Intestinal absorption of biotin in the rat

We examined the absorption of biotin using the in vivo intestinal loop technique. Jejunal segments from male rats were filled with solutions containing [3H]biotin and [14C]inulin in Krebs-Ringer phosphate buffer, pH 6.5. Absorption was determined on the basis of luminal tritium disappearance after correction for inulin recovery. At biotin concentrations of 0.1 and 5.0 microM, luminal biotin disappearance was linear for at least 10 min. At biotin concentrations ranging from 2.3 nM to 75 microM, 10-28% of the administered dose was absorbed in 10 min. The concentration dependence of luminal biotin disappearance is consistent with the presence of both saturable and nonsaturable (linear) components of biotin uptake, with estimated Km = 9.6 microM and Jmax = 75.2 pmol/(2.5 cm loop X min). The rate constant for nonsaturable uptake is 3.1 pmol/(2.5 cm loop X min X microM). We conclude that at biotin concentrations less than 5 microM, biotin absorption proceeds largely by the saturable process, whereas at concentrations above 25 microM, nonsaturable uptake predominates. Additional studies demonstrated significantly less biotin uptake in the ileum than in the jejunum, a finding in agreement with previous in vitro studies.     

Dietary biotin intake modulates the pool of free and protein-bound biotin in rat liver

The current studies were undertaken to analyze the relationships among dietary biotin intake, hepatic free biotin and hepatic protein-bound biotin in rats. The biotin status of rats was manipulated through dietary intervention to model moderate biotin deficiency, adequacy, supplementation and pharmacologic biotin supplementation (0, 0.06, 0.6 and 100 mg/kg, respectively). Urinary biotin excretion was directly related to biotin intake, but no difference between biotin-adequate and biotin-supplemented rats was detected. In contrast, plasma biotin was directly and significantly regulated by biotin intake at every intake level. A hepatic free biotin pool was directly demonstrated in these studies, and like plasma, its size was directly related to dietary biotin intake. The relationship between dietary biotin intake and protein-bound biotin was also analyzed. Moderate biotin deficiency markedly decreased the abundance of each biotinylated polypeptide in rat liver. Biotin supplementation did not significantly elevate the abundance of biotinylated pyruvate, propionyl CoA, methylcrotonyl CoA or acetyl CoA carboxylase 1. The abundance of biotinylated acetyl CoA carboxylase 2, however, was significantly higher in biotin-supplemented rats. Pharmacologic biotin intake significantly reduced the abundance of biotinylated propionyl CoA and methylcrotonyl CoA carboxylase. These results indicate the following: 1) moderate biotin deficiency reduces free and protein bound biotin; 2) biotin intakes in rats that mimic the currently recommended daily value (DV) do not result in full protein biotinylation; and 3) pharmacologic supplementation may reduce the abundance of functional carboxylases.     

Effect of dietary cystine on methionine metabolism in rat liver

Cystine supplementation of adequate diets resulted in significantly higher hepatic levels of betaine-homocysteine methyltransferase. Other changes occurred but were a function of the basal diet. When the latter contained 0.25% methionine + 0.5% cystine, the additional cystine caused a markedly lower hepatic cystathionine synthase activity and lower levels of both adenosylmethionine and serine. The metabolic effect of these changes may be enhanced methionine retention and diminished transsulfuration.     

Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake.

Measurements of intake and uptake of cadmium in relation to diet composition were carried out in 57 nonsmoking women, 20-50 years of age. A vegetarian/high-fiber diet and a mixed-diet group were constructed based on results from a food frequency questionnaire. Duplicate diets and the corresponding feces were collected during 4 consecutive days in parallel with dietary recording of type and amount of food ingested for determination of the dietary intake of cadmium and various nutrients. Blood and 24-hr urine samples were collected for determination of cadmium, hemoglobin, ferritin, and zinc. There were no differences in the intake of nutrients between the mixed-diet and the high-fiber diet groups, except for a significantly higher intake of fiber (p < 0.001) and cadmium (p < 0.002) in the high-fiber group. Fecal cadmium corresponded to 98% in the mixed-diet group and 100% in the high-fiber diet group. No differences in blood cadmium (BCd) or urinary cadmium (UCd) between groups could be detected. There was a tendency toward higher BCd and UCd concentrations with increasing fiber intake; however, the concentrations were not statistically significant at the 5% level, indicating an inhibitory effect of fiber on the gastrointestinal absorption of cadmium. Sixty-seven percent of the women had serum ferritin < 30 micrograms/l, indicating reduced body iron stores, which were highly associated with higher BCd (irrespective of fiber intake). BCd was mainly correlated with UCd, serum ferritin, age, anf fibre intake. UCd and serum ferritin explained almost 60% of the variation in BCd.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intestinal calcium and lead absorption: effects of dietary lead and calcium

The combined effects of dietary calcium (Ca) and lead (Pb) status on intestinal Ca and Pb absorption and related parameters were investigated in young growing chicks. Dietary Pb intake resulted in two remarkable, apparently independent and essentially opposite effects on intestinal Ca and Pb absorption, depending on dietary Ca and Pb levels and duration of treatment. The initial response (1 week) to Ca deficiency was stimulated Ca absorption and calbindin-D level, regardless of dietary Pb intake. The later response (2 weeks) was a reversal, by Pb, of the early phase stimulation. Intestinal Pb absorption was similarly enhanced by Ca deficiency initially, and this response was also inhibited by prolonged dietary Pb intake. Ingestion of Pb by chicks fed adequate Ca resulted in generally elevated intestinal Ca absorption and calbindin-D levels after both 1 and 2 weeks. Intestinal Pb absorption was also increased in the adequate Ca situation, but only after 2 weeks at the lower levels of dietary Pb. The results underscore the complicated nature of Pb-Ca interactions and demonstrate the importance of thorough characterization of the animal model system.     

Effect of dietary methionine on utilization of tissue selenium from dietary selenomethionine for glutathione peroxidase in the rat

To study the effect of dietary methionine on the bioavailability of Se from selenomethionine ([Se]Met), weanling rats were first loaded with Se by feeding 0.5 mg Se as [Se]Met per kg diet of a low methionine (0.17% by analysis) torula yeast-based diet for 21 d, and then were fed an Se-deficient diet (less than 0.02 mg Se/kg) supplemented with 0, 0.4 or 0.9% methionine for 28 d. Plasma, liver and muscle Se increased 2.6-, 2.5- and 2.2-fold, respectively, during [Se]Met supplementation, and then the tissue Se declined exponentially during the Se-deficient diet period. Plasma, liver and muscle glutathione peroxidase (GSH-Px) activities decreased 43-50% during the [Se]Met supplementation period in spite of the increase in tissue Se. When these [Se]Met-loaded rats were fed the Se-deficient diet and supplemented with methionine, tissue GSH-Px activities increased significantly within 3 to 7 d, but then decreased for the remainder of the experiment. Calculation of the percentage of tissue Se present as Se in GSH-Px indicated that substantial Se from dietary [Se]Met was stored in tissues in a form different from GSH-Px when a low methionine diet was fed. These results indicate that the dietary methionine level can modulate the availability of Se from dietary [Se]Met and from stored tissue [Se]Met; the inability of stored [Se]Met to provide Se for GSH-Px synthesis over a prolonged period of time suggests that [Se]Met may not be an optimum form for Se supplementation.     

Effect of dietary pectin on iron absorption and turnover in the rat

The influence of dietary pectin on iron absorption and retention was studied in rats. Basal diet with low and normal iron levels were fed with and without addition of 2% citrus pectin. After 40 days rats were fasted for 24 hours and were given 59Fe in dilute HCl with or without 2% pectin by gavage. Whole-body counting techniques were employed to monitor 59Fe absorption and turnover. Rats maintained on low iron diet absorbed and retained a much higher proportion of 59Fe than rats maintained on normal level of iron. Dietary pectin at the level fed in this study had no influence on iron uptake and/or turnover in rats.     

Intestinal absorption of Cd in vitro.

Everted gut sacs from the rat were utilized to characterize the movement of Cd across the intestinal tract. Total uptake of Cd (tissue content plus serosal fluid content) after incubation for 30 min as a function of the Cd concentration in mucosal fluid (range 5 μm to 3.4 mm) exhibited first-order kinetics. However, tissue Cd concentrations approached a steady state (1–5 μm Cd/g tissue) within 30-min incubation with mucosal concentrations greater than 1.2 × 10^?4m. Serosal fluid demonstrated an increased rate of accumulation of Cd at the higher mucosal fluid concentrations. This increased rate preceded the attainment of a steady state in tissue Cd by approximately 10 min. These results are consistent with the hypothesis that Cd diffuses into the intestinal tissue where part is bound and the remainder passes into the serosal fluid. As the tissue concentration of Cd approaches a steady state, increasing amounts of Cd move into the serosal fluid.     

Intestinal iron absorption: regulation by dietary & systemic factors

Iron is an essential trace metal in human metabolism. However, imbalances in iron homeostasis are prevalent worldwide and have detrimental effects on human health. Humans do not have the ability to remove excess iron and therefore iron homeostasis is maintained by regulating the amount of iron entering the body from the diet. Iron is present in the human diet in number of different forms, including heme (from meat) and a variety of non-heme iron compounds. While heme is absorbed intact, the bioavailability of non-heme iron varies greatly depending on dietary composition. A number of dietary components are capable of interacting with iron to regulate its solubility and oxidation state. Interestingly, there is an emerging body of evidence suggesting that some nutrients also have direct effects on the expression and function of enterocyte iron transporters. In addition to dietary factors, body iron status is a major determinant of iron absorption. The roles of these important dietary and systemic factors in regulating iron absorption will be discussed in this review.     

Intestinal microflora and gastrointestinal adaptation in the rat in response to non-digestible dietary polysaccharides

1. A comparison was made of the effect of a fibre-free diet and diets containing non-digestible polysaccharides on rat caecal and colonic physiology and microflora. 2. All polysaccharide-containing diets led to enlargement of the caecum and colon, associated with increased weight of contents, and of tissue. Carboxymethylcellulose (CMC) had the most marked effect and animals given this also had watery faeces. 3. The density of bacteria in the caecum and colon varied significantly with diet and the proportion of aerobic bacteria in the flora was increased by the CMC diet. 4. In vitro, CMC and hydroxypropylmethylcellulose were poorly fermented. 5. There was a high correlation (caecum r 0.93; colon r 0.94) between tissue weight and wet weight of organ contents but no correlation with bacterial density, number of bacteria per organ, moisture content or short-chain fatty acid content. 6. It is concluded that caecal and colonic enlargement is due to tissue hypertrophy in response to increased bulk of contents, irrespective of the nature of that bulk which varies with diet; it is unlikely that short-chain fatty acids or other microbial metabolites are the stimulus for the trophic response seen when non-digestible dietary polysaccharides are fed to rats.     

Intestinal iron absorption in chronic alcoholics.

Chronic alcohol misusers frequently accumulate significant amounts of excess iron, but the mechanism of this loading is unknown. In vivo whole-body retention studies demonstrated, on average, a two-fold increase in intestinal iron absorption in six male chronic alcoholics. Degrees of iron loading as assessed by serum ferritin or hepatic iron levels did not correlate with alcohol consumption or liver function tests. In vitro studies of iron uptake at varying medium iron concentrations by duodenal mucosa biopsies showed increased iron uptake by tissue from the chronic alcoholics, particularly at the highest medium iron concentration used. Analysis of the uptake data showed similar Michaelis-Menten kinetic constants for uptake by tissue from control subjects and alcoholics. The analysis showed, in addition, a linear component for 59Fe uptake. This component was five-fold greater for the tissue from the chronic alcoholics compared to the controls at the highest medium iron concentration. 57Co-cyanocobalamin was included in the incubation medium as a tissue extracellular fluid marker (ECF). It was found that the apparent distribution volume of the ECF marker, reflecting tissue permeability, was 75% higher for the biopsies from the alcoholics compared to control subjects. These results, together with the previous reports of enhanced in vitro and in vivo intestinal permeability to 51Cr-EDTA in chronic alcoholics, indicate that unregulated increased iron absorption via the non-carrier-mediated paracellular route contributes to the iron overload in chronic alcoholics.