The total area of the human adult gut mucosa is not in the order of tennis lawn, rather is that of half a badminton court.

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A recently developed method to isolate gastric glands from the rabbit gastric mucosa (Berglindh and Obrink 1976) was used to study the effects of some common gastric secretagogues. Three parameters were investigated: 1) Respiratory activity; 2) Intraglandular accumulation of the weak base aminopyrine; 3) Quantitative morphology of the parietal cells. The following substances were tested: Histamine, cAMP, db-cAMP, aminophylline, carbachol and pentagastrin. The strongest effect was obtained with db-cAMP which dose-dependently stimulated the respiration up to 200%, increased the aminopyrine accumulation 80% and altered the parietal cell morphology from a typically resting to a typically stimulated state. cAMP also stimulated the respiration but was about 10 times less effective on a molar basis than the dibutyryl form. Histamine, like db-cAMP, stimulated the respiration in a dose-dependent manner and strongly increased the aminopyrine accumulation. The morphological changes were, however, not of the same magnitude as after db-cAMP. Aminophylline, tested only for respiratory activity, stimulated the oxygen consumpation moderately. Carbachol induced a transient increase in both the oxygen consumption and in the aminopyrine accumulation with a peak value after approximately 15 minutes for both, but gave no significant morphological alterations. Pentagastrin, finally, was incapable of inducing changes in any of the three parameters. Aminopyrine was also found to accumulate approx. 50 times in unstimulated, morphologically resting glands. This seems to indicate that there might be acid sites already in resting glands.

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The hormone gastrin stimulates acid secretion by releasing histamine from gastric enterochromaffin-like (ECL) cells and induces ECL cell proliferation in vivo. This study uses a > 90% pure ECL cell preparation in culture to compare gastrin effects on histamine release, histidine decarboxylase (HDC) activity, and DNA synthesis. Gastrin and the cholecystokinin octapeptide (CCK-8, nonsulfated) induced histamine release from ECL cells (24-96 h of primary culture) within 5 min of incubation [concentration eliciting 50% of maximal response (EC50), 4 and 2 x 10(-11) M, respectively]. The CCK-B antagonist L-365,260 inhibited this effect [concentration inhibiting 50% of maximal response (IC50), 2 x 10(-8) M], whereas the CCK-A antagonist L-364,718 (10(-8) M) and the tyrosine kinase inhibitor genistein (10(-4) M) had no effect. Histamine release was associated with a biphasic elevation of intracellular Ca2+. Gastrin stimulated HDC activity two- to threefold after 60 min of incubation (EC50, 10(-10) M). Gastrin also increased DNA synthesis in ECL cells, with an EC50 of 1.7 x 10(-12) M as measured by the incorporation of 5-bromo-2'-deoxyuridine (BrdU). Positive nuclear immunostaining increased two- to threefold in up to 20% of ECL cells after 48-96 h of incubation. This effect was inhibited by L-365,260 (IC50, 5 x 10(-9) M) and by genistein (10(-4) M) but was not altered by L-364,718 (10(-8) M). The antisecretory drugs omeprazole, lansoprazole, and pantoprazole did not affect BrdU incorporation in isolated ECL cells. In conclusion, acute and chronic gastrin effects on the ECL cell are mediated via CCK-B receptors but differ in apparent receptor affinity and signal transduction pathways.

Monoclonal antibodies were prepared against a purified membrane fraction from hog gastric mucosa containing the H+ + K+ ATPase. On sodium dodecyl sulfate gels the molecular weight of this fraction corresponds to a single band of about 95,000. In contrast, on isoelectric focusing gels three groups of peptides are resolved with isoelectric points of 5.7, 6.2, and 8.5. One of the monoclonal antibodies (HK111) was shown to react selectively with the acidic peptide, whereas another antibody (HK113) reacted with the alkaline peptide, showing that the three peptides were antigenically distinct. Both monoclonal antibodies selectively labeled the parietal cell, and antibody HK111 labeled the tubulovesicles of the resting parietal cell and the microvilli of the secretory canaliculus of the secreting cell. This finding suggests translocation of membrane from the tubulovesicles to the secretory surface on stimulation.

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International audienceAbstract Aims: Roux-en-Y gastric bypass surgery is the most efficient treatment of morbid obesity but the mechanisms of action are still poorly understood. The aim of this study was to explore the Roux-limb mucosa after gastric bypass surgery, focusing on basic morphology and inflammation. Methods and Results: Jejunal mucosal samples from the Roux-limb were gathered from eight patients at time of surgery and six to eight months post-surgery. Histological evaluation of inflammation and morphometric investigations were performed, mitotic frequency was assessed using immunohistochemistry and inflammatory markers and Angiotensin (Ang) II receptors were detected using western blot. Mitotic frequency increased and villous surface area decreased in the Roux-limb mucosa but no signs of active inflammation were observed after surgery. Protein analyses showed increased levels of nicotineamide adenine dinucleotidephosphate (NADPH)-oxidase, myeloperoxidase (MPO) and the Ang II type 1(AT1) receptor after surgery, whereas the levels of inducible nitric oxide synthase (iNOS), nitrotyrosine and the Ang II type 2(AT2) receptor remained constant Conclusion: These results indicate that the phenotype of the jejunal mucosa changes once exposed to un-digested food and the increased microbial load in the Roux-limb after surgery