Inhibitory effect of captan in the small intestine absorption capacity of the mouse

1994 ◽  
Vol 53 (5) ◽  
Author(s):  
S.J. Iturri ◽  
J. Soto
Keyword(s):  
Small Intestine ◽  
Inhibitory Effect ◽  
Absorption Capacity ◽  
Small Intestine Absorption

Inhibitory Effect of Baicalin on Disaccharidase in Small Intestine

2009 ◽  
Vol 7 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Shu-Jing GU ◽  
Li LIU ◽  
Yao-Wu LIU ◽  
Xin-Yue JING ◽  
Xiao-Dong LIU ◽  
...  
Keyword(s):  
Small Intestine ◽  
Inhibitory Effect

scholarly journals Dietary ascorbic acid lowers the concentration of soluble copper in the small intestinal lumen of rats

1994 ◽  
Vol 71 (5) ◽  
pp. 701-707 ◽  
Author(s):  
G. J. Van Den Berg ◽  
S. YU ◽  
A. G. Lemmens ◽  
A. C. Beynen
Keyword(s):  
Ascorbic Acid ◽  
Small Intestine ◽  
Liquid Phase ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Intestinal Lumen ◽  
Distal Intestine ◽  
Small Intestinal ◽  
Ascorbic Acid Supplementation

We tested the hypothesis that ascorbic acid in the diet of rats lowers the concentration of soluble Cu in the small intestine, causing a decrease in apparent Cu absorption. Male rats were fed on diets adequate in Cu (5 mg Cu/kg) without or with 10 g ascorbic acid/kg. The diet with ascorbic acid was fed for either 6 or 42 d. Ascorbic acid depressed tissue Cu concentrations after a feeding period of 42, but not after 6 d. Dietary ascorbic acid lowered apparent Cu absorption after 6, but not after 42 d. The lowering of tissue Cu concentrations after long-term ascorbic acid feeding may have increased the efficiency of Cu absorption, and thus counteracted the inhibitory effect of ascorbic acid. Dietary ascorbic acid caused a significant decrease in the Cu concentrations in the liquid phase of both the proximal and distal parts of the small intestinal lumen. This effect was due to both a decrease in the amount of Cu in the liquid digesta and an increase in the volume of the liquid phase; only the latter effect for the distal intestine was statistically significant. We conclude that ascorbic acid supplementation lowers Cu absorption by decreasing the concentration of soluble Cu in the small intestine.

Intestinal distribution of intrinsic factor and vitamin B12 absorption

1965 ◽  
Vol 208 (1) ◽  
pp. 14-17 ◽  
Author(s):  
Kunio Okuda ◽  
Katsumi Sasayama
Keyword(s):  
Small Intestine ◽  
Vitamin B12 ◽  
Large Intestine ◽  
Intrinsic Factor ◽  
Vitamin B ◽  
Vitamin B12 Absorption ◽  
Small Intestine Absorption

Evidence is presented that intrinsic-factor (IF) activity is present in the small intestine as far down as the ileal end. Physiologic doses of radioactive vitamin B12 without IF were applied directly into various levels of the intestine by surgical and other means in man and rats, and significant absorption was obtained from the small intestine. Absorption inhibition by ethylenediaminetetraacetate and its counteraction by Ca ion demonstrated that such absorption was dependent on IF action. The large intestine was shown to be incapable of physiologic absorption of vitamin B12, and IF was totally ineffective. It is proposed that physiologically, gastric IF descends with some activity in the small intestine, where more of the food vitamin B12 is liberated by digestion and subjected to IF.

scholarly journals Tolerance to low-digestible carbohydrates: symptomatology and methods

2001 ◽  
Vol 85 (S1) ◽  
pp. S17-S21 ◽  
Author(s):  
Philippe Marteau ◽  
Bernard Flourié
Keyword(s):  
Small Intestine ◽  
Breath Test ◽  
Absorption Capacity ◽  
Subjective Symptoms ◽  
Intersubject Variability ◽  
Intrasubject Variability ◽  
Hydrogen Breath Test ◽  
Experimental Conditions ◽  
Double Blind ◽  
Double Blind Placebo

Low-digestible carbohydrates (LDCs) are incompletely or not absorbed in the small bowel and fermented in the colon. They are usually well tolerated but may also have some dose-related undesirable effects due to their natural osmotic potential and/or excessive fermentation: borborygmi, excessive flatus, bloating, abdominal cramps and eventually diarrhoea. There is an important intersubject variability in the tolerance to LDCs because of differences in absorption capacity, motility pattern, colonic response and intestinal sensitivity. There is also a great intrasubject variability, depending on the type of LDC, dosage and type of consumption. Absorption of LDC in the small intestine can be assessed using hydrogen breath test or intubation techniques or analysis of ileostomy effluents. Double-blind, placebo-controlled studies are required to assess the subjective symptoms of intolerance, and the experimental conditions may influence the results.

scholarly journals Active Sugar Transport by the Small Intestine

1968 ◽  
Vol 52 (3) ◽  
pp. 482-494 ◽  
Author(s):  
Robert G. Faust ◽  
Mary G. Leadbetter ◽  
Regina K. Plenge ◽  
Alston J. McCaslin
Keyword(s):  
Small Intestine ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Density Gradient Centrifugation ◽  
Gradient Centrifugation ◽  
Sugar Transport ◽  
Initial Step ◽  
Inhibitory Effect ◽  
Glucose Binding ◽  
Brush Borders

Tris-disrupted and intact brush border membrane preparations from mucosa of hamster jejunum were capable of preferentially binding actively transported D-glucose in a similar manner. Density gradient centrifugation of the Tris-disrupted brush borders indicated that D-glucose was bound to a fraction containing the cores or inner material of the microvilli. The properties of this binding were examined with the Tris-disrupted brush border preparation. Actively transported sugars competitively inhibited preferential D-glucose binding, whereas no effect was observed with nonactively transported sugars. Neither actively nor nonactively transported amino acids affected D-glucose binding. D-Glucosamine, which is not actively transported, was inhibitory to preferential D-glucose binding as well as to the active transport of D-glucose by everted sacs of hamster jejunum. No inhibitory effect was observed with the same concentration of D-galactosamine. Preferential D-glucose binding was also inhibited by sulfhydryl-reacting compounds, Ca2+, and Li+ ions. On the other hand, Mg2+ was shown to be stimulatory and Na+, NH4+, and K+ had no effect on this phenomenon. The results of these experiments suggest that preferential D-glucose binding to brush borders is related to the initial step in active sugar transport by the small intestine.

scholarly journals Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY

1999 ◽  
Vol 276 (2) ◽  
pp. G550-G555 ◽  
Author(s):  
Xiao-Tuan Zhao ◽  
John H. Walsh ◽  
Helen Wong ◽  
Lijie Wang ◽  
Henry C. Lin
Keyword(s):  
Small Intestine ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Inhibitory Effect ◽  
Proximal Half

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat ( P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist ( P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist ( P< 0.05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

Sign in / Sign up

Export Citation Format

Share Document