Biomedical subjects

A A Masclee

Publications and source records attributed to A A Masclee.

At least 55 records · Page 3Linked to original sources

PubMed1999

Does jejunal feeding activate exocrine pancreatic secretion?

BACKGROUND: The upper small bowel is of pivotal importance for the stimulation of exocrine pancreatic secretion in response to a meal. We hypothesize that more distal delivery of nutrients into the small intestine will result in less activation of pancreatic secretion. MATERIALS AND METHODS: Eight healthy subjects (3 male, 5 female; age 23 +/- 1 years) participated in two experiments, performed in random order. Subjects were intubated with a 4-lumen tube. Duodenal outputs of pancreatic enzymes and bilirubin were measured by aspiration using a recovery marker. The distal opening was used for continuous administration of a mixed liquid meal and located at either the ligament of Treitz or 60 cm further distally. Gallbladder volume was measured and blood samples were drawn for determination of gastrointestinal hormones. The duration of each experiment was 4 h; with 1 h fasting and 3 h continuous administration of nutrients. RESULTS: During proximal jejunal feeding, pancreatic enzyme output increased significantly over basal levels. No significant increase over basal levels was observed during distal jejunal feeding. Bilirubin output and gallbladder contraction were significantly (P < 0.05) reduced during distal compared to proximal jejunal feeding. No significant differences were found in plasma levels of CCK, PYY and neurotensin between proximal and distal jejunal feeding. CONCLUSION: Continuous feeding in the distal jejunum does not stimulate exocrine pancreatic secretion but maintains gallbladder contraction, although to a lesser extent. These effects are not related to hormonal changes but probably reduced activation of the enteropancreatic reflexes.

Adult↗

PubMed1999

Effect of gastrin on proximal gastric motor function in humans.

UNLABELLED: The present study was performed to investigate the effect of gastrin on proximal gastric motor and sensory function. Ten healthy volunteers participated in three experiments performed in random order during: (A) continuous intravenous infusion of saline (control) or (B) gastrin (15 pmol kg-1 h-1) reaching postprandial serum gastrin levels or (C) gastrin infusion (15 pmol kg-1 h-1) preceded by acute acid inhibition with intravenous omeprazole. Proximal gastric function was evaluated using a barostat with stepwise pressure and volume distensions and volume measurements during set pressure (MDP + 2 mmHg). Gastrin significantly increased the intragastric volume compared to control during MDP + 2 mmHg (276 +/- 39 mL vs. 159 +/- 9 mL; P < 0.01) and reduced phasic slow volume wave frequency (from 1.4 +/- 0.1 to 0.7 +/- 0.1 per min; P < 0.01). During isobaric distensions gastrin increased gastric compliance (42 +/- 4 mL mmHg-1 vs. 31 +/- 3 mL mmHg-1; P < 0.05). These effects of gastrin infusion were completely abolished by pretreatment with omeprazole. Symptom perception decreased during gastrin infusion and was more dependent on pressure and wall tension than on volume. IN CONCLUSION: gastrin may have a role in regulating proximal gastric mechanics by inducing fundic relaxation and increasing gastric wall compliance. The effect of gastrin is dependent on acid secretion.

Adult↗

PubMed1999

Effect of bombesin on esophageal motility in humans.

We have investigated the effect of bombesin on esophageal motility and explored the mechanism of action of bombesin. Eight healthy subjects were studied in random order during intravenous administration of (1) bombesin, (2) bombesin + vagal cholinergic receptor blockade with atropine and (3) bombesin + somatostatin. Lower esophageal sphincter pressure (LESP) and esophageal body motility were recorded continuously by Dent-sleeve manometry. Bombesin significantly (p < 0.01) increased LESP from 20 +/- 2 mmHg to 43 +/- 6 mmHg. Neither atropine nor somatostatin significantly reduced the bombesin-induced increases in LESP. Bombesin significantly (p<0.05) increased peristaltic wave amplitude (from 61 +/- 4 to 105 +/- 9 mmHg) and duration (from 2.9 +/- 0.2 to 4.8 +/- 0.3 s) in the mid and distal part of the esophagus. Neither atropine nor somatostatin significantly reduced the esophageal body motor response to bombesin. In conclusion (1) bombesin significantly increases LESP and affects esophageal body motility by increasing peristaltic wave amplitude and duration and (2) the effect of bombesin on esophageal motility is not dependent on vagal cholinergic mechanisms and is not mediated by the action of gastrointestinal hormones released by bombesin.

Adult↗

PubMed1999

The role of the barostat in human research and clinical practice.

BACKGROUND: The barostat is a recently developed device used to study the physiology and pathophysiology of the motor and sensory functions of the gastrointestinal tract. It can monitor volume changes while maintaining a set constant pressure and deliver controlled distensions of gastrointestinal organs. Simultaneously, motility and visceral perception may be assessed. The barostat has contributed to the understanding of physiological processes in the gastrointestinal tract with regard to regulation of tone, compliance, enteric reflexes, sensation and processing of signals to and from the gut. In addition, the barostat has been used to study various gastrointestinal disorders. In functional bowel disorders, objective abnormalities in visceral sensitivity and enteric reflexes have been demonstrated. Numerous other diseases, gastrointestinal in origin as well as systemic diseases affecting the gut, have been studied. In the near future, the barostat may become a clinically useful tool for the objective diagnosis of motor and sensitivity disorders of the gut and for monitoring the effectiveness of therapy.

Baroreflex↗

PubMed1999

Effect of insulin and glucose on basal and cholecystokinin-stimulated exocrine pancreatic secretion in humans.

Pancreaticobiliary secretion is reduced during acute hyperglycemia. In nondiabetics, this inhibitory effect also may result from hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin (CCK)-stimulated pancreaticobiliary secretion. Nine healthy volunteers (age, 22-52 years) were studied on three occasions in random order during (a) intravenous saline (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mM), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/L, glucose at 4-5 mM). Duodenal outputs of bilirubin, amylase, trypsin, and bicarbonate were measured under basal conditions and during CCK infusion (0.25 and 0.5 IDU/kg/h). Basal pancreaticobiliary secretion was significantly (p < 0.05) reduced during both HG and HI. During low-dose CCK stimulation, HG significantly (p < 0.05) reduced bilirubin and trypsin output compared with control. In contrast, HI did not significantly reduce pancreatic enzyme and bilirubin output during low-dose CCK infusion. During high-dose CCK infusion, neither HI nor HG influenced pancreatic enzyme and bilirubin output. Pancreatic bicarbonate output was not influenced by CCK and remained significantly (p < 0.05) reduced during HI and HG compared with control. It is concluded that during both acute hyperglycemia and euglycemic hyperinsulinemia, basal pancreaticobiliary secretion is significantly reduced. CCK-stimulated pancreatic enzyme and bilirubin output is significantly reduced only during hyperglycemia. The inhibitory effect of hyperglycemia on pancreaticobiliary secretion in healthy volunteers may occur independent of insulin.

Adult↗

PubMed1999

Cholecystokinin secretion in patients with chronic pancreatitis and after different types of pancreatic surgery.

UNLABELLED: Cholecystokinin (CCK) secretion may be affected in patients with chronic pancreatitis (CP), but little is known on the effect of pancreatic surgery on CCK secretion. We measured CCK secretion (radioimmunoassay, RIA) in response to bombesin infusion (100 ng/kg/20 min) for 120 min to test CCK secretory capacity, to ingestion of a liquid diet (400 kcal) for 120 min, and in response to a solid fat-rich meal (500 kcal) for 120 min. These studies were performed in 45 patients with CP (25 with exocrine insufficiency), 15 patients after duodenum-preserving pancreatic head resection (DPRHP), 18 patients after the Whipple operation, 12 patients after distal pancreatectomy (DP), and 35 control subjects. In CP patients, the CCK secretory capacity was preserved, but the postprandial CCK response was reduced, depending on meal composition and the presence of exocrine insufficiency. In patients after Whipple's operation, CCK secretory capacity and postprandial CCK secretion were significantly (p < 0.05) reduced. In patients after DPRHP, CCK secretory capacity was not affected, but the postprandial CCK response was significantly (p < 0.05) reduced, depending on meal composition and the presence of exocrine insufficiency. In patients after DPRHP, fasting plasma CCK levels were significantly (p < 0.01) increased, pointing to the absence of feedback inhibition on CCK secretion by intraluminal enzymes. After DP, the CCK secretory capacity was not affected. IN CONCLUSION: alterations in CCK secretion are observed in patients with chronic pancreatitis and after pancreatic surgery. These alterations are related not only to the disease process (exocrine insufficiency) but also to the type of surgery and type of stimulus.

Adult↗

PubMed1999

Motor and sensory function of the proximal stomach in reflux disease and after laparoscopic Nissen fundoplication.

OBJECTIVE: After Nissen fundoplication, dyspeptic symptoms such as fullness and early satiety develop in >30% of patients. These symptoms may result from alterations in proximal gastric motor and sensory function. METHODS: We have evaluated proximal gastric motor and sensory function using an electronic barostat in 12 patients after successful laparoscopic Nissen fundoplications (median follow-up; 12 months). Twelve age- and gender-matched patients with severe gastroesophageal reflux disease (GERD) and 12 healthy volunteers served as controls. Studies were performed in the fasting state and after meal ingestion. Gastric emptying tests were performed in all patients. Vagus nerve integrity was measured by the response of pancreatic polypeptide (PP) to insulin hypoglycemia. RESULTS: Minimal distending pressure and proximal gastric compliance were not significantly different between post-Nissen patients, GERD patients, and healthy controls. Postprandial relaxation of the stomach, however, was significantly (p < 0.05) reduced post-Nissen (267 +/- 34 ml), compared with controls (400 +/- 30 ml) and GERD (448 +/- 30 ml). Postprandial relaxation was significantly (p < 0.01) prolonged in GERD patients. Postprandial relaxation of the stomach correlated with gastric emptying of solids (r = 0.62; p = 0.01). Gastric emptying of solids became significantly (p < 0.05) faster after fundoplication. Postprandial fullness was significantly (p < 0.05) increased in the operated patients. CONCLUSIONS: Post-Nissen patients have a significantly reduced postprandial gastric relaxation and significantly accelerated gastric emptying, which may explain postoperative dyspeptic symptoms. The abnormalities result from fundoplication and not from vagus nerve injury or reflux per se, because in reflux patients gastric relaxation and gastric emptying are prolonged.

Adult↗

PubMed1999

Effect of intravenous amino acids on interdigestive antroduodenal motility and small bowel transit time.

BACKGROUND: Patients on total parenteral nutrition have an increased risk of developing gallstones because of gall bladder hypomotility. High dose amino acids may prevent biliary stasis by stimulating gall bladder emptying. AIMS: To investigate whether intravenous amino acids also influence antroduodenal motility. METHODS: Eight healthy volunteers received, on three separate occasions, intravenous saline (control), low dose amino acids (LDA), or high dose amino acids (HDA). Antroduodenal motility was recorded by perfusion manometry and duodenocaecal transit time (DCTT) using the lactulose breath hydrogen test. RESULTS: DCTT was significantly prolonged during LDA and HDA treatment compared with control. The interdigestive motor pattern was maintained and migrating motor complex (MMC) cycle length was significantly reduced during HDA compared with control and LDA due to a significant reduction in phase II duration. Significantly fewer phase IIIs originated in the gastric antrum during LDA and HDA compared with control. Duodenal phase II motility index was significantly reduced during HDA, but not during LDA, compared with control. CONCLUSIONS: Separate intravenous infusion of high doses of amino acids in healthy volunteers: (1) modulates interdigestive antroduodenal motility; (2) shortens MMC cycle length due to a reduced duration of phase II with a lower contractile incidence both in the antrum and duodenum (phase I remains unchanged whereas the effect on phase III is diverse: in the antrum phase III is suppressed and in the duodenum the frequency is increased); and (3) prolongs interdigestive DCTT.

Adult↗

PubMed1999

Gall bladder emptying in severe idiopathic constipation.

BACKGROUND: It has been suggested that slow transit constipation (STC) may be part of a panenteric motor disorder. AIM: To evaluate motility of an upper gastrointestinal organ, the gall bladder, in 16 patients with STC and 20 healthy controls. METHODS: Gall bladder emptying (ultrasonography) was studied in response to neural, cephalic-vagal stimulation with modified sham feeding (MSF) for 90 minutes and in response to hormonal stimulation with cholecystokinin (CCK, 0.5 IDU/kg/h) for 60 minutes. RESULTS: Fasting gall bladder volume in patients with STC (17 (2) cm(3)) was significantly (p<0. 01) reduced compared with that in controls (24 (2) cm(3)). Gall bladder emptying in response to MSF was significantly reduced in patients with STC expressed both as percentage emptying (11 (5)% versus 22 (3)%; p<0.05) and as absolute emptying (2.1 (0.7) cm(3) versus 4.9 (0.7) cm(3); p<0.02). However, percentage gall bladder emptying in response to CCK was not different between patients and controls (73 (4)% versus 67 (4)%) although the absolute reduction in gall bladder volume was significantly (p<0.05) smaller in patients (10.7 (1.1) cm(3) versus 15.3 (1.4) cm(3)). CONCLUSIONS: Patients with slow transit constipation have smaller fasting gall bladder volumes, impaired gall bladder responses to vagal cholinergic stimulation, but normal gall bladder responses to hormonal stimulation with CCK. These results point to abnormalities in gastrointestinal motility proximal from the colon in slow transit constipation and more specifically, impaired neural responsiveness.

Adult↗

PubMed1998

Influence of hyperglycemia on the satiating effect of CCK in humans.

In the present study the effects of intraduodenal (i.d.) fat (endogenous CCK) and of CCK infusion on satiety were studied during normo-and hyperglycemic conditions. Eight healthy subjects participated in two protocols consisting of two experiments each. First protocol: (a) normoglycemia (control) with i.d. emulsified fat (i.d. fat) infusion, (b) acute hyperglycemia (HG) with plasma glucose levels stabilized at 15 mmol/L and i.d. fat infusion. In the second protocol the effect of exogenous cholecystokinin (CCK) on satiety was studied during normo- and hyperglycemia. Intraduodenal fat (Intralipid 10%) was infused at a dose of 1 g/h via a nasoduodenal tube in the first protocol, whereas in the second protocol CCK-33 was infused intravenously at a dose of 0.5 IDU/kg x h. Satiety was scored using visual analog scales (VAS). Plasma CCK levels were determined at regular intervals. During infusion of i.d. fat and i.v. CCK the VAS scores of wish to eat, hunger, and prospective feeding decreased significantly (p<0.05) in the normoglycemic experiments. During hyperglycemia satiety did not significantly change in the basal period; however, the scores of wish to eat, hunger, and prospective feeding increased significantly (p<0.05) when i.d. fat or i.v. CCK was administered. Plasma CCK levels in the basal and the stimulated period were not significantly different between normo- and hyperglycemia. In summary, the present study shows that in healthy humans volunteers 1) during normoglycemic conditions satiety can be induced by very low dose of i.d. fat and by CCK infusion, 2) during hyperglycemia the effect of i.d. fat and CCK on satiety are reversed, resulting in increased appetite.

Adult↗

PubMed1998

Effects of hyperglycemia and hyperinsulinemia on satiety in humans.

Hyperglycemia may influence satiety. One mechanism by which glucose could influence food intake is hyperinsulinemia. Therefore, we investigated the short-term effects of acute hyperglycemia and euglycemic hyperinsulinemia on satiety. Six healthy volunteers (aged 20 to 26 years) were studied for 240 minutes on three separate occasions in random order during (1) intravenous (i.v.) saline (control), (2) acute hyperglycemic hyperinsulinemia (HG) with plasma glucose at 15 mmol/L, and (3) euglycemic hyperinsulinemia (HI) with plasma insulin at 80 mU/L and glucose at 4 to 5 mmol/L. Subjective criteria for appetite like the wish to eat, prospective feeding intentions ("How much food do you think you can eat?"), and feelings of hunger and fullness were scored on a 100-mm visual analog scale (VAS) at 30-minute intervals. Appetite was also measured every 60 minutes with the use of a food selection list (FSL). Appetite (prospective feeding intentions, feelings of hunger, and the wish to eat) gradually increased over basal levels during control conditions and HI. In contrast, prospective feeding intentions and feelings of hunger gradually decreased during HG and were significantly (P < .05) reduced versus basal and control levels during the last hour of the experiment. The wish to eat followed the same pattern. Feelings of fullness did not significantly change in all three experiments. Total food selection was not significantly decreased during HG, but the preference for fat-rich or carbohydrate-rich items tended to be reduced. The study suggests that in humans hyperglycemia induces satiety. This effect seems not to be mediated by insulin, since HI had no effect on appetite. However, a potentiating effect of endogenous insulin on the satiating effect of high blood glucose levels cannot be excluded.

Adult↗

PubMed1998

Effect of insulin on basal and cholecystokinin-stimulated gallbladder motility in humans.

BACKGROUND/AIMS: Acute hyperglycemia inhibits gallbladder contraction. In non-diabetic subjects this inhibitory effect may result from endogenous hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin-stimulated gallbladder motility. METHODS: Gallbladder volume (ultrasonography) and duodenal bilirubin output were studied simultaneously in nine healthy volunteers (age 20-52 years) on 3 separate occasions in random order during: (a) saline infusion (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mmol/l), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/l, glucose at 4-5 mmol/l). After a 2-h basal clamp period, cholecystokinin was infused intravenously for 60 min at 0.25 IDU x kg(-1) x h(-1), followed by another 60 min at 0.5 IDU x kg(-1) x h(-1). RESULTS: HI and HG significantly (p<0.05) reduced basal duodenal bilirubin output compared to control, while basal gallbladder volume did not change. At the low dose cholecystokinin, gallbladder emptying during HG (25+/-3%) and HI (39+/-4%) was significantly (p<0.01) reduced compared to control (61+/-4%). The inhibitory effect of HG was significantly (p<0.05) stronger compared to HI. Duodenal bilirubin output during the low dose cholecystokinin was significantly (p<0.05) reduced by HG, but not by HI. No inhibitory effect of HG and HI on gallbladder emptying and duodenal bilirubin output was observed with the high dose of cholecystokinin. CONCLUSIONS: In healthy subjects acute hyperglycemia and euglycemic hyperinsulinemia reduce basal duodenal bilirubin output and inhibit gallbladder emptying stimulated by low dose cholecystokinin. These results suggest that insulin is involved in the inhibitory effect of hyperglycemia on basal and cholecystokinin-stimulated gallbladder motility.

Adult↗

PubMed1998

Effect of amino acids on lower esophageal sphincter characteristics and gastroesophageal reflux in humans.

The effect of a commercially available mixed amino acids solution, when given either intravenously or intragastrically, on lower esophageal sphincter (LES) pressure, frequency of transient LES relaxations (TLESRs) and gastroesophageal reflux (GER) was investigated in six healthy volunteers. LES pressure and esophageal pH were simultaneously recorded on three separate occasions 1 hr before (basal) and 3 hr during intravenous or intragastric infusion of amino acids (250 mg protein/kg/hr) or saline (control). No significant changes in LES pressure were seen in the control experiment. Intravenous amino acids caused a rapid and sustained (P < 0.01) decrease in LES pressure whereas intragastric amino acids decreased LES pressure only gradually and temporarily (P < 0.01). In the three experiments no significant differences were observed in TLESR frequency, the number of GER episodes, the mechanism of reflux, or duration of acid exposure. In healthy subjects both intragastric and, especially, intravenous infusion of amino acids significantly decrease LES pressure but do not affect the frequency of TLESRs or GER episodes during a continuous liquid gastric load.

Adult↗

PubMed1998

Obese women are less sensitive for the satiety effects of bombesin than lean women.

OBJECTIVE: The aim of this study was to investigate whether infusion of bombesin, when combined with a gastric preload, influence satiety and foot intake in obese and lean healthy women. DESIGN: Double blind, placebo controlled study. SETTING: Department of Gastroenterology, Leiden University Medical Center, The Netherlands. SUBJECTS: Obese (n = 7) and lean (n = 7) healthy women. INTERVENTIONS: Intravenous infusion of bombesin (0.09 nmol/kg ideal weight/h) or placebo for 165 min. Gastric preload of banana slices was administered at time 60 min. Meal ingestion started at time 75 min (banana slices). Food intake was calculated and satiety was measured by visual analog scales. RESULTS: During infusion of bombesin the amount of food eaten by the lean individuals (193+/-37 g) was significantly reduced compared to saline infusion (365+/-42 g, P < 0.05). However, bombesin induced no significant feeding suppression in obese women when compared to saline (241+/-46 vs 301+/-45 g, respectively). The decrease in food intake during bombesin infusion compared to saline was significantly greater in lean subjects (173+/-30 g) than in obese subjects (59+/-35 g; P < 0.05). Only in lean subjects subjective preprandial hunger feelings were significantly affected by bombesin infusion. CONCLUSIONS: Infusion of bombesin, when combined with a gastric preload, inhibits food intake and increases satiety in lean women. Obese women are less sensitive for these bombesin induced satiety effects.

Adult↗

PubMed1998

Interdigestive antroduodenal motility and gastric acid secretion.

BACKGROUND: In humans, interdigestive acid secretion and antroduodenal motility are closely related with cyclic variations in acid secretion, synchronous with the various phases of the migrating motor complex (MMC). Duodenal acidification inhibits antral motility, but little is known about the effect of acute acid inhibition on antroduodenal motility. AIM: To study the effect of acute acid inhibition on antroduodenal motility. SUBJECTS: Ten healthy volunteers (four men and six women: age range 20-31 years). METHODS: Antroduodenal motility (perfusion manometry) and gastric acid secretion (continuous aspiration with recovery marker) were measured simultaneously. Each subject was studied twice in random order during (1) intravenous infusion of saline for one-two complete MMC cycles and (2) during acute acid inhibition with intravenous famotidine (bolus 20 mg, continuous infusion 4 mg/h) for one-two complete MMC cycles or at least 240 min. RESULTS: In the saline study, acid output in phase III (2.1 +/- 0.3 mmol/10 min) and late phase II (1.7 +/- 0.2 mmol/10 min) was significantly (P<0.05) increased over early phase II and phase I (1.2 +/- 0.2 and 1.2 +/- 0.2 mmol/10 min, respectively). Famotidine increased gastric pH to above pH 6 within 30 min. After acid inhibition, duration of MMC cycle during famotidine (106 +/- 8 min) was not significantly different from the saline experiment (133 +/- 14 min). Phase distribution of the MMC cycle was not significantly different between famotidine (I, II and III: 12 +/- 3, 82 +/- 3 and 5 +/- 1%) and saline (I, II and III: 13 +/- 3, 83 +/- 3 and 4 +/- 1%). CONCLUSIONS: Gastric acid secretion varies cyclically with interdigestive antroduodenal motility. Acute acid inhibition with intravenous famotidine does not significantly affect interdigestive antroduodenal motility.

Adult↗

PubMed1998

Effects of somatostatin on proximal gastric motor function and visceral perception.

BACKGROUND: Somatostatin affects gastrointestinal motility and secretion and visceral sensation, but little is known about its effects on the proximal stomach. AIM: To evaluate the effects of somatostatin on proximal gastric motor function and perception of symptoms. METHODS: Six healthy subjects participated in two experiments performed in random order during continuous intravenous infusion of saline or somatostatin (250 microg/h). Proximal gastric motor function was evaluated using a barostat. We performed pressure and volume distensions and a barostat procedure (minimal distending pressure + 2 mmHg). Symptoms were evaluated at regular intervals using visual analogue scales (VAS). RESULTS: Neither minimal distending pressure nor gastric fundal tone were significantly different between somatostatin and saline. Pressure-volume curves during distensions were not influenced by somatostatin. However, phasic volume waves were significantly (P < 0.001) reduced by somatostatin, and somatostatin significantly (P < 0.05) reduced symptom perception of fullness and abdominal pressure during stepwise distensions.

Adult↗

PubMed1998

Hyperglycaemia reduces gastrin-stimulated gastric acid secretion in humans.

BACKGROUND: Recent studies have pointed to the role of plasma glucose in the regulation of gastrointestinal function. METHODS: We have investigated the effect of acute hyperglycaemia on gastric acid secretion and pancreatic polypeptide (PP) release. Gastric acid output was measured under basal conditions and in response to intravenous infusion of gastrin-17 in two doses: 5 pmol kg-1 h for 60 min and 15 pmol kg-1 h for another 60 min. Seven healthy subjects were studied during normoglycaemia and during acute hyperglycaemia at 15 mmol L-1. Acid output was measured by continuous aspiration using phenol red as recovery marker. Plasma PP levels were determined at regular intervals. RESULTS: Gastrin infusion at 5 pmol kg-1 h significantly (P < 0.05) increased acid output both during normoglycaemia and during hyperglycaemia. Gastrin infusion at 15 pmol kg-1 h further and significantly (P < 0.05) increased the acid output during both experiments. Hyperglycaemia significantly (P < 0. 05) reduced basal acid output (2.5 +/- 0.9 vs. 6.3 +/- 1.9 mmol h-1), low-dose gastrin stimulated acid output (6.5 +/- 1.7 vs. 13.0 +/- 1. 8 mmol h-1) and high-dose gastrin stimulated acid output (11.7 +/- 3. 0 vs. 19.4 +/- 3.0 mmol h-1) compared with normoglycaemia. Plasma PP levels were not stimulated by gastrin-17 infusion and were significantly (P < 0.05) reduced during hyperglycaemia. CONCLUSIONS: (a) Basal and gastrin-17-stimulated gastric acid secretion are reduced during hyperglycaemia; (b) infusion of gastrin-17 to physiological post-prandial levels does not affect plasma PP levels; (c) plasma PP levels are reduced during hyperglycaemia, suggesting vagal-cholinergic inhibition of gastric acid secretion during hyperglycaemia.

Adult↗

PubMed1998

Dose-dependent inhibition of postprandial gallbladder motility and plasma hormone secretion during acute hyperglycemia.

BACKGROUND: Actual blood glucose concentrations influence gastrointestinal function. We investigated whether in healthy subjects the inhibitory effect of acute hyperglycemia on gallbladder motility is dose-dependent. METHODS: Seven healthy volunteers were studied on four separate occasions in random order during euglycemia and during hyperglycemic clamping, at 4 mmol/l, 8 mmol/l, 12 mmol/l, and 16 mmol/l, respectively. Gallbladder volumes (ultrasonography) and plasma hormone release were studied before and after ingestion of a meal. RESULTS: Postprandial gallbladder contraction was significantly (P < 0.05) and dose-dependently inhibited during the hyperglycemic experiments at 8, 12, and 16 mmol/l (56%+/-8%, 49%+/-8%, and 30%+/-5%, respectively) compared with euglycemia (68%+/-6%). Postprandial cholecystokinin release was significantly (P < 0.05) reduced compared with euglycemia only at a plasma glucose level of 16 mmol/l (116+/-28 versus 159+/-13 pmol x l(-1) x 120 min). Plasma pancreatic polypeptide secretion, as an indirect measure of vagal-cholinergic tone, was significantly (P < 0.05) and dose-dependently reduced during hyperglycemia at 8, 12, and 16 mmol/l. CONCLUSION: In healthy subjects acute hyperglycemia significantly and dose-dependently inhibits postprandial gallbladder motility. Future studies on gallbladder motility should take into account the influence of plasma glucose, because already at postprandial glucose levels gallbladder motility is reduced.

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