Pattern of Gastric Emptying in Functional Dyspepsia. An Ultrasonographic Study

We assessed the ultrasonographic pattern of gastric emptying in patients with functional dyspepsia, evaluating its relationship with symptoms. Twenty dyspeptic patients, with slight (group A) and severe (group B) symptoms, and 10 controls (group C) underwent ultrasonographic study of gastric emptying by measuring postprandial variations of the antral area at regular intervals. The time at which the antral area returned to the basal value was assumed to be the final emptying time. The final emptying time was significantly longer in both group A (294 +/- 42 min) and group B (340 +/- 36 min) compared to controls (244 +/- 21 min), but no significant difference was observed between them. A significantly (P < 0.05) greater dilation of the antral area was found at 50 min in group B compared to group A patients. A different pattern of antral motor function rather than a delay of gastric emptying correlates with the severity of symtoms in dyspeptic patients.     

Inhibitory effect of galanin on postprandial gastrointestinal motility and gut hormone release in humans

Galanin was infused intravenously in 8 healthy volunteers at a dose of 40 pmol/kg.min for 1 h to investigate the pharmacologic effects of this peptide on postprandial gastrointestinal motility and gut peptide release in humans. Galanin strongly inhibited gastrointestinal motility. Gastric emptying was significantly delayed, with the time taken to empty 50% of the gastric contents increasing from 59.0 +/- 4.8 min (control infusion) to 99.3 +/- 4.7 min (galanin infusion). Mouth-to-cecum transit time increased from 67.5 +/- 6.9 to 126.3 +/- 18.5 min. Galanin potently suppressed the initial postprandial rise in plasma concentrations of glucose, insulin, peptide tyrosine tyrosine, neurotensin, enteroglucagon, pancreatic glucagon, somatostatin, and pancreatic polypeptide, but did not change gastric inhibitory polypeptide, motilin, peptide histidine methionine, and gastrin concentrations compared with control. The results indicate that an infusion of galanin has potent effects on the gastrointestinal tract in humans. The changes in motor activity in particular suggest that the local galaninergic innervation could have an important physiologic role in the control of human gastrointestinal propulsive motor activity.     

Ghrelin stimulates gastric emptying and hunger in normal-weight humans

CONTEXT: Ghrelin is produced primarily by enteroendocrine cells in the gastric mucosa and increases gastric emptying in patients with gastroparesis. MAIN OBJECTIVE: The objective of the study was to evaluate the effect of ghrelin on gastric emptying, appetite, and postprandial hormone secretion in normal volunteers. DESIGN: This was a randomized, double-blind, crossover study. SUBJECTS: Subjects included normal human volunteers and patients with GH deficiency. INTERVENTION: Intervention included saline or ghrelin (10 pmol/kg.min) infusion for 180 min after intake of a radioactively labeled omelette (310 kcal) or GH substitution in GH-deficient patients. MAIN OUTCOME MEASURES: Measures consisted of gastric empty-ing parameters and postprandial plasma levels of ghrelin, cholecystokinin, glucagon-like peptide-1, peptide YY, and motilin. RESULTS: The emptying rate was significantly faster for ghrelin (1.26 +/- 0.1% per minute), compared with saline (0.83% per minute) (P < 0.001). The lag phase (16.2 +/- 2.2 and 26.5 +/- 3.8 min) and half-emptying time (49.4 +/- 3.9 and 75.6 +/- 4.9 min) of solid gastric emptying were shorter during ghrelin infusion, compared with infusion of saline (P < 0.001). The postprandial peak in plasma concentration for cholecystokinin and glucagon-like peptide-1 occurred earlier and was higher during ghrelin infusion. There was no significant effect of ghrelin on plasma motilin or peptide YY. There was no difference in gastric emptying before and after GH substitution. CONCLUSION: Our results demonstrate that ghrelin increases the gastric emptying rate in normal humans. The effect does not seem to be mediated via GH or motilin but may be mediated by the vagal nerve or directly on ghrelin receptors in the stomach. Ghrelin receptor agonists may have a role as prokinetic agents.     

Effect of motilin on gastric emptying in patients with diabetic gastroparesis.

Erythromycin markedly accelerates gastric emptying, possibly because it acts as a motilin agonist. In the present study, the effect of an equipotent dose of motilin was tested. In six patients with severe diabetic gastroparesis, gastric emptying of liquids and solids was examined scintigraphically after motilin or placebo in a double-blind crossover study. Motilin (10 pmol.kg-1.min-1) or saline was infused over a 90-minute period starting 5 minutes before breakfast. Motilin markedly accelerated emptying. For liquids, the half-emptying time was reduced from 51 +/- 6 to 22 +/- 11 minutes (P less than 0.01) and for solids from 111 +/- 4 to 51 +/- 12 minutes (P less than 0.01). The mean increase in plasma motilin levels was 1315 +/- 342 pg/mL, corresponding to an effective infusion rate of about 4 pmol.kg-1.min-1. In the control experiments, basal motilin levels (173 +/- 17 pg/mL) were within the normal range but increased steadily postprandially, reaching 321 +/- 25 pg/mL at the end of the study period, probably reflecting gastric distension. The postprandial increase in pancreatic polypeptide level was blunted compared with accepted normal values but was more pronounced during motilin infusion, i.e., 650 +/- 217 vs. 279 +/- 66 pg/mL (P less than 0.01), probably because of the improved emptying. Our data show that motilin accelerates gastric emptying in diabetic gastroparesis and support the hypothesis that erythromycin's effect is mediated through motilin receptors.     

Gastric emptying is accelerated in obese type 2 diabetic patients without autonomic neuropathy.

OBJECTIVE: To clarify the impact of type 2 diabetes mellitus on the gastric emptying rate. MATERIAL AND METHODS: Using a double-isotope scintigraphic technique, we assessed the gastric emptying of a standard liquid-solid meal in 13 obese type 2 diabetic patients without autonomic neuropathy (age: 47.4 +/- 8.6 yr, body mass index: 33.9 +/- 4.8 kg/m(2), glycaemia: 9.1 +/- 2.6 mmol/l) and in 7 controls with similar sex ratio, age, BMI and body fat distribution. RESULTS: The half gastric emptying time for the liquid phase was not significantly different between diabetic patients and controls (respectively: 52.7 +/- 14.5 min and 63.1 +/- 15.2 min). However, the half gastric emptying time for the solid phase was significantly shortened in diabetic patients versus controls (respectively 88.8 +/- 23.2 min in diabetic patients and 113.6 +/- 26.9 min in controls; p<0.04). Furthermore, a negative relationship was highlighted between the half gastric emptying time for the solid phase and basal glycaemia (r=-0.65, p<0.02) in diabetic patients. No significant relationship was found between gastric emptying parameters and cardiac autonomic nerve function, insulin or gastrin levels. CONCLUSION: Solid gastric emptying is accelerated in obese type 2 diabetic patients without patent autonomic neuropathy when compared to obese non diabetic patients.     

Gallbladder emptying and somatostatin and cholecystokinin plasma levels in celiac disease

OBJECTIVE: Gallbladder hypomotility in celiac disease has been attributed to decreased cholecystokinin secretion. The possible influence of somatostatin, which inhibits gallbladder motility, however, has never been evaluated. In this study gallbladder emptying and cholecystokinin and somatostatin plasma levels were evaluated in response to a fatty meal in patients with celiac disease at diagnosis and after long-term gluten-free diet and in controls. METHODS: Gallbladder volume and plasma levels of cholecystokinin and somatostatin were measured by ultrasonography and radioimmunoassay, respectively, at 0 time and 30, 60, 75, and 90 min after an oral fatty meal (227 kcal, 45% fat) in 10 celiac patients at diagnosis and after 18 months of successful gluten-free diet and in 10 healthy subjects. The pattern of gallbladder emptying was evaluated by mixed factorial analysis of variance and the curve fitting by multiple regression analysis. RESULTS: Patients at diagnosis had significantly greater fasting gallbladder volume and higher somatostatin plasma levels than controls (25.7 +/- SD 9.7 ml vs 16.8 +/- 7.0 ml, p = 0.021 and 9.3 +/- 4.6 vs 4.8 +/- 3.4 pmol/L, p = 0.023, respectively), significantly lower fatty meal-induced gallbladder ejection fraction (55 +/- 11.2% vs 76 +/- 7.2%, p = 0.005), and cholecystokinin peak and smaller area under the cholecystokinin secretion curve (3.1 +/- 2.3 pmol/L vs 10.5 +/- 6.9 pmol/L, p = 0.028 and 157 +/- 142 pmol/L/90 min vs 453 +/- 229 pmol/L/90 min, p = 0.028, respectively). The two groups had a similar emptying pattern (p = 0.8913) expressed by a significant quadratic term of the emptying function (p = 0.0001). The mean overall emptying volume was significantly greater in patients than in controls (p = 0.0007). Gluten-free diet normalized these findings. CONCLUSIONS: In patients at diagnosis, elevated somatostatin levels were associated with increased gallbladder fasting volume, whereas decreased cholecystokinin secretion was responsible for the reduced gallbladder emptying. Gluten-free diet reversed these abnormalities.     

Defective gallbladder emptying and cholecystokinin release in celiac disease. Reversal by gluten-free diet

Normal volunteers (n = 6), patients with untreated celiac disease and subtotal villous atrophy (n = 6), patients with nonresponsive celiac disease (n = 2), and patients with celiac disease on a gluten-free diet with a virtually normal biopsy specimen (n = 6) drank a liquid fat meal after an overnight fast. Gallbladder emptying was monitored by using 99mTc-eHIDA, and blood samples were taken for cholecystokinin estimation by radioimmunoassay after high-performance liquid chromatography. The half-times of gallbladder emptying were 20.4 +/- 2.9 min (mean +/- SEM) for normals and 22.1 +/- 2.8 min in treated patients with celiac disease (NS). In patients with untreated celiac disease half-times were 154.3 +/- 10.3 min (p less than 0.02 vs. normals and treated patients with celiac disease), and in 2 nonresponsive patients, half-times were 40.7 and 37.3 min. Integrated plasma cholecystokinin responses were 473 +/- 87 and 436 +/- 137 pmol X L-1 X 30 min-1 in normals and treated patients with celiac disease (NS). In untreated patients with celiac disease values were 16 +/- 9 pmol X L-1 X 30 min-1 (p less than 0.001 vs. normals and treated patients with celiac disease), and in nonresponsive patients values were 442 and 322 pmol X L-1 X 30 min-1. In 2 patients studied before and during gluten-free diet half-times for gallbladder emptying changed from 168.9 and 302.4 min to 20.1 and 23.4 min, and cholecystokinin responses changed from 0 and 45 to 623 and 298 pmol X L-1 X 30 min-1. Cholecystokinin immunoreactivity cochromatographing with cholecystokinin-octapeptide was responsible for 50%-60% of circulating cholecystokinin in normals and in treated patients but the small amount of cholecystokinin that was released in untreated patients with celiac disease cochromatographed with cholecystokinin-33/39. We conclude that there is a reversible defect of gallbladder emptying and cholecystokinin release in celiac disease.     

Proximal and distal gut hormone secretion in irritable bowel syndrome

OBJECTIVE: Sensory and motor dysfunctions of the gut are both important characteristics of irritable bowel syndrome (IBS). Several gut peptides contribute to the regulation of gastrointestinal function but little is known about gut hormone secretion in IBS. MATERIAL AND METHODS: We evaluated perceptual thresholds and fasting and postprandial plasma levels of proximal (cholecystokinin (CCK), motilin) and distal (peptide YY) gut peptides up to 1 h after ingestion of a high caloric meal in 99 IBS patients and 40 age- and gender-matched healthy controls. RESULTS: Fasting plasma CCK levels were significantly elevated in patients (1.2+/-0.8 pM) compared with those in controls (0.8+/-0.7 pM, p=0.006), as was the incremental postprandial CCK response (72+/-73 versus 40+/-42 pM.60 min, respectively; p=0.003). No differences in fasting and postprandial motilin or PYY levels were found. The postprandial PYY response was significantly increased in hypersensitive compared to normosensitive patients (215+/-135 versus 162+/-169 pM, p=0.048). Patients with a diarrhoea predominant bowel habit had higher fasting motilin levels compared to constipated patients or alternating type IBS patients (82.1+/-36.5 versus 60.8+/-25.1 versus 57.5+/-23.9 pM, one-way ANOVA p=0.003). CONCLUSIONS: IBS patients have increased fasting and postprandial plasma levels of CCK. Changes in plasma levels of motilin and PYY may contribute to the clinical expression of IBS, such as the presence of visceral hypersensitivity or a predominant bowel habit.     

Gastrointestinal hormone abnormalities and G and D cells in functional dyspepsia patients with gastric dysmotility

AIM: To investigate the relationship between gastric dysmotility, gastrointestinal hormone abnormalities, and neuroendocrine cells in gastrointestinal mucosa in patients with functional dyspepsia (FD). METHODS: Gastric emptying was assessed with solid radiopaque markers in 54 FD patients, and the patients were divided into two groups according to the results, one with delayed gastric emptying and the other with normal gastric emptying. Seventeen healthy volunteers acted as normal controls. Fasting and postprandial plasma levels and gastroduodenal mucosal levels of gastrointestinal hormones gastrin, somatostatin (SS) and neurotensin (NT) were measured by radioimmunoassay in all the subjects. G cells (gastrin-producing cells) and D cells (SS-producing cells) in gastric antral mucosa were immunostained with rabbit anti-gastrin polyclonal antibody and rabbit anti-SS polyclonal antibody, respectively, and analyzed quantitatively by computerized image analysis. RESULTS: The postprandial plasma gastrin levels, the fasting and postprandial plasma levels and the gastric and duodenal mucosal levels of NT were significantly higher in the FD patients with delayed gastric emptying than in those with normal gastric emptying and normal controls. The number and gray value of G and D cells and the G cell/D cell number ratio did not differ significantly between normal controls and the FD patients with or without delayed gastric emptying. CONCLUSION: Our findings suggest that the abnormalities of gastrin and NT may play a role in the pathophysiology of gastric dysmotility in FD patients, and the abnormality of postprandial plasma gastrin levels in FD patients with delayed gastric emptying is not related to the changes both in the number and gray value of G cells and in the G cell/D cell number ratio in gastric antral mucosa.     

Abnormalities of serotonin metabolism and their relation to symptoms in untreated celiac disease.

BACKGROUND AND AIMS: Serotonin (5-hydroxytryptamine [5-HT]) is a key modulator of gut function that in excess causes nausea, vomiting, and diarrhea. We recently showed that patients with post-infective irritable bowel syndrome have increased postprandial release of 5-HT associated with low-grade T-cell mediated inflammation. Celiac disease is another common disease in which a T-cell enteropathy is associated with increased mucosal 5-HT levels. Our aim was to determine how this inflammatory lesion influenced 5-HT bioavailability and how changes in 5-HT related to the symptoms of nausea, vomiting, and diarrhea seen in untreated celiac patients. METHODS: Fasting plasma and platelet 5-HT and postprandial plasma 5-HT levels were measured after a high-carbohydrate meal in celiac patients (n = 18) and healthy controls (n = 18) using high-pressure liquid chromatography. Dyspepsia was assessed during the postprandial period using a questionnaire. Finally, we compared the histology and mucosal 5-HT levels in duodenal biopsy specimens from celiac patients and controls. RESULTS: Celiac patients had increased 5-HT-containing enterochromaffin cell numbers and significantly higher peak plasma 5-HT levels (P = .0002), postprandial area under the curve (P = .0006), and platelet 5-HT stores (P = .031) than controls. Peak 5-HT levels correlated significantly with postprandial dyspepsia scores (P = .005). Celiac patients had higher duodenal 5-HT levels (P = .007) than controls. CONCLUSIONS: Celiac disease is associated with increased mucosal 5-HT content and enhanced 5-HT release from the upper small bowel, which correlates with postprandial dyspepsia. Serotonin excess may mediate dyspeptic symptoms in untreated celiac disease.     

Gastric clearance of radiopaque markers in the evaluation of gastric emptying rate

BACKGROUND: The study of gastric emptying rate of solids using radiopaque indigestible solid markers has been a poorly employed technique because some kinds of markers do not leave the stomach at the same time as the meal but during the interdigestive migrating motor complex (IMMC). The aim of this study was to evaluate whether markers of particular shape and size can be successfully employed for this purpose. METHODS: Twenty-eight non-ulcer dyspeptic (NUD) patients and 20 healthy volunteers received a standard solid meal (790 Kcal) together with 20 small polyethylene radiopaque cylinders (5 mm x 2 mm in diameter). Gastric emptying rate was evaluated by ultrasound while the emptying of markers was simultaneously followed by X-rays using a brilliance intensifier. RESULTS: Final emptying time (FET = time when the antrum area returns to fasting size) of digestible solids was 355+/-35 min in NUD patients versus 265+/-20 min in controls (P < 0.001). The gastric emptying curve of digestible solids correlated with emptying of markers both in NUD patients (r= +0.96) and in controls (r= +0.93). CONCLUSIONS: The assessment of gastric clearance of radiopaque cylinders of 2 mm x 5 mm in size is a reliable tool for the study of gastric emptying rate of digestible solids. This is a readily available and easily performed test in any radiology unit.     

The effect of acute oral erythromycin on gallbladder motility and on upper gastrointestinal symptoms in gastrectomized patients with and without gallstones: a randomized, placebo-controlled ultrasonographic study

OBJECTIVE: Gastrectomy might be a risk factor for cholelithiasis and gallbladder stasis might play a major role. We studied fasting and postprandial gallbladder motility with 600 mg oral erythromycin or placebo in gastrectomized patients (with and without gallstones) and controls. METHODS: Seventeen patients operated on for gastric cancer (subtotal gastrectomy: n = 10, total gastrectomy: n = 7) were compared with 20 sex- and body-size matched healthy controls. Subjects randomly received erythromycin or placebo 30 min before the ingestion of a standard 200 ml liquid test meal. Gallbladder volume was estimated by ultrasonography until 120 min after test meal. A visual analog scale monitored GI perception of appetite, satiety, nausea, abdominal fullness and epigastric pain. RESULTS: Gastrectomized patients had increased fasting gallbladder volume (35.9 +/- 3.4 ml versus 21.0 +/- 1.4 ml, p = 0.0005) with faster postmeal emptying (T/2 14.8 +/- 1.1 min versus 23.5 +/- 1.5 min, p = 0.00019) than controls. Six patients developed small and asymptomatic gallstones, which did not influence gallbladder motility. In these patients, fasting gallbladder volume increased with time after surgery (r = +0.82, p = 0.047). Perception of satiety, abdominal fullness, and epigastric pain after ingestion of the test meal were all significantly greater in patients than in controls. Erythromycin significantly enhanced gallbladder emptying during fasting (p = 0.001) and postprandially in both patients and controls (0.002 < p < 0.017) and significantly reduced postmeal satiety and epigastric discomfort in gastrectomized patients. CONCLUSIONS: Increased fasting volume might be a form of stasis, predisposing patients to gallstone formation. Erythromycin improves fasting and postprandial gallbladder emptying and decreases upper GI symptoms in gastrectomized patients.     

Function of the proximal stomach after partial versus complete laparoscopic fundoplication

OBJECTIVES: After antireflux surgery, more than 30% of patients develop dyspeptic symptoms such as fullness and early satiety. We have previously shown that these symptoms are related to fundoplication-induced changes in proximal gastric motor and sensory function, especially impaired postprandial relaxation. We hypothesize that impaired fundus relaxation may be more pronounced after complete versus partial fundoplication. METHODS: Fasting and postprandial proximal gastric motor and sensory function were measured with an electronic barostat in patients after laparoscopic partial (n = 14) and complete (n = 14) fundoplication, in gastroesophageal reflux disease (GERD) patients (n = 12), and in healthy control subjects (n = 15). Gastric emptying and vagus nerve function tests were performed in all patients. RESULTS: Minimal distending pressure (MDP) and proximal gastric compliance were not significantly different among patients after antireflux surgery, GERD patients, and healthy controls. Maximal postprandial fundus relaxation was significantly (p < 0.01) reduced in patients after partial (267 +/- 32 ml) and complete (294 +/- 34 ml) fundoplication compared with GERD patients (448 +/- 30 ml) and healthy controls (409 +/- 25 ml). Sensations of fullness were not significantly different between patients with partial and complete fundoplication. There was a significant positive correlation between the postoperative duration and the degree of postprandial fundus relaxation (r = 0.67; p < 0.001). CONCLUSIONS: Both after complete and after partial fundoplication, proximal gastric motor function is affected, with impaired postprandial relaxation and increased sensation of fullness. These alterations are not related to the type of fundoplication but correlate significantly with the duration of the postoperative period.     

Obesity does not increase effects of synthetic ghrelin on human gastric motor functions

BACKGROUND & AIMS: Ghrelin is secreted by the stomach and stimulates food intake. Obese individuals have lower fasting plasma ghrelin levels but increased appetite, suggesting greater responses to endogenous ghrelin in obesity. The aim of this study was to compare effects of exogenous ghrelin (at a dose that stimulates growth hormone [GH] release in the physiologic range) versus placebo on gastric emptying, gastric volume, and postprandial symptoms and determine whether body mass (ranging from normal weight to obesity) influences responses to ghrelin. METHODS: After intravenous bolus synthetic human ghrelin (0.33 mug/kg) or saline, we measured plasma GH, gastric volume, and gastric emptying by combined (99m)Tc-single-photon emission computed tomography and scintigraphy ((111)In egg meal, 300 kcal) and postprandial symptoms using visual analogue scales. RESULTS: In 25 obese subjects (5 men and 20 women; body mass index [BMI], 36 +/- 4 kg/m(2)) and 13 female normal-weight (BMI, 22 +/- 2 kg/m(2)) subjects of similar ages, ghrelin increased GH levels (15.0 +/- 2.4 ng/mL) at 40 minutes postinjection and tended to decrease fasting gastric volumes compared with placebo (P = .059). There were no effects of BMI on treatment response and no differences between ghrelin and saline on postprandial (P = .09) or change in (postprandial minus fasting) gastric volumes, gastric emptying, or aggregate postprandial symptoms. Effects of ghrelin did not differ between obese and normal-weight participants. CONCLUSIONS: At doses that stimulate physiologic GH plasma levels, synthetic ghrelin tended to decrease fasting gastric volumes without altering postprandial volumes or gastric emptying in a predominantly female cohort. The data are not consistent with the hypothesis that higher body mass is associated with increased gastric responsiveness to ghrelin.     

Postprandial gut peptide plasma levels in women with idiopathic slow-transit constipation

BACKGROUND: As abnormalities of circulating gut regulatory peptides may have pathogenetic relevance in chronic idiopathic slow-transit constipation, we measured fasting and postprandial levels of plasma pancreatic polypeptide, motilin, cholecystokinin, neurotensin, and somatostatin in women with the disease. Results were compared with those of women with normal bowel habits. METHODS: Eight women with slow-transit constipation and 10 healthy women were studied. Blood samples were taken at regular intervals in fasting conditions and for 3 h after a standard solid-liquid meal (550 kcal). Gut peptide plasma levels were measured with a radioimmunoassay. RESULTS: Fasting gut peptide levels and postprandial pancreatic polypeptide responses were normal in constipated patients, in whom, however, motilin levels did not increase after the meal, and postprandial concentration-time curves of cholecystokinin, neurotensin, and somatostatin were delayed. Mean +/- standard error of the mean peak times in patients and in controls were, respectively, 99 +/- 14.7 and 46 +/- 4.1 min (P < 0.01, Mann-Whitney test) for cholecystokinin, 135 +/- 9.8 and 60 +/- 3.9 min (P < 0.01) for neurotensin, and 111 +/- 17.7 and 51 +/- 6.0 min (P < 0.05) for somatostatin. CONCLUSIONS: Patients with slow-transit constipation have abnormal postprandial patterns of motilin, cholecystokinin, neurotensin, and somatostatin.     

Impaired release of peptide YY in patients with proctocolectomy and ileal pouch-anal anastomosis.

BACKGROUND: Peptide YY (PYY) is a gut hormone produced by endocrine cells in the distal small bowel, colon, and rectum. PYY inhibits upper gastrointestinal secretory and motor functions. The aim of this study was to determine whether basal and postprandial plasma PYY levels in patients with proctocolectomy and ileal pouch-anal anastomosis (IPAA) are reduced and to determine the relationship between plasma PYY and plasma cholecystokinin (CCK) levels. METHODS: Plasma concentrations of PYY and CCK were measured before and after ingestion of a standardized breakfast in 14 IPAA patients and in 12 healthy control subjects. RESULTS: Basal PYY was slightly lower in the IPAA patients than in the controls (8.3 +/- 0.3 versus 9.3 +/- 1.1 pM; not significant). Ingestion of the meal induced a small but significant increase of PYY to a maximum of 10.9 +/- 0.9 pM in patients. Integrated postprandial PYY was markedly reduced in patients when compared with the controls (1725 +/- 66 pM*180min versus 3194 +/- 480 pM*180 min; P < 0.005). Plasma PYY concentrations were inversely correlated with plasma CCK concentrations in the 2nd and 3rd h after the meal (r = -0.86; P = 0.0001). CONCLUSION: PYY release in response to meal ingestion is markedly reduced but not completely absent in patients with proctocolectomy and ileal pouch-anal anastomosis. The inverse relationship between circulating PYY and CCK in the late postprandial phase is compatible with a negative feedback regulation of CCK release by endogenous PYY.     

Abnormalities of upper gut motility in patients with slow-transit constipation.

OBJECTIVE: To further delineate motor activity of the upper gastrointestinal tract in patients with slow-transit constipation. DESIGN: A prospective study comparing healthy volunteers with patients with a clinical diagnosis of slow-transit constipation. METHODS: Eighteen patients with clinical diagnosis of slow-transit constipation and 10 healthy controls were included in the study. Fasting antroduodenal motility was measured by perfusion manometry for at least one complete cycle of the migrating motor complex or a maximum of 300 min. Oesophageal manometry, gastric emptying and orocaecal transit time measurements were also performed. RESULTS: At least one complete cycle of the migrating motor complex was observed in all controls, but in only nine patients (P < 0.01 versus control). The migrating motor complex cycle was incomplete (n = 5) or phase 3 activity was absent (n = 4) in the other patients. The incidence of clustered contractions was significantly increased in slow-transit constipation (P = 0.05 versus controls). The area under the contraction curve during late phase 2 (1509+/-296 mmHg x s) in patients with a complete cycle was significantly smaller than that in controls (2997+/-614 mmHg x s; P = 0.05). Orocaecal transit time was not significantly different among patients and controls, but oesophageal motility was abnormal in five of 18 patients and gastric emptying was abnormal in eight of 15 patients. CONCLUSION: Abnormalities of upper gut motility occur frequently in patients with slow-transit constipation. Interdigestive antroduodenal motility is characterized by (i) absence or prolonged duration of the migrating motor complex, (ii) an increased number of clustered contractions, or (iii) a decreased motility during late phase 2 of the migrating motor complex.     

Gastric myoelectrical activity, gastric emptying, and correlations with symptoms and fasting blood glucose levels in diabetic patients

BACKGROUND: The aims of this study were to determine the electrogastrogram (EGG) changes and gastric emptying rates in diabetic patients and to investigate the correlation between upper gastrointestinal symptoms, fasting blood glucose, and gastric myoelectrical abnormalities. METHODS: Fourteen patients with long-standing type 1 diabetes mellitus and dyspepsia symptoms participated in the study. EGG recordings were obtained 30 minutes before and during a 2-hour radionuclide gastric emptying test for a solid meal. Fasting blood glucose was determined immediately before the gastric emptying study. Symptoms of nausea, vomiting, early satiety, abdominal bloating, and pain were rated from 0 to 3. RESULTS: Nine patients (64%) had delayed gastric emptying with 84.6 +/- 4.5% retention at 2 hours. Seven patients (50%) had abnormal EGG findings. The postprandial power change in the EGG of the patients with delayed gastric emptying (-0.48 +/- 0.16 dB) was decreased compared with patients with normal gastric emptying (4.7 +/- 2.6 dB) (P = 0.079). In patients with abnormal EGGs, the mean symptom score was significantly higher than patients with normal EGGs (2.42 +/- 0.13 versus 2.0 +/- 0.16; P < 0.05). Compared with normal gastric emptying patients, patients with delayed gastric emptying had higher but not significantly different symptom scores (2.31 +/- 0.11 versus 2.08 +/- 0.30; P = 0.225). There was no significant difference in fasting glucose levels in delayed (252 +/- 61.2 mg/dl) versus normal (378 +/- 82 mg/dl) gastric emptying or abnormal (288 +/- 86.4 mg/dl) EGGs versus patients with normal (304 +/- 57.6 mg/dl) EGGs. CONCLUSIONS: Overall, 78% (11 of 14) of patients with diabetes had either gastric motility or myoelectrical abnormalities. Patients with abnormal EGGs had more severe symptom scores. In diabetic patients with symptoms of gastropathy, an EGG may provide an important screening test for diagnosing abnormal gastric motility.     

Clinical relevance of scintigraphic measurement of gastric emptying of a solid-liquid meal in the dumping syndrome.

Gastric emptying of the solid and liquid components of an ordinary meal was evaluated by a dual isotopic technique in 36 patients referred to our hospital for early postprandial symptoms induced by various esophageal and/or gastric operations. Patients were classified as typical (n = 11), equivocal (n = 9) or improbable (n = 16) dumpers, in accordance with their presenting symptoms, as assessed before gastric emptying measurement. Patients with typical dumping symptoms displayed, as expected, significant acceleration of gastric emptying of liquids (t1/2: 18 +/- 6 min. vs. 48 +/- 7 min. in healthy controls; p less than 0.02), and also exhibited a dramatic enhancement of gastric emptying of solids (t1/2: 11 +/- 1 min. vs. 126 +/- 12 min. in healthy controls; p less than 0.001) and a complete loss of solid-liquid discrimination (7 +/- 6 min. vs. 78 +/- 7 min. in healthy controls; p less than 0.01). Mean gastric emptying rates for equivocal and improbable dumpers were not significantly different from those of healthy controls, but individual results were very heterogeneous; they included stasis, acceleration, or both disorders, and were not predictable by analysis of symptoms alone. Thus gastric emptying of solids as well as liquids is accelerated in symptomatic dumping patients, and objective evaluation of the emptying of both solid and liquid gastric emptying is essential in atypical dumpers, in order to characterize their disorders and prescribe the most rational treatment.     

Interdigestive cycling and post-prandial release of pancreatic polypeptide in severe obesity

Changes in pancreatic polypeptide plasma concentrations have been reported in obesity. It has been suggested that altered PP plasma levels may play a role in the abnormal food intake observed in obesity. Earlier studies, however, have not considered the physiological fluctuations of PP during fasting. We examined PP plasma concentrations in 12 subjects with severe obesity and in 10 normal subjects during the entire cycle of interdigestive motility and after the administration of a standard mixed meal. Obese patients and healthy controls showed similar fluctuations of PP during individual phases of the migrating motor complex (MMC) and reached their peak PP plasma levels (134 +/- 35 (s.e.m.) pg/ml in controls vs 113 +/- 17 pg/ml in obese subjects) during phase III activity. Following the test meal, prompt release of PP occurred which was significantly higher than basal values at each 15 min interval during the first postprandial hour in both controls and obese patients. The integrated PP postprandial response at 60 min did not differ between obese patients (163 +/- 15 pg/ml.h) and controls (198 +/- 37 pg/ml.h; n.s.). A putative causal role for PP in obesity thus seems very unlikely.