Oxytocin and cholecystokinin secretion in women with colectomy

BACKGROUND: Cholecystokinin (CCK) concentrations in plasma have been shown to be significantly higher in colectomised subjects compared to healthy controls. This has been ascribed to reduced inhibition of CCK release from colon. In an earlier study CCK in all but one woman who was colectomised, induced release of oxytocin, a peptide present throughout the gastrointestinal (GI) tract. The aim of this study was thus to examine if colectomised women had a different oxytocin response to CCK compared to healthy controls. METHODS: Eleven women, mean age 34.4 ± 2.3 years, who had undergone colectomy because of ulcerative colitis or constipation were studied. Eleven age-matched healthy women served as controls. All subjects were fasted overnight and given 0.2 μg/kg body weight of CCK-8 i.v. in the morning. Samples were taken ten minutes and immediately before the injection, and 10, 20, 30, 45, 60, 90 and 120 min afterwards. Plasma was collected for measurement of CCK and oxytocin concentrations. RESULTS: The basal oxytocin and CCK concentrations in plasma were similar in the two groups. Intravenous injection of CCK increased the release of oxytocin from 1.31 ± 0.12 and 1.64 ± 0.19 pmol/l to 2.82 ± 0.35 and 3.26 ± 0.50 pmol/l in controls and colectomised women, respectively (p < 0.001). Given the short half-life of CCK-8 in plasma, the increased concentration following injection could not be demonstrated in the controls. On the other hand, in colectomised women, an increase of CCK in plasma was observed for up to 20 minutes after the injection, concentrations increasing from 1.00 ± 0.21 to a maximum of 1.81 ± 0.26 pmol/l (p < 0.002). CONCLUSION: CCK stimulates the release of oxytocin in women. There is no difference in plasma concentrations between colectomised and controls. However, colectomy seems to reduce the metabolic clearance of CCK. The hyperCCKemia in patients who had undergone colectomy is consequently not only dependent on CCK release, but may also depend on reduced clearance

Release of tryptophan and serotonin into the portal vein of the isolated perfused rat small intestine

To investigate the release of serotonin from intestinal enterochromaffin cells, we used an in vitro technique which allows studies excluding overlapping influences from outside the gut. The entire small intestine of rats fed a standard or tryptophan-enriched (3% of total) diet was totally isolated by ligatures with the exception of the superior mesentric artery and portal vein that supply and drain the intestine. Simultaneously to the vascular perfusion (Krebs-Ringer bicarbonate buffer, 0,4% human albumin, 5 m M glucose, 0.6 m M glutamine) the gut lumen was infused (buffer or 0.1 N HCL). Acidification of the gut lumen resulted in an increment of venously released tryptophan and serotonin. After feeding tryptophan-enriched food the release of tryptophan was increased. However, the total amount of released serotonin after tryptophan diet did not differ as compared to that after standard diet. Addition of a monoamino-oxidase inhibitor (pargyline) to the arterial perfusate enhanced the released amount of serotonin 3-fold in the portal venous effluent (at a concentration of 1 m M but not 0.1 m M ). Recovery studies done by arterial infusions of serotonin (1 µ M , 10µ M ) and evaluation of the amounts venously released revealed a high loss of infused serotonin (40%–70%). Our data suggest gut-born serotonin to more likely play a paracrine role than a role as a classical hormone.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47538/1/433_2005_Article_BF01852260.pd

Les lipides, protéines et glucides stimulent la sécrétion de cholécystokinine intestinale chez le porc

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Plasma and tissue levels of digestive regulatory peptides during postnatal development and weaning in the calf

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