Plasma Cholecystokinin, Plasma Peptide YY and Gallbladder Motility in Patients with Slow Transit Constipation: Effect of Intestinal Stimulation

Abstract

Background/Aim: Because cholecystokinin and peptide YY are gut hormones with potent effects on gastrointestinal motility, we determined whether abnormalities of cholecystokinin and peptide YY exist in slow transit constipation. Methods: Plasma concentrations of these hormones before, during and after intraduodenal infusion of a liquid meal in 21 patients with slow transit constipation were compared with the results in 8 healthy controls. Results: Fasting levels of plasma cholecystokinin (3.1 ± 0.2 vs. 2.4 ± 0.2 pM; p = 0.02) were higher in patients. Basal plasma peptide YY (11.4 ± 1.4 vs. 8.9 ± 0.7 pM; p = 0.1) tended to be higher in patients. After the meal (60–90 min), incremental cholecystokinin (p < 0.05), but not peptide YY, was significantly higher in patients. During intraduodenal infusion of the meal (0–60 min), incremental plasma cholecystokinin (251 ± 20 pM·min) and peptide YY (1,146 ± 186 pM·min) in patients were almost similar to control values (262 ± 22 and 901 ± 166 pM·min). Gallbladder volumes before, during and after the meal were not different between the 2 groups. Gastric emptying of a solid meal was delayed in the majority of patients (12 of 18). Abnormalities of plasma cholecystokinin were observed only in patients with delayed gastric emptying. Conclusion: Plasma levels of cholecystokinin are elevated in the fasting state and decrease more slowly after stimulation, but maximum release in response to intestinal nutrients is not altered in patients with slow transit constipation. The abnormality seems to be confined to a subgroup of patients with delayed gastric emptying.

Symptoms and Pathophysiological Correlations in Patients with Constipation and Functional Dyspepsia

“…However, this finding has not been confirmed by multivariate statistics, which, conversely, showed only a risk association between severe postprandial fullness, delayed gastric emptying and impaired gallbladder contraction. Interestingly, these results confirm the risk association existing between delayed gastric emptying and postprandial fullness [17, 18], but also suggest that postprandial fullness may be associated with reduced gallbladder contraction, which probably involves a neurohormonal mechanism mediated by an altered CCK release [1, 19, 20]. …”

Pathophysiology of constipation in the older adult

“…Excessive nitric oxide was found in ICC preparations from the distal colon of patients with STC [49] . A decrease in serotonin immunoreactivity in the muscular mucosa and circular muscle was identified in patients who underwent subtotal colectomy for colonic inertia [50] . How changes in the release of various neurotransmitters contribute to the pathogenesis of STC has not been described in detail.…”

Chronic idiopathic slow transit constipation: pathophysiology and management

“…Fasting and postprandial plasma levels of PP have been found to be high and postprandial PYY level to be low in patients with ISTC [52]. On the other hand, an increase in the number of large intestinal PYY cells and unchanged fasting and postprandial plasma levels of PP and PYY in patients with ISTC have been reported [53–55]. Serotonin‐cell density in the large intestine (Fig.…”