Background-Hyperglycaemia delays gastric emptying, both in healthy controls and in patients with diabetes mellitus. These changes in antroduodenal motility are likely to constitute the mechanism through which gastric emptying of solids is delayed during high blood glucose concentrations in these diabetic patients. (Gut 1997; 40: 641-646)

We examined the relationship of interdigestive gallbladder emptying with the different phases of the migrating motor complex (MMC) and with plasma levels of cholecystokinin (CCK) and motilin. In 10 volunteers 20 cycles of the MMC were recorded. In 11 cycles phase III occurred in antrum and duodenum (group 1). In nine cycles phase III was observed only in duodenum (group 2). In group 1 gallbladder emptying started at 30% of total cycle length and continued until the end of the cycle. Maximal gallbladder emptying was 33.3 +/- 3.3% (SE). In group 2 gallbladder emptying also started at 30% of total cycle length but ended at 60%. Maximal gallbladder emptying in this group was 24.3 +/- 3.1% (P < 0.05). Motilin levels were higher in group 1 than in group 2 during phase IIB (240.1 +/- 28.5 and 142.1 +/- 30.9 pg/ml, respectively, P < 0.05) and during phase III (210.8 +/- 24.3 and 93.5 +/- 12.5 pg/ml, respectively, P < 0.05). We conclude that: 1) phase III activities starting in the antrum are preceded by greater and prolonged gallbladder emptying, higher motilin levels, and higher intraduodenal bile acid concentrations than phase III activities starting in the duodenum and 2) no relationship between interdigestive gallbladder motility and CCK levels could be demonstrated.

Reports on motor abnormalities in Type 1 (insulin-dependent) diabetes mellitus are inconsistent. In 20 Type 1 diabetic patients and in 11 control subjects antroduodenojejunal manometry was performed under euglycaemic conditions in order to examine the prevalence of gastric and small intestinal motor abnormalities in relation to dyspeptic symptoms and the degree of cardiac autonomic neuropathy. In diabetic patients compared to control subjects phase III (regular, high-amplitude contractile activity at maximal frequency) involved the gastric antrum less often (12 vs 35%, p < 0.05), the duration of phase I (motor quiescence) was shorter (6 +/- 1 vs 21 +/- 4 min, p < 0.002) and in phase II (irregular motor activity) the frequency of duodenal and jejunal contractions was higher. After a meal the duration of the fed state was shorter in diabetic patients with symptoms during the study than in diabetic patients without symptoms and than in control subjects (57 +/- 27 vs 157 +/- 11 and 140 +/- 13 min, p < 0.02). Postprandial antral hypomotility was seen in diabetic patients with symptoms only in the first 30 min after the meal. One hour after the meal the frequency of duodenal and jejunal contractions was again higher in diabetic patients. In diabetic patients compared to control subjects more burst activity (clusters of non-propagated high-amplitude contractile activity at maximal frequency) was seen (7.9 +/- 1.6 vs 0.8 +/- 0.5% of the total time of study, p < 0.002). No correlation was found between manometric parameters and the degree of cardiac autonomic neuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

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Background: Acromegalic patients treated three times daily with subcutaneous injections of the somatostatin analogue octreotide frequently develop gallstones, due to suppressed cholecystokinin release and impaired gall‐bladder emptying. Aim: To elucidate the effects of a new long‐acting octreotide formulation (Sandostatin LAR) on gall‐bladder emptying, cholecystokinin release and gallstone formation. Methods: Postprandial gall‐bladder and gastric emptying were determined by ultrasonography and cholecystokinin release was measured in seven patients on days 0, 14, 28, and 75 (Sandostatin LAR, 20 mg intramuscularly on days 1, 30, and 60). Results: During treatment, fasting gall‐bladder volumes increased from 26.5 ± 3.2 mL to 61.4 ± 7.5 mL, but postprandial cholecystokinin release and gall‐bladder emptying (from 63.9 ± 3.8% to 12.3 ± 3.5%) were severely suppressed. Gallstones formed in six out of seven patients within 8 months of treatment. Gastric emptying did not change during the therapy. Conclusions: The risk of gallstone formation is greatly increased during Sandostatin LAR. This is probably related to profound suppression of cholecystokinin release and gall‐bladder emptying.