol/g at 90 min, and levels were maintained above 20 nmol/g until 180 min. This resulted in a significant increase in the small intestine EGCG AUC (4621.80 +/- 1958.72 vs. 1686.50 +/- 757.07 (nmol/g.min)). EGCG appearance in the colon and the feces of piperine-cotreated mice was slower than in mice treated with EGCG alone. The present study demonstrates the modulation of the EGCG bioavailablity by a second dietary component and illustrates a mechanism for interactions between dietary chemicals.     

Effects of lycopene supplementation on plasma and tissue lycopene levels in various rodent strains

Lycopene has been shown to have various biologic effects, and rats and mice are often used for elucidating its in vivo effects and mechanisms. Here, we compared plasma and tissue lycopene levels in F344 rats, BALB/c mice, nude mice, and gerbils by oral supplementation with lycopene (20 mg/kg BW x 2d) every other morning for 10 days. We found that livers accumulated substantially more lycopene than kidneys and that the hepatic lycopene contents varied greatly in these animals, with gerbils being most efficient (1432 +/- 235 nmol/g), followed by nude mice (524 +/- 133 nmol/g), F344 rats (28 +/- 11 nmol/g), and BALB/c mice (5 +/- 2 nmol/g). Plasma lycopene concentrations also varied greatly, of which the highest was found in gerbils (667 +/- 160 nmol/L), followed by nude mice (224 +/- 51 nmol/L), then by BALB/c mice and F344 rats (198 +/- 52 and 139 +/- 41 nmol/L, respectively). Interestingly, plasma and tissue beta-carotene concentrations in these animals were markedly decreased by lycopene supplementation. To determine the steady-state levels of plasma lycopene, we fed 10 gerbils with lycopene (20 mg/kg BW x 2d) for 20 days, and we found a steady-state level of plasma lycopene between 597 to 722 nmol/L. Our results demonstrate that gerbils and nude mice are better accumulators than F344 rats and BALB/c mice, and that the former species may be more useful for studying the in vivo effects of lycopene.     

Development of a dietary model for the study of mild zinc deficiency in humans and evaluation of some biochemical and functional indices of zinc status

After a 1-wk baseline period, a dietary regimen was developed to induce mild zinc deficiency in 15 males (aged 25.3 +/- 3.3 y, mean +/- SD). The regimen consisted of 1 wk on a liquid diet containing 0.6 mg Zn/d and molar ratios of phytate to zinc (phy:Zn) and of phytate X calcium to zinc [(phy X Ca): Zn] of 209 and 4116, respectively, followed by 6 wk on a diet based on soy protein and egg albumin containing 4 mg Zn/d and with phy:Zn and (Ca X phy):Zn of 70 and 2000, respectively. Subjects were then repleted with 30 mg Zn/d for 2 wk. Fasting blood and urine samples were taken weekly. Changes were observed in mean plasma (mumol/L) and urinary zinc (mumol/d): baseline 97.0 +/- 10.9 and 8.0 +/- 2.7, depletion 80.1 +/- 13.4 and 4.3 +/- 2.3, and repletion 100.8 +/- 13.6 and 8.2 +/- 3.1, respectively (P less than 0.05); taste acuity (0.05 less than P less than 0.10); and cellular immune responses (P less than 0.05). Activities of plasma angiotensin-1-converting enzyme and acidic alpha-D-mannosidase were unchanged. Mild zinc deficiency was induced by the dietary regimen.     

Protocatechuic acid is the major human metabolite of cyanidin-glucosides

The metabolic fate of dietary anthocyanins (ACN) has not been fully clarified in humans. In all previous studies, the proportion of total ACN absorbed and excreted in urine was <1% intake. This study aimed to elucidate the human metabolism of cyanidin-glucosides (CyG) contained in blood orange juice (BOJ). One liter of BOJ, containing 71 mg CyG, was consumed by 6 healthy, fasting volunteers. Blood, urine, and fecal samples were collected at baseline and at different times up to 24 h after juice consumption. The content of native CyG, glucuronidated/methylated derivatives, and various phenolic acids was determined by HPLC/MS/MS. The serum maximal concentration of cyanidin-3-glucoside (Cy-3-glc) was 1.9 +/- 0.6 nmol/L and that of protocatechuic acid (PCA) was 492 +/- 62 nmol/L at 0.5 h and 2 h after juice consumption, respectively. The calculated total amounts in plasma corresponded for Cy-3-glc to 0.02% and for PCA to 44% of CyG ingested. CyG and glucuronidated/methylated metabolites, but not PCA, were detected in urine. ACN recovered in 24-h urine collections represented approximately 1.2% of the ingested dose. Both CyG (1.90 +/- 0.04 nmol/g) and PCA (277 +/- 0.2 nmol/g) were recovered in 24-h fecal samples. Data explained the metabolic fate of 74% of BOJ ACN. PCA was for the first time, to our knowledge, identified in humans as a CyG metabolite, accounting for almost 73% of ingested CyG. A high concentration of PCA may explain the short-term increased plasma antioxidant activity observed after intake of cyanidin-rich food and it can also contribute to the numerous health benefits attributed to dietary ACN consumption.     

Values of water-soluble vitamins in blood and urine of Japanese young men and women consuming a semi-purified diet based on the Japanese Dietary Reference Intakes

We investigated the levels of water-soluble vitamins except for vitamin B6 in the blood and urine of Japanese college male (n = 10) and female (n = 10) students. They consumed for 7 d a semi-purified diet based on Japanese Dietary Reference Intakes to assess the Recommended Dietary Allowances (RDA) for water-soluble vitamins and to present some new normal values for blood and urine levels of water-soluble vitamins in Japanese. The blood and the 24-h urine samples were collected on the last day of the experiment and measured. The values of total vitamin B1 in whole blood, total vitamin B2 in whole blood, total cyanocobalamin in serum, total nicotinamide in whole blood, total pantothenic acid in whole blood, total folates in serum, total biotin in serum, and ascorbic acid in plasma were 104+/-17 pmol/mL (mean+/-SD), 216+/-25 pmol/mL, 0.34+/-0.05 pmol/mL, 59.1+/- 5.0 nmol/ mL, 2.45+/-0.37 nmol/mL, 15.6+/-4.6 pmol/mL, 8.3+/-0.5 pmol/mL, and 62+/-10 nmol/mL, respectively, in males, and 90+/-23, 234+/-18, 0.67+/-0.20, 61.9+/-6.0, 2.48+/-0.30, 30.2+/-8.6, 8.4+/-0.3, and 67+/-14, respectively, in females. There was a significant difference in the values of cyanocobalamin and total folates between men and women. The urinary excretion of vitamin B1, vitamin B2, cyanocobalamin, sum of the catabolic metabolites of nicotinamide, pantothenic acid, folates, biotin, and ascorbic acid were 665+/-114 nmol/d, 562+/-325 nmol/d, 93+/-31 pmol/d, 84+/-26 micromol/d, 9.3+/-2.3 micromol/d, 19.4+/-2.8 nmol/d, 83+/-18 pmol/d, and 148+/-51 micromol/d, respectively, in males, and 495+/-212, 580+/-146, 145+/-49, 83+/-19, 16.9+/-1.3, 22.7+/-2.7, 83+/-23, and 140+/-51, respectively, in females. There was a significant difference in the urinary excretion of cyanocobalamin, pantothenic acid and total folates between men and women. These values will be useful for the nutritional assessment of water-soluble vitamins for Japanese, although the examination period was short. In future, an experiment with various age groups and re-evaluation by repeated experiments will provide more accurate values.     

Magnesium, zinc, and copper status of US Navy SEAL trainees

Magnesium, zinc, and copper status of 270 US Navy Sea, Air, and Land (SEAL) trainees was determined from dietary intakes and biochemical profiles. Although mean intakes exceeded the Recommended Dietary Allowances or the Estimated Safe and Adequate Intake range, intakes of 34%, 44%, and 37% of the trainees were below the recommendations for Mg, Zn, and Cu, respectively. Mean plasma concentrations were 0.85 +/- 0.004 mmol/L, 13.4 +/- 0.2 mumol/L, and 16.5 +/- 0.2 mumol/L for Mg, Zn, and Cu respectively. Mean 24-h urinary excretions were 5.7 +/- 0.2 mmol, 11.1 +/- 0.3 mumol, and 0.05 +/- 0.003 mumol, for Mg, Zn, and Cu, respectively. The data provided by the present study should be useful for comparing other physically active male populations.     

Neither glutamine nor arginine supplementation of diets increase glutamine body stores in healthy growing rats

The aim of the work was to resolve whether glutamine and arginine supplemented diets affect plasma and tissue (muscle, liver and intestinal mucosa) glutamine concentrations, as well as glutaminase and glutamine synthetase specific activities. The trial was performed in growing rats fed 10% protein diets for 3 weeks. Protein sources were: whey proteins (W); whey proteins+free glutamine (WG); whey proteins+arginine (WA); and casein+wheat protein hydrolysate+acid whey (39:39:22), as source containing protein-bound glutamine (CGW). Rats fed the control diet (6.4% glutamine) (W) showed comparable glutamine body stores to those of rats fed the WG diet. In fact, glutamine sup- plementation down-regulated the hepatic glutamine synthetic capacity of growing rats (W/WG: 6.8+/-0.3 vs 6.0+/-0.2 nmol/min/mg protein). Arginine supplementation of the diet (up to 9% of the protein content) resulted in a decrease in plasma and tissue glutamine concentrations (W/WA: plasma, 1218+/-51 vs 1031+/-48 micromol/L; liver 7.5+/-0.4 vs 6.5+/-0.2 micromol/g; muscle: 5.7+/-0.2 vs 4.0+/-0.2 micromol/g). These data suggest that glutamine supplementation of the diet does not increase plasma and tissue glutamine concentrations in healthy growing rats, while the addition of arginine to the diet decreases glutamine body stores.     

Intestinal excretion of endogenous zinc in Guatemalan school children

The intestine is the major route of excretion of endogenous zinc (Zn) and has a key role in maintaining Zn homeostasis. The principal objective of this paper is to provide an interpretative report of quantities of endogenous fecal Zn (EFZ) excreted by rural Guatemalan school children fed either normal or low phytate maize as their principal food staple. EFZ was measured by a Zn stable isotope technique. EFZ did not differ between control and low phytate maize groups. The overall EFZ (n = 53) was (mean +/- SD) 1.56 +/- 0.69 mg Zn/d or 0.07 +/- 0.03 mg Zn x kg body wt(-1) x d(-1). EFZ was not correlated with the quantity of Zn absorbed. The estimated EFZ at the level of absorption that matched the physiologic requirement (EFZ(PR)) did not differ from the above mean value. The EFZ(PR) of 0.07 +/- 0.03 mg Zn/kg body wt is twice the value currently used in the estimation of Dietary Reference Intakes. Supported by other recent childhood data, these results suggest that the current estimates of EFZ(PR) used in the calculation of Zn requirements for children are misleadingly low.     

Riboflavin and riboflavin-derived cofactors in adolescent girls with anorexia nervosa

BACKGROUND: Thyroid hormones, riboflavin, riboflavin cofactors, and organic acids were assessed in girls with anorexia nervosa. OBJECTIVE: The objective was to examine the effect of malnutrition and low thyroid hormone concentrations on erythrocyte and plasma riboflavin metabolism and their relation with urinary organic acid excretion. DESIGN: Seventeen adolescent girls with anorexia nervosa [body mass index (BMI; in kg/m2): 14.8 +/- 2.2] and 17 age-matched, healthy girls (control subjects; BMI: 20.5 +/- 2.2) took part in the feeding study. Erythrocyte and plasma riboflavin as well as riboflavin cofactors (flavin mononucleotide and flavin adenine dinucleotide) were assessed by HPLC, whereas urinary organic acids were assessed by gas chromatography-mass spectrometry. RESULTS: Anorectic patients who began a feeding program had higher erythrocyte riboflavin (3.5 +/- 2.2 compared with <0.1 nmol/mol hemoglobin; P < 0.001), lower plasma flavin adenine dinucleotide (57.8 +/- 18.5 compared with 78.5 +/- 54.3 nmol/L; P < 0.05), and higher urinary ethylmalonic acid (7.12 +/- 4.39 compared with 1.3 +/- 2.8 micromol/mmol creatinine; P < 0.001) and isovalerylglycine (7.65 +/- 4.78 compared with 3.8 +/- 0.9 micromol/mmol creatinine; P < 0.05) concentrations than did control subjects. Triiodothyronine concentrations were low and negatively correlated with plasma riboflavin concentrations (r = -0.69, P < 0.01). Not all patients showed improvements in these biochemical indexes after 30 d of refeeding. CONCLUSIONS: The low triiodothyronine concentrations observed in anorexia nervosa could alter the extent of riboflavin conversion into cofactors, thus leading to high erythrocyte riboflavin concentrations, low plasma flavin adenine dinucleotide concentrations, and high rates of ethylmalonic acid and isovalerylglycine excretion.