Effects of galacto-oligosaccharide ingestion on the mucosa-associated mucins and sucrase activity in the small intestine of mice.

BACKGROUND: Galacto-oligosaccharides (GOS) are non-digestible oligosaccharides with short galactosyl chain units produced by lactose fermentation which are considered as prebiotics. Only few studies have investigated the effects of GOS medium-term ingestion on the small intestinal epithelium characteristics. AIM OF THE STUDY: In this study, we evaluated the consequences of GOS ingestion on small intestinal mucosal morphology, on brush-border membrane enzyme activities and on mucin content in BALB/c mice. METHODS: Mice received the experimental diets for 4 weeks and then the small intestine was collected to measure sucrase, lactase and alkaline phosphatase activities, to study the villus heights in the jejunum mucosa and to determine mucosal mucin content as well as MUC-2 and MUC-4 mRNAs expression by qRT-PCR. RESULTS: Our results showed that GOS has no detectable effect on the intestine villus height but increased the total protein content by twofold. Sucrase activity was significantly increased in the intestinal mucosa recovered from animals fed the GOS diet without any detectable modification of lactase and phosphatase activities. Interestingly, GOS was also able to increase sucrase activity in cultured Caco-2 cells raising the view that they likely act directly on these cells. Furthermore, GOS was found to markedly increase O-linked glycoproteins associated with the intestinal mucosa without modifying MUC-2, MUC-4 mRNAs expression. Lastly, TNF-alpha mRNA expression was also not modified after GOS ingestion. CONCLUSIONS: These results suggest that, in BALB/c mice, 4-week GOS ingestion is able to increase the small intestinal mucosa-associated mucin content and enterocyte-associated sucrase activity without modifying villus height.

Colonic luminal ammonia and portal blood L-glutamine and L-arginine concentrations: a possible link between colon mucosa and liver ureagenesis.

The highest ammonia concentration in the body is found in the colon lumen and although there is evidence that this metabolite can be absorbed through the colonic epithelium, there is little information on the capacity of the colonic mucosa to transfer and metabolize this compound. In the present study, we used a model of conscious pig with a canula implanted into the proximal colon to inject endoluminally increasing amounts of ammonium chloride and to measure during 5 h the kinetics of ammonia and amino acid concentration changes in the portal and arterial blood. By injecting as a single dose from 1 to 5 g ammonia into the colonic lumen, a dose-related increase in ammonia concentration in the portal blood was recorded. Ammonia concentration remained unchanged in the arterial blood except for the highest dose tested, i.e. 5 g which thus apparently exceeds the hepatic ureagenesis capacity. By calculating the apparent net ammonia absorption, it was determined that the pig colonic epithelium has the capacity to absorb 4 g ammonia. Ammonia absorption through the colonic epithelium was concomitant with increase of L-glutamine and L-arginine concentrations in the portal blood. This coincided with the expression of both glutamate dehydrogenase and glutamine synthetase in isolated colonic epithelial cells. Since L-glutamine and L-arginine are known to represent activators for liver ureagenesis, we propose that increased portal concentrations of these amino acids following increased ammonia colonic luminal concentration represent a metabolic link between colon mucosa and liver urea biosynthesis.