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At least 55 records · Page 3Linked to original sources
PubMed1991

Nonabsorbable marker and single, random stool samples used for measuring intestinal absorption of macronutrients in infants and children.

To measure intestinal absorption by using a single, random stool sample, polyethylene glycol (PEG), 1 g/d, and a constant diet were given to healthy infants, with a constant PEG-to-macronutrient ratio. After 10 d equilibration, apparent intestinal absorption of macronutrients was estimated from a standard 3-d metabolic balance and compared with that estimated by using the ratio of PEG to macronutrients in a single random sample of feces. Correlation coefficients for this comparison were 0.649, 0.715, and 0.924 for nitrogen, carbohydrate, and fat, respectively. Additionally, apparent intestinal absorptions estimated from two separate consecutive 3-d metabolic-balance studies were compared, showing correlation coefficients of 0.106, 0.653, and 0.463 for nitrogen, carbohydrate, and fat, respectively. The random sample-marker technique appears to be acceptable for measuring apparent absorption of macronutrients and is at least as accurate as a standard 3-d metabolic-balance study.

Child, Preschool↗
PubMed1991

The effect of exercise associated with acute poisoning with potassium nitrate and sodium nitrite on the processes of intestinal absorption of D-xylose in rats.

The intestinal absorption of D-xylose was studied during acute poisoning of male Wistar rats receiving intragastrically potassium nitrate and sodium nitrite and small intestine perfusion with these compounds. The metabolic parameters, Na+/K(+)-ATPase, alkaline phosphatase, oxygen uptake, and lactic acid level, were assessed in the small intestine mucosa one hour after administration of these compounds. Exercise was demonstrated to reduce the intestinal absorption of D-xylose, to raise the level of lactic acid, and to increase the oxygen uptake by the small intestine mucosa, but caused no changes in the activity of Na+/K(+)-ATPase or alkaline phosphatase. Also, exercise failed to change the direction of the toxic effects of sodium nitrite but increased potassium nitrate toxicity as evidenced by reduced absorption of D-xylose from the intestine despite lack of changes of the enzymes Na+/K(+)-ATPase and alkaline phosphatase in the mucosa.

Alkaline Phosphatase↗
PubMed1988

Passive and carrier-mediated intestinal absorption components of captopril.

The intestinal absorption mechanism of captopril was investigated in fasted rats using a single-pass perfusion method. Captopril and captopril disulfide were analyzed by HPLC. A modified boundary-layer solution was applied to determine the apparent intestinal wall permeabilities (Pw*). The results indicated that captopril is very permeable in the small intestine but not in the colon, and the permeability in the small intestine is both pH and concentration dependent. The estimated parameters for the carrier are: Km*, 6 mM; Jmax*, 12 mM; and Pc*, 2. There is also a significant passive component to captopril absorption in the small intestine. Furthermore, the intestinal permeability of captopril was significantly decreased by the withdrawal of sodium from the perfusate (3 times), and the addition of 85 mM of gly-gly (2.5 times), 15 mM of gly-pro (4 times), dipeptide mixture (4.5 times), 0.5 mM of 2,4-dinitrophenol (4 times), and 10 mM of cephradine (6 times). This is the first demonstration that an angiotensin converting enzyme (ACE) inhibitor is at least in part transported by a carrier-mediated process in the intestine via the peptide carrier system. In addition, the results showed that the peptide carrier system can transport a substrate without a "N" terminal nitrogen atom.

Animals↗
PubMed1987

Intestinal absorption and metabolism of homoursodeoxycholic acid in rats.

Intestinal absorption, hepatic biotransformation and intestinal bacterial modification of the C25 homolog of ursodeoxycholic acid, homoursodeoxycholic acid, and its glycine conjugate, glycohomoursodeoxycholic acid, were studied in rats. Homoursodeoxycholic acid, like ursodeoxycholic acid, was efficiently absorbed from the intestine and rapidly excreted into the bile. Most (greater than 95%) of the absorbed homoursodeoxycholic acid was found to undergo beta-oxidation to form two C23 bile acids, norursodeoxycholic acid and nor-beta-muricholic acid during passage through the liver. Bacterial modification of homoursodeoxycholic acid was very similar to that of ursodeoxycholic acid. In the rat intestinal tract, glycohomoursodexycholic acid was deconjugated to form unconjugated homoursodeoxycholic acid which was then 7 beta-dehydroxylated to form homolithocholic acid.

Animals↗
PubMed1985

Intestinal absorption and metabolism of norcholic acid in rats.

Intestinal absorption and hepatic and intestinal bacterial biotransformations of norcholic acid, the C23 homologue of cholic acid, were studied in the rats. Norcholic acid, like cholic acid, was efficiently absorbed from the intestine and quickly secreted into the bile. Unlike the C24 bile acid, however, which is secreted by rat liver as its taurine conjugate, the C23 bile acid appeared in the bile predominantly as the unconjugated form. conjugated form. Bacterial modification of norcholic acid was similar to but less extensive than that of cholic acid. A considerable part of norcholic acid was left unchanged during its passage through the intestinal tract. A major bacterial metabolite of norcholic acid was the 7-dehydrogenation product, 7-ketonordeoxycholic acid, rather than the 7-dehydroxylation product, nordeoxycholic acid, though the reverse is true for cholic acid.

Animals↗
PubMed1987

Intestinal absorption of choline in rats.

The intestinal absorption of choline, an endogenous quaternary ammonium, from the rat jejunum has been investigated with an in situ ligated loop method and an in vitro everted sac method. Choline was absorbed rapidly from the ligated jejunum and structural analogs inhibited choline absorption competitively. In in vitro experiments, choline was transported from the mucosal fluid to the intracellular fluid against a concentration gradient and the rate of tissue uptake was highly affected by incubation temperature, aerobic condition and the presence of a metabolic inhibitor, 2,4-dinitrophenol. The tissue accumulation of choline was saturable at concentrations below 100 microM and, above this concentration the uptake ratio of choline (medium to tissue) was almost constant. One mM hemicholinium-3, which is well known to inhibit choline uptake by neurons through the choline specific carrier, also significantly inhibited choline uptake, especially at concentrations of choline below 100 microM. The fact that the choline uptake is linear in the presence of hemicholinium-3 shows that choline is partially absorbed by passive diffusion. The difference between the total tissue accumulation and choline uptake by the passive diffusional pathway followed Michaelis-Menten kinetics and the apparent Kt of 47 microM and Vmax of 4.1 nmol/ml intracellular fluid/min were determined by an in vitro everted sac method. These findings suggested that, a lower concentrations, choline was absorbed from the rat intestine mainly by an active transport system.

Animals↗
PubMed1978

Effects of vasoactive intestinal polypeptide on intestinal absorption and blood flow.

1. Intestinal absorption and blood flow in anaesthetized dogs was determined after I.V. infusion of vasoactive intestinal polypeptide (VIP) (1.75-175 ng/min) to determine the contribution of the cardiovascular changes to transport. 2. 22Na and 3H2O were utilized to determine the unidirectional fluxes of Na and H2O from saline perfused through the ileal lumen and the clearances of 3H2O were used to determine total and absorptive site blood flow. 3. Net Na and H2O absorption were reversed to secretion by VIP at 175 ng/min due to a significant decrease in unidirectional absorptive fluxes and smaller increases in secretory fluxes. 4. Arterial pressure and absorptive site blood flow were reduced in proportion to the changes in Na and H2O fluxes. 5. Total and absorptive site blood flow decreased and the blood flow resistances increased. 6. Prior treatment with guanethidine to suppress sympathetic effects did not greatly affect the responses to VIP. Prior treatment with atropine to suppress cholinergic effects inhibited most of the effects of VIP. 7. Absorptive site blood flow was linearly related to absorptive fluxes of Na and H2O but with different slopes for results from atropinized dogs as compared to those from dogs given VIP alone or VIP plus guanethidine. 8. It was concluded that VIP reduces gut absorption through a generalized cardiovascular effect and also through a mechanism which depends on the release of ACh by the gut.

Animals↗
PubMed1978

Intestinal absorption of fluoride preparations.

Gastric intestinal absorption of five different preparations of sodium fluoride was measured by means of ten hour urinary excretion. Best absorption was by nonenteric coated sodium fluoride. All three enteric coated preparations showed poorer absorption, with marked individual variations. Florical, the currently available preparation, showed better absorption than any enteric coated tablets and only slightly less than sodium fluoride alone. For active cochlear otospongiosis two capsules three times a day should be prescribed.

Administration, Oral↗
PubMed1988

Epithelial cell proliferation and intestinal absorptive function during starvation and refeeding in the rat.

1. Intestinal epithelial cell production and intestinal absorption were measured in fed, starved and refed rats. 2. Four days' starvation significantly decreased the crypt cell production rate (CCPR), absorption, small intestinal length and crypt cell population. 3. There was an immediate increase in absorption 1 day after refeeding, which preceded a slower increase in CCPR. The absorption rate then decreased progressively after refeeding, and was significantly lower than control levels 1 week after refeeding. The CCPR, however, increased more gradually, reaching control levels after 2 days and then 'overshooting' control values. 4. There was no significant change in the crypt cell population immediately after refeeding; thus we propose that the initial increase in absorption on refeeding is either due to an accelerated maturation rate of the enterocytes or to the migration of enterocytes from the base of the villus to the functional zone. 5. The rapid recruitment of absorptive function appeared to be a 'one-off' event, the villus compartment then having to wait for increased cell production in the crypts to repopulate the villi.

Animals↗
PubMed1988

Intestinal absorption of calcium in newborn piglets. Role of vitamin D.

The role of vitamin D for intestinal absorption of Ca was studied in neonatal piglets. Piglets of normal phenotype (heterozygotes) and piglets which suffered from pseudo-vitamin D deficiency rickets, type I, which were devoid of renal 25-cholecalciferol-1-hydroxylase were used for the experiments. Intestinal absorption of Ca was measured after an oral dose of 3-7 MBq 45CaCl2. Intestinal absorption of Ca was the same in heterozygotes and homozygotic rachitic piglets during the first 3-4 weeks of life. Ca absorption began to decline in rachitic piglets at the age of 4 weeks. In 8-week-old rachitic piglets intestinal Ca absorption was 50% of control piglets. Body weights of heterozygotes and rachitic piglets were the same at birth and no different weight gains were seen between the two groups during the first 4-5 weeks of life. No differences were observed during the first weeks of life in the concentrations of plasma Ca, inorganic-phosphate and alkaline-phosphatase activity between the groups. Hypocalcemia and hypophosphatemia developed in rachitic piglets between the 3rd and 5th weeks of life. Concentrations of 1,25-(OH)2D3 in plasma declined in heterozygote piglets from 130 +/- 26 to 88 +/- 19 pg/ml and in rachitic piglets from 67 +/- 37 to 23 +/- 11 pg/ml during the first 6 weeks. An intestinal nuclear 1,25-(OH)2D3 receptor was absent in neonatal piglets of both experimental groups. It is concluded that intestinal absorption of Ca in piglets during the first 2-4 weeks of life is independent of vitamin D.

Alkaline Phosphatase↗
PubMed1990

Differential effect of steroids and chloroquine on the intestinal absorption of aluminium and calcium.

In rats with normal renal function the intestinal absorption of aluminium appears to be partly vitamin D dependent. To further characterise the similarities between the absorption of aluminium and calcium we investigated the effects of dihydroxylated vitamin D metabolites, prednisolone, and chloroquine (CQ) in Sprague-Dawley rats with normal or reduced renal function. The latter agents interfere with lysosomal functions and have been reported to reduce the intestinal absorption of calcium, whereas vitamin D metabolites may stimulate the absorption of both aluminium and calcium. To assess the intestinal absorption of aluminium we monitored urinary aluminium excretion and serum aluminium concentrations following an oral load of 410 mumol aluminium. Calcium absorption was calculated from the differences between an orally administered dose of 45calcium and faecal excretion. In vitamin-D-deficient rats cholecalciferol and calcitriol augmented urinary aluminium excretion to a similar degree subsequent to an oral load whereas 24R,25(OH)2D3 was without an apparent effect. In vitamin-D-replete rats with normal renal function CQ (225 mg/kg i.p.; 3 days) as well as prednisolone (25 mg/kg; 7 days) significantly reduced calcium absorption (% dose) (CQ: 39 +/- 5%, prednisolone: 42 +/- 3%, control: 58 +/- 11%). In contrast neither drug reduced urinary aluminium excretion (CQ: 519 +/- 92, prednisolone: 494 +/- 137, control: 469 +/- 187 nmol/5 days) or the postload increase in serum aluminium following oral exposure. When aluminium was administered intravenously recovery of aluminium was comparable between treatment groups and controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1990

Acute effects of ursodeoxycholic and chenodeoxycholic acid on the small intestinal absorption of bile acids.

The effects of ursodeoxycholic acid and chenodeoxycholic acid on the small-intestinal absorption of endogenous bile acids were studied in patients with ileostomies who served as a model to investigate small-intestinal absorption in humans. In the control period, the eight patients excreted 327 +/- 91 (mean +/- standard error of the mean) mumol/8 h cholic acid and 214 +/- 38 mumol/8 h chenodeoxycholic acid by their ileal fluid. Following ursodeoxycholic acid administration (500 mg), ileal excretion of cholic acid increased to 517 +/- 96 mumol/8 h, and that of chenodeoxycholic acid increased to 337 +/- 42 mumol/8 h, indicating decreased absorption of these bile acids. Following chenodeoxycholic acid administration (500 mg), no significant increase of cholic acid excretion was observed, whereas chenodeoxycholic acid excretion increased as expected. It is concluded that following ursodeoxycholic acid administration the absorption of common bile acids from the small intestine decreases markedly. This effect of ursodeoxycholic acid on intestinal absorption of common bile acids probably is responsible for the decrease of their plasma concentrations, the reduction of their pool sizes, the increase of their fractional turnover rates, and most likely also contributes to the increased hepatic synthesis of cholic acid.

Adult↗
PubMed1976

Intestinal absorption of phosphate: action of protein synthesis inhibitors and glucocorticoids in the rat.

The effect of actinomycin D, cycloheximide and glucocorticoids on the intestinal absorption of phosphate was studied. The effective intestinal absorption of 32P and 47Ca was determined simultaneously in intact rats in vivo using a whole body counter. Both, actinomycin D and cycloheximide caused a significant diminution of the intestinal absorption of phosphate whereas calcium absorption was not altered. Experiments with the in situ ligated loop technique were performed to eliminate the possibility that the action of the protein synthesis inhibitors could be due to an altered intestinal motility effect. Phosphate absorption was also significantly diminished under this condition. On the other hand, the administration of glucocorticoids produced a significant inhibition of phosphate and calcium absorption in the rat in vivo. The reported results indicate that proteins and/or enzymes with a rapid turn-over are involved in the mechanism of phosphate intestinal absorption, and confirm previous observations that phosphate and calcium are transported across the intestine by different mechanisms.

Animals↗
PubMed1986

Intestinal absorption in the mechanically obstructed rat intestine: protection by prostaglandins.

Intestinal obstruction inhibits amino acid absorption. The inhibition, being dependent on the pathological changes of the absorptive epithelium, was considered as an index of injury and measured after varying periods of obstruction and after pretreatment with clindamycin, indomethacin, 16,16-dimethyl-PGE2 or arachidonic acid. A reduction in amino acid uptake was apparent after 2h of obstruction and was increasingly evident after 4, 6 and 18 h. During the late phase (after 6 h), inhibition was partly prevented by pretreatment with clindamycin, but the antibiotic was ineffective during the early phase (within the first 2 h). Bacterial colony counts of luminal contents of rats obstructed for 2 h, were not different from counts obtained in controls, but significantly lower than counts in rats that have been obstructed for 6 h. Pretreatment of rats with 16,16-dimethyl-PGE2 or with arachidonic acid prevented the early inhibitory effects of the obstruction. The findings suggest that the early inhibition in amino acid uptake may be related to metabolic changes that are correctable by the administration of 16,16-dimethyl-PGE2 or of arachidonic acid. The inhibition, during the late phase, is mainly related to an overgrowth of the enteric bacteria.

16,16-Dimethylprostaglandin E2↗
PubMed1976

Intestinal absorption of L-tryptophan in scleroderma.

The purpose of this investigation was to study the intestinal absorption of L-tryptophan and to assess the absorptive function of the intestine in scleroderma. The oral L-tryptophan loading test was performed in 31 cases of systemic scleroderma (progressive systemic sclerosis, PSS) and 3 cases of localized scleroderma. Serum levels of tryptophan and urinary excretion of indole-acetic acid (IAA) and indican (IS) were determined in order to assess intestinal absorption of tryptophan. In 10 cases the D-xylose test and in 4 cases Schilling's test was also performed. Furthermore, in vitro binding of L-tryptophan by plasma proteins in PSS and in other skin diseases as controls was studied. The normal increase in serum tryptophan after loading was noted in 17 cases (in 14 cases of PSS with a mild, slow progression in 3 cases of PSS with a severe, rapidly progressing course). In 10 of these cases, urinary excretion of IAA was higher than normal and in normal and in 3 cases excretion of urinary IS was also above normal. On the other hand, in 14 cases of severe, rapidly progressing PSS and in 2 of 3 cases of widespread linear scleroderma, serum levels of tryptophan were markedly depressed after loading, while urinary excretion of IAA and IS was normal. In all 4 cases studied, Schilling's test was normal, and only in 2 of 10 cases of PSS was the D-xylose test abnormal. It is concluded that in the majority of cases of PSS, intestinal absorpiton of tryptophan is normal as also is the absorptive function of the intestine. The slight rise in serum tryptophan after loading in some cases of PSS may be a result of increased binding of tryptophan by albumin.

Adolescent↗
PubMed1986

Metabolic acidosis enhances 1,25(OH)2D3-induced intestinal absorption of calcium and phosphorus in rats.

The effect of metabolic acidosis on the intestinal absorption of calcium (Ca) and phosphorus (P), plasma vitamin D metabolites and urinary excretion of Ca in adult rats treated with a small dose of 1,25(OH)2D3 were investigated. The rats in the experimental group received 1.8% ammonium chloride (NH4Cl) and a commercial chow, and their pair-fed controls received 0.45% NaCl. Both groups were given subcutaneously 1,25(OH)2D3. Intestinal absorption of Ca and P was measured by gut sac uptake of 45Ca and 32P. In the acidotic rats, duodenal, jejunal and ileal 45Ca uptake as well as jejunal and ileal 32P uptake were significantly increased. Plasma 1,25(OH)2D, 25(OH)D and 24,25(OH)2D were similar in both groups. 1,25(OH)2D3 treatment induced a greater calciuria in acidotic rats and increased their fractional excretion (FE) of Ca. An additional experiment showed increased 45Ca uptake by duodenum at a pH of 7.0 compared to pH 7.4. The present study suggests that NH4Cl-induced metabolic acidosis may enhance the effect of 1,25(OH)2D3 on intestinal absorption of Ca and P in the rat. However, the data from the study cannot exclude the possibility that acidosis may have a direct, vitamin D-independent effect on the intestine.

Acidosis↗