Inhibition Of Intestinal Absorption Research Articles

Inhibition of Intestinal Absorption by Bile Acids

Inhibition of Intestinal Absorption by Bile Acids

Inhibition of Intestinal Absorption by Bile Acids

Inhibition of Intestinal Absorption by Bile Acids

フザレノンX投与ラットにおけるグルコース腸吸収阻害について

フザレノンX投与ラットにおけるグルコース腸吸収阻害について

Reduction of serum phenylalanine levels in PKU rats with intestinal absorption inhibitors of phenylalanine (PHE): 61

It has been often suggested that inhibition of the intestinal absorption of PHE would be a new approach for PKU treatment. We have previously shown that a PKU model for dietetic studies is obtained by means of the synergistic inhibition of Phenylalanine-Hydroxylase with p-chlorophenylalanine + cotrimoxazole (daily intraperitoneal injection of the 2 inhibitors leads to hyperphenylalaninemia without need for a phenylalanine load). Addition of beta-2-thienylalanine (THI) or phenylalaninol (PHE-ol) to the diet (1g%) significantly reduced phenylalaninemia: PHE: 1.30 ± 0.30, + THI : 0.70 ± 0.27, + PHE-ol:0.87 + 0.29 mmol/l. However, the effectiveness of THI or PHE-ol was mainly dependent on diet quality: with 5 isonitrogenous-isoosmotic diets (amino acids, lactalbumin & its hydrolysate, casein & its hydrolysate), decrease of serum PHE with THI or PHE-ol only occurred with high PHE diets (inhibitor/PHE molar ratio 1.4), without significant difference between results with intact or hydrolysed protein diets. It has been claimed that amino acid (AA) changes in serum, liver and brain, induced by hyperPHE, could explain disturbed protein synthesis in PKU; we confirm such changes in our PKU model (mainly: essential AA decrease in serum, liver and brain), however AA imbalance did not disappear on THI or PHE-ol supplemented diets. These data suggest that PHE analogues (such THI or PHE-ol)used in diets to decrease intestinal absorption of PHE cannot ensure serum PHE reduction comparable to that obtained with PHE restricted diets.

Pharmacological properties of galenic preparations. II. Intestinal absorption inhibitor of alkaloid in the Scopolia extract.

Pharmacological properties of galenic preparations. II. Intestinal absorption inhibitor of alkaloid in the Scopolia extract.

Gastrin Inhibition of Intestinal Absorption in Dogs

We compared the effects of endogenous gastrin and exogenous pentapeptide on intestinal absorption of sodium, potassium, water, and glucose. Jejunal and ileal loops were isolated from the rest of the gut in anesthetized dogs, and a physiological solution containing these substances was instilled in the loops for 15-min periods. Absorption was determined by the recovery of water and solutes in the solution evacuated from the loops. Intravenous pentagastrin (5.0 μg per kg-hr) inhibited absorption of sodium, potassium, and water from the ileum and jejunum and glucose from the ileum. Endogenously released gastrin (evoked by instilling a 5% acetylcholine solution in the stomach to bathe the antral mucosa) caused inhibition of absorption of sodium, potassium, water, and glucose from both jejunal and ileal loops. Intravenously administered secretin had no effect on intestinal absorption in this preparation.

Inhibition of intestinal absorption and improvement of oral glucose tolerance by biguanides in the normal and in the streptozotocin-diabetic rat.

In the rat the assumption of a primary effect of moderate doses of biguanides on intestinal absorption is supported by the following results: 1. The tolerance to parenteral glucose administration was not improved. — 2. Afteroral pretreatment the hyperglycaemia induced byoral glucose was decreased. — 3. After pretreatmentin vivo the transport of glucose through the intestinal wall was inhibited. — 4. The intestinal glucose transport was inhibited alsoin vitro in the presence of biguanides at concentrations to be expected in intestinal tissuein vivo after efficient doses. — 5. In the streptozoocin-diabetic rat there was a strong correlation between the feeding state and the hypoglycaemie effect of biguanides. In streptozotocin-diabetic rats previously starved and then refed, the hypoglycaemie effect decreased with decreasing doses of the diabetogenic agent. — 6. The relative potency of various biguanides was similar with regard to their effects on hyperglycaemia and on the intestinal glucose transport. — The results suggest, however, that in the rat further events, probably triggered by the inhibition of intestinal absorption, are involved in the mechanism of action of biguanides.

The inhibition of intestinal absorption of phenylalanine in the rhesus monkey.

Summaryβ-2-Thienylalanine, cycloleucine, and parachlorophenylalanine have been shown to acutely reduce intestinal absorption of an oral phenylalanine load. Combined with phenylalanine, they reduce plasma tryptophan levels more than phenylalanine alone.Whether their oral administration will be of benefit in allowing a more liberal diet in phenylketonuric children requires more investigation.

Pharmacologic and toxicologic evaluation of 2-( N-tetradecyl- N-ethylamino)-2-methyl-1,3-propanediol hydrochloride, an inhibitor of intestinal absorption

2-( N-Tetradecyl- N-ethylamino)-2-methyl-1,3-propanediol hydrochloride (I) and Cetrimide caused a dose responsive inhibition of growth rate of rats which is, at least in part, due to a decrease in food and water consumption. The pharmacologic profile of I does not resemble that of the centrally acting anorexigenic agent, d-amphetamine. The acute toxicity of I in rodents is low, and hyperplasia and marked keratosis of the epithelium of the esophagus and nonglandular portion of the stomach were the only histopathologic changes observed. Pathologic evidence of toxicity was not observed in cats, dogs, or monkeys given active doses of I. The correlation in potency between Cetrimide and I as surfactants, as irritants to mucous membranes, as irreversible noncompetitive inhibitors of induced contractions of the isolated ileum and jejunum, and as inhibitors of active transport in the gastrointestinal tract suggest that these compounds interfere locally with the energy mechanisms of the cells of the alimentary canal. This, in combination with local irritation of the esophagus, may be responsible for the observed anorexigenic effects of these compounds.

Inhibition of intestinal absorption.

Journal Article INHIBITION OF INTESTINAL ABSORPTION Get access P.A. SANFORD, Ph.D. P.A. SANFORD, Ph.D. Department of Physiology, University of Sheffield Search for other works by this author on: Oxford Academic PubMed Google Scholar British Medical Bulletin, Volume 23, Issue 3, September 1967, Pages 270–274, https://doi.org/10.1093/oxfordjournals.bmb.a070570 Published: 01 September 1967

AUTORADIOGRAPHIC STUDY OF SUGAR AND AMINO ACID ABSORPTION BY EVERTED SACS OF HAMSTER INTESTINE

Autoradiographs were prepared from frozen sections of everted sacs of hamster jejunum which had been incubated in vitro with C(14)- or H(3)-labeled sugars and amino acids. When such tissue was incubated in 1 mM solutions of L-valine or L-methionine, columnar absorptive cells at tips of villi accumulated these amino acids to concentrations ranging from 5 to 50 millimoles per liter of cells. Quantitative data were obtained by microdensitometry of C(14) autoradiographs. Similar, though less striking, results were obtained with the sugars: galactose, 3-0-methylglucose, alpha-methylglucoside, and 6-deoxyglucose. In all cases the marked "step-up" in concentration occurred near the brush border of the cell, and a "step-down" in concentration occurred at the basal pole of the cell. Known inhibitors of intestinal absorption, e.g., phlorizin in the case of sugars, blocked the concentrative step at the luminal border of the absorptive cell. It is inferred from these data that active transport systems for sugars and amino acids reside in the brush border region of the cell. Additional evidence suggests that the basal membrane of the cell may be the site of both a diffusion barrier and a weak transport system directed into the cell.

Enhancement of inhibition of intestinal absorption by cetrimide-phloridzin combination.

Enhancement of inhibition of intestinal absorption by cetrimide-phloridzin combination.