scholarly journals Influence of cholecalciferol (vitamin D3) on the initial kinetics of the uptake of calcium ions by rat small-intestinal mucosa (Short Communication)

1973 ◽  
Vol 134 (2) ◽  
pp. 667-669 ◽  
Author(s):  
J. M. O'Donnell ◽  
M. W. Smith

The uptake of Ca2+ by isolated small-intestinal mucosa from vitamin D-depleted and -repleted rats was analysed for the effects of vitamin D on initial kinetics. The rapid association of Ca2+ with the tissue, which is complete within 1min, was unaffected by the vitamin, whereas the subsequent, linear, uptake was significantly increased. Neither the tissue space accessible to inulin nor the permeability to thiourea was influenced by vitamin D treatment.

1968 ◽  
Vol 109 (3) ◽  
pp. 457-467 ◽  
Author(s):  
D. R. Fraser ◽  
E. Kodicek

1. The mechanism of vitamin D esterification in the rat was studied with liver, small-intestinal mucosa, pancreatic juice and blood plasma as enzyme sources and [1−3H]cholecalciferol, [U−14C]ergocalciferol and [4−14C]cholesterol as substrates. 2. No esterification of vitamin D could be detected with liver preparations nor with homogenates or acetone-dried powder extracts of intestinal mucosa. 3. Pancreatic juice esterified [1−3H]cholecalciferol with oleic acid, and specificity studies indicated that a cholesterol-esterifying enzyme was using vitamin D as substrate. 4. Plasma cholesterol-esterifying enzyme also esterified vitamin D. 5. The specificity of the esterification reaction is discussed in relation to (a) the molecular structure of the substrates and (b) their availability, in a micellar solution, to the enzyme. 6. It is concluded that cholesterol-esterifying enzymes esterify vitamin D in vivo during absorption from the small intestine and while it is transported in blood.


2009 ◽  
Vol 102 (9) ◽  
pp. 1285-1296 ◽  
Author(s):  
Maud Le Gall ◽  
Mélanie Gallois ◽  
Bernard Sève ◽  
Isabelle Louveau ◽  
Jens J. Holst ◽  
...  

Sodium butyrate (SB) provided orally favours body growth and maturation of the gastrointestinal tract (GIT) in milk-fed pigs. In weaned pigs, conflicting results have been obtained. Therefore, we hypothesised that the effects of SB (3 g/kg DM intake) depend on the period (before v. after weaning) of its oral administration. From the age of 5 d, thirty-two pigs, blocked in quadruplicates within litters, were assigned to one of four treatments: no SB (control), SB before (for 24 d), or after (for 11–12 d) weaning and SB before and after weaning (for 35–36 d). Growth performance, feed intake and various end-point indices of GIT anatomy and physiology were investigated at slaughter. The pigs supplemented with SB before weaning grew faster after weaning than the controls (P < 0·05). The feed intake was higher in pigs supplemented with SB before or after weaning (P < 0·05). SB provided before weaning improved post-weaning faecal digestibility (P < 0·05) while SB after weaning decreased ileal and faecal digestibilities (P < 0·05). Gastric digesta retention was higher when SB was provided before weaning (P < 0·05). Post-weaning administration of SB decreased the activity of three pancreatic enzymes and five intestinal enzymes (P < 0·05). IL-18 gene expression tended to be lower in the mid-jejunum in SB-supplemented pigs. The small-intestinal mucosa was thinner and jejunal villous height lower in all SB groups (P < 0·05). In conclusion, the pre-weaning SB supplementation was the most efficient to stimulate body growth and feed intake after weaning, by reducing gastric emptying and intestinal mucosa weight and by increasing feed digestibility.


1984 ◽  
Vol 259 (4) ◽  
pp. 2452-2456 ◽  
Author(s):  
M C Blaufuss ◽  
J I Gordon ◽  
G Schonfeld ◽  
A W Strauss ◽  
D H Alpers

2021 ◽  
Vol 9 (3) ◽  
pp. 547
Author(s):  
Daniel Sánchez ◽  
Iva Hoffmanová ◽  
Adéla Szczepanková ◽  
Věra Hábová ◽  
Helena Tlaskalová-Hogenová

The ingestion of wheat gliadin (alcohol-soluble proteins, an integral part of wheat gluten) and related proteins induce, in genetically predisposed individuals, celiac disease (CD), which is characterized by immune-mediated impairment of the small intestinal mucosa. The lifelong omission of gluten and related grain proteins, i.e., a gluten-free diet (GFD), is at present the only therapy for CD. Although a GFD usually reduces CD symptoms, it does not entirely restore the small intestinal mucosa to a fully healthy state. Recently, the participation of microbial components in pathogenetic mechanisms of celiac disease was suggested. The present review provides information on infectious diseases associated with CD and the putative role of infections in CD development. Moreover, the involvement of the microbiota as a factor contributing to pathological changes in the intestine is discussed. Attention is paid to the mechanisms by which microbes and their components affect mucosal immunity, including tolerance to food antigens. Modulation of microbiota composition and function and the potential beneficial effects of probiotics in celiac disease are discussed.


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