The use of biochemical parameters for a qualitative and quantitative assessment of ischemic damage to the small-intestinal mucosa

1987 ◽  
Vol 7 (12) ◽  
pp. 917-923 ◽  
Author(s):  
Ludo Filez ◽  
Willy Stalmans ◽  
Freddy Penninkx ◽  
Raymond Kerremans ◽  
Karel Geboes

Lactate dehydrogenase has been measured in the small-intestinal mucosa in order to assess its value as a marker for the effects of ischemia and of reperfusion. The decrease in specific activity of the enzyme illustrates the deleterious effect of reperfusion on the quality of the remaining epithelial cells. However, this parameter fails to detect the loss of epithelial cells, which is the major event during ischemia as well as during reperfusion. In contrast, the expression of enzyme activity per g protein of the underlying intestinal muscle allowed us, in addition, to assess quantitatively the loss of epithelial cells, in good agreement with the histological data.

1994 ◽  
Vol 267 (1) ◽  
pp. G59-G66
Author(s):  
J. F. White

Methods are described for isolating the cell nests, subepithelial clusters of germinative cells, from salamander intestinal mucosa and for growing the nests in culture into polarized monolayers of intestinal epithelial cells. Cells were viable in culture for up to 3 wk. The capacity of the monolayer cells to engage in membrane transport was evaluated using the patch-clamp technique in the whole cell mode. L-Valine (25 mM) induced an inward current in small intestinal cells of 25.8 +/- 5.7 pA and depolarized the cell membrane 14.5 +/- 1.6 mV. L-Alanine and L-phenylalanine were similarly effective, whereas D-valine was ineffective. The Km of the transporter for valine was 90 mM. Replacement of bath Na with tris(hydroxymethyl)aminomethane eliminated the inward current induced by valine. The basal (solute-independent) inward current was also reduced by Na+ replacement. Glucose did not induce a Na+ current. In contrast to the effect of valine on small intestinal cells, large intestinal cells were unresponsive to valine. It is concluded that the cultured small intestinal cells possess Na-amino acid but not Na-sugar cotransport. This profile of behavior is characteristic of undifferentiated small intestinal cells. Primary cultures of salamander small intestinal cells should be useful for studying enterocyte function and the developmental biology of the small intestinal mucosa.


1974 ◽  
Vol 142 (3) ◽  
pp. 545-553 ◽  
Author(s):  
Peter R. Flanagan ◽  
S. H. Zbarsky

Phosphodiesterase II activity was determined by using a synthetic substrate, the 2,4-dinitrophenyl ester of thymidine 3′-phosphate. The enzyme activity was determined in fractions obtained by differential centrifugation of homogenates of epithelial cells from the small intestinal mucosa of guinea pigs and rats. In guinea-pig preparations phosphodiesterase II occurred with highest specific activity in those fractions rich in succinate dehydrogenase and acid phosphatase. A lysosomal location for the guinea-pig enzyme was indicated by its structure-linked latency and by its association with particles that under-went a characteristic decrease in equilibrium density when Triton WR-1339 was injected into the animals. With rat preparations a much greater proportion of the phosphodiesterase II activity was found in the soluble fraction after ultracentrifugation. The rat enzyme exhibited a lower degree of latency and administration of Triton WR-1339 had no effect. The rat enzyme further differed from that of the guinea pig in other respects; it was more labile at 60°C, it exhibited a lower pH optimum and it had a higher molecular weight as determined by gel-filtration chromatography.


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.


Sign in / Sign up

Export Citation Format

Share Document