Biomedical subjects

I Biemond

Publications and source records attributed to I Biemond.

At least 37 records · Page 2Linked to original sources

PubMed1999

Medium chain triglycerides activate distal but not proximal gut hormones.

BACKGROUND AND AIMS: Compared to long chain triglycerides (LCT), medium chain triglycerides (MCT) are considered an attractive caloric source in malabsorptive diseases because of their favorable physico-chemical characteristics. The use of MCTis, however, limited by the occurrence of gastrointestinal symptoms such as diarrhoea. We have, therefore, investigated the effects of MCT and LCT on proximal (cholecystokinin; CCK) and distal (peptide YY; PYY) gut hormone secretion. METHODS: Eight healthy volunteers participated in four experiments performed in random order during continuous intraduodenal administration for 360 min of a) saline (control); b) LCT15 mmol/h; c) MCT15mmol/h (equimolar); d) MCT 30 mmol/h (equicaloric). Plasma CCK and PYY were determined at regular intervals (radioimmunoassay). Duodenocecal transit (DCTT) was measured by lactulose H(2)breath test. RESULTS: DCTT during LCT (105 +/- 11 min) was not significantly different from saline (111 +/- 10 min). Both low dose MCT (54 +/- 5 min) and high dose MCT (61 +/- 6 min) significantly accelerated DCTT (P< 0.05). Plasma CCK increased significantly (P< 0.05) during LCT but not during MCT or saline. PYY increased significantly (P< 0.05) not only during LCT, but also during low and high dose MCT but not during saline. CONCLUSIONS: Intraduodenal MCTs a) accelerate intestinal transit; b) do not stimulate CCK release; c) but stimulate release of the distal gut hormone PYY. These results suggest that MCTs are not rapidly absorbed in the proximal gut but probably reach the ileocolonic region and stimulate PYY release.

Adult↗

PubMed1999

Serum gastrin and chromogranin A during medium- and long-term acid suppressive therapy: a case-control study.

BACKGROUND: Serum chromogranin A (CgA) is regarded as a reliable marker of neuroendocrine proliferation. We previously described increased serum CgA levels during short-term profound gastric acid inhibition. AIM: To investigate serum gastrin and CgA levels in dyspeptic patients during continuous medium- (6 weeks to 1 year), or long-term (1-8 years) gastric acid suppressive therapy. PATIENTS AND METHODS: 114 consecutive dyspeptic patients referred for upper gastrointestinal endoscopy were enrolled in a cross-sectional, case-control study [62 patients on continuous antisecretory therapy, either with proton pump inhibitors (n = 47) or H2-receptor antagonists (H2RA) (n = 15) for gastro-oesophageal reflux disease with or without Barrett's oesophagus or functional dyspepsia, and 52 age- and sex-matched patients without medical acid inhibition and with normal endoscopic findings (control group)]. Omeprazole doses ranged from 20 mg to 80 mg daily and ranitidine from 150 mg to 450 mg daily. Fasting serum CgA and serum gastrin levels were measured by radioimmunoassay (reference values: serum CgA < 4.0 nmol/L; serum gastrin < 85 ng/L). RESULTS: Fasting serum CgA levels positively correlated with serum gastrin in the entire study population (r = 0. 55, P = 0.0001). Median serum CgA values were higher in patients treated with a proton pump inhibitor than H2RA [2.8 (2.0-5.9) nmol/L vs. 2 (1.9-2.3) nmol/L, P < 0.002] and controls [2.8 (2.0-5.9) nmol/L vs. 1.8 (1.5-2.2) nmol/L, P < 0.0001) and did not differ between patients treated with H2RA or controls. Serum gastrin and CgA levels in patients on proton pump inhibitor therapy positively correlated with the degree and duration of acid inhibition. Patients on long-term proton pump inhibitor therapy had significantly higher fasting serum gastrin and CgA than those on medium-term proton pump inhibitor therapy [127 (73-217) ng/L vs. 49 (29-78) ng/L, P < 0.0001 and 4.8 (2.8-8) ng/L vs. 2.1 (1.9-2.6) ng/L, P < 0.001]. No such relation was found in patients on medium- vs. long-term H2RA. Overall, patients with positive Helicobacter pylori serology had higher serum gastrin and CgA levels than those with negative H. pylori serology [51 (27-119) ng/L vs. 27 (14-79) ng/L, P = 0.01, 2.4 (1.9-3.4) nmol/L vs. 2.0 (1.7-2.5) nmol/L, P = 0.05]. CONCLUSIONS: During long-term continuous proton pump inhibitor treatment, serum gastrin and CgA levels are significantly elevated compared to H2RA treatment and nontreated dyspeptic controls. H. pylori infection seems to affect gastric ECL cell secretory function. Increased serum CgA values during long-term profound gastric acid inhibition could reflect either gastric enterochromaffin-like cell hyperfunction or proliferative changes.

Adult↗

PubMed1999

Antroduodenal motility and small bowel transit during continuous intraduodenal or intragastric administration of enteral nutrition.

BACKGROUND: Gastrointestinal intolerance is observed more frequently during intraduodenal (ID) tube feeding than during intragastric (IG) feeding, possibly because it evokes a stronger gastrointestinal response and accelerates small bowel transit. We have investigated whether the accelerated small bowel transit during ID feeding results from alterations in antroduodenal motility pattern. DESIGN: The effect of IG and ID infusion of a polymeric diet (Nutrison, 125 kcal h-1) on antroduodenal motility, small bowel transit time (SBTT) and gastrointestinal hormone release was studied in nine healthy subjects. These subjects were studied on three occasions for 6 h during fasting, continuous IG or ID feeding. RESULTS: Phase III recurrence time was significantly prolonged during IG feeding compared with fasting (240 +/- 51 vs. 136 +/- 24 min; P < 0.05). None of the subjects had recurrence of phase III during ID feeding; the fed motor pattern remained present. Parameters of fed motility (mean amplitude and motility index) were not significantly different between IG and ID feeding, although the frequency of antral and duodenal contractions was lower during ID than during IG feeding. SBTT was significantly accelerated during ID compared with IG feeding and with fasting (58 +/- 8 vs. 73 +/- 9 and 83 +/- 10 min respectively; P < 0.05). Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels were significantly higher during ID than during IG feeding. Peptide YY (PYY) levels were significantly higher during ID than during fasting, but not during IG feeding CONCLUSIONS: During intraduodenal feeding, a fed motility pattern is preserved, whereas during intragastric feeding transition from a fed to a fasting motor pattern is observed in over 50% of the subjects. These differences may be related to augmented hormone release during intraduodenal feeding.

Adult↗

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

Faecal parameters in the assessment of activity in inflammatory bowel disease.

BACKGROUND: Determination of inflammatory activity is helpful when assessing the efficacy of drugs in therapeutic trials and in facilitating management of individual patients with inflammatory bowel disease (IBD). Faecal parameters have been hypothesized to be more specific than non-faecal measurements in the assessment of intestinal inflammation. METHODS: Review of the literature on faecal measurements in IBD. RESULTS AND CONCLUSIONS: Leakage of various proteins and leukocyte products into the intestinal lumen can be assessed and quantified in stool specimens and serve as a measurement of inflammatory activity. Several of these faecal parameters are raised in patients with IBD. There is a considerable overlap between patients with active and those with inactive disease, however, and the correlation of the faecal parameters with disease activity indices is often low. The value of alpha1-antitrypsin measurement in faeces in the assessment of intestinal inflammation has been well established. Further studies in patients with IBD are needed to determine whether other faecal parameters, such as lactoferrin, tumour necrosis factor alpha, PMN-elastase, lysozyme, leucocyte esterase, immunoglobulin A, among others, are more accurate or cost-effective than measurement of alpha1-antitrypsin in the stools of such patients.

Clinical Laboratory Techniques↗

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

Differential features of gastric cancer patients, either Helicobacter pylori positive or Helicobacter pylori negative.

BACKGROUND: Helicobacter pylori infection is associated with an increased risk of gastric cancer. In Helicobacter pylori negative patients, factors different from those in Helicobacter pylori positive patients may be involved in gastric carcinogenesis. METHODS: Thirty-nine recently diagnosed consecutive patients with gastric cancer were investigated. Gastric biopsies were obtained for detection of Helicobacter pylori (by immunohistochemistry), non-Helicobacter pylori flora (by modified Giemsa and culture) and histological assessment according to the Sydney classification by Haematoxylin-Eosin staining. In serum samples, Helicobacter pylori antibodies were determined by IgG enzyme-linked immunosorbent assay, IgA enzyme-linked immunosorbent assay, and Western blotting. Furthermore, serum gastrin, pepsinogen A and C and plasma chromogranin A were determined. RESULTS: Helicobacter pylori was detected by immunohistochemistry in 53.8%, by IgG in 56.4%, by IgA in 33.3%, and by Western blotting in 74.4% of the 39 patients. Ten patients (25.6%) were negative by both histology and serology. Non-Helicobacter pylori flora was detected in 27 of the 39 patients (69.2%) with a similar frequency in Helicobacter pylori positive and negative patients. Helicobacter pylori positivity was found significantly more often in diffuse than intestinal type carcinoma patients (p < 0.05). Elevated gastrin levels and antrum-sparing atrophic gastritis were more frequent in Helicobacter pylori negative than in Helicobacter pylori positive patients (p < 0.05). CONCLUSIONS: In 10 out of 39 gastric cancer patients, no evidence of previous or current Helicobacter pylori infection could be demonstrated. Non-Helicobacter pylori was found in 69.2% of patients regardless of the Helicobacter pylori status. Further studies are needed to establish the contribution of non-Helicobacter pylori flora as well as antrum-sparing atrophic gastritis with hypergastrinaemia to the development of gastric cancer.

Aged↗

PubMed1998

Fecal lysozyme in assessment of disease activity in inflammatory bowel disease.

This study was undertaken to determine whether measurement of fecal lysozyme is helpful in determining disease activity in inflammatory bowel disease. In 112 patients with Crohn's disease, 46 patients with ulcerative colitis, and 40 controls, fecal lysozyme concentration was measured. Results were correlated with CDAI and AI in Crohn's disease and with Truelove and Witts' grading in ulcerative colitis. Fecal lysozyme concentration (mean +/- SEM) was significantly (P < 0.001) higher in Crohn's disease (75 +/- 14 microg/g) and ulcerative colitis (238 +/- 33 microg/g) than in controls (6 +/- 1 microg/g). There was only a weak correlation between fecal lysozyme concentration and CDAI (r = 0.32; P = 0.001) and AI (r = 0.38; P < 0.0005) in patients with Crohn's disease and with Truelove and Witts' grading (r = 0.47; P = 0.001) in ulcerative colitis. When CDAI > or = 150 or AI > or = 100 were used as the standard for active disease, fecal lysozyme concentration was elevated in 78% of patients with active colonic Crohn's disease. In ulcerative colitis fecal lysozyme concentration was increased in active disease (95% in grade II and 94% in grade III) as compared 33% in grade I. Measurement of fecal lysozyme is of little help in diagnosing and determining disease activity of inflammatory bowel disease as whole, but it may be of help for diagnosis and assessment of activity of colonic IBD.

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

Hypergastrinaemia during long-term omeprazole therapy: influences of vagal nerve function, gastric emptying and Helicobacter pylori infection.

AIM: elucidate the mechanisms that lead to severe hypergastrinaemia during long-term omeprazole therapy for gastro-oesophageal reflux disease (GERD). PATIENTS AND METHODS: A total of 26 GERD patients were studied during omeprazole maintenance therapy. Twelve patients with severe hypergastrinaemia (gastrin > 400 ng/L) were compared with 14 control patients (gastrin < 300 ng/L). Helicobacter pylori serology and a laboratory screen were obtained in all patients. Gastric emptying was scored by the evidence of food remnants upon endoscopy 12 h after a standardized meal. Gastric antrum and corpus biopsies were analysed for histological parameters, as well as somatostatin and gastrin concentrations. All patients underwent a meal-stimulated gastrin test and the hypergastrinaemia patients also underwent a vagal nerve integrity assessment by pancreatic polypeptide testing (PPT). RESULTS: Severe hypergastrinaemia patients had a longer duration of treatment (80 vs. 55 months; P = 0.047) and were characterized by a higher prevalence of H. pylori infection (9/12 vs. 2/14, P = 0.004), corpus mucosal inflammation and atrophic gastritis (P < 0.04). This was reflected in lower serum pepsinogen A concentrations (mean +/- S.E.M. 53.6 +/- 17.9 vs. 137 +/- 16.0 mg/L, P = 0.03), pepsinogen A/C ratio (1.8 +/- 0.3 vs. 4.1 +/- 0.6, P = 0.005) and mucosal somatostatin concentrations (2.75 +/- 0.60 vs. 4.48 +/- 1.08 mg/g protein, P = 0.038). Two patients in the hypergastrinaemia group had signs of delayed gastric emptying, but none in the normogastrinaemia group did (P = N.S.). In addition, both groups had a normal meal-stimulated gastrin response. CONCLUSION: Severe hypergastrinaemia during omeprazole maintenance therapy for GERD is associated with the duration of therapy and H. pylori infection, but not with abnormalities of gastric emptying or vagal nerve integrity.

Aged↗

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

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.

Adult↗

PubMed1998

Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects.

BACKGROUND: The reason for the high prevalence of mild cobalamin (vitamin B-12) deficiency in the elderly is poorly understood. OBJECTIVE: We aimed to determine the reason for this high prevalence. DESIGN: We examined cobalamin intake, the presence and severity of atrophic gastritis, the presence of Helicobacter pylori infection, and plasma cobalamin and methylmalonic acid (MMA) concentrations in 105 healthy, free-living, older subjects aged 74-80 y. RESULTS: Mild cobalamin deficiency, ie, low to low-normal plasma cobalamin concentrations (< 260 pmol/L) and elevated plasma MMA concentrations (> 0.32 micromol/L), were found in 23.8% of subjects; 25.7% of subjects were not cobalamin deficient (plasma cobalamin > or = 260 pmol/L and plasma MMA < or = 0.32 micromol/L). Six subjects (5.8%), including 1 with mild cobalamin deficiency, had dietary cobalamin intakes below the Dutch recommended dietary intake of 2.5 microg/d. Mildly cobalamin-deficient subjects had lower total (diet plus supplements) cobalamin intakes (median: 4.9 microg/d; 25th and 75th percentiles: 3.9, 6.4) than did non-cobalamin-deficient subjects (median: 6.3 microg/d; 25th and 75th percentiles: 5.4, 7.9) (P = 0.0336), mainly because of less frequent use of cobalamin supplements (8% compared with 29.6%; chi2 = 3.9, P = 0.048). Atrophic gastritis was found in 32.4% of the total study group: mild to moderate in 19.6% and severe in 12.7%. The prevalence of severe atrophic gastritis, but not mild-to-moderate atrophic gastritis, was higher in mildly cobalamin-deficient subjects (25%) than in non-cobalamin-deficient subjects (3.7%) (chi2 = 4.6, P = 0.032). The prevalence of immunoglobulin G antibodies to H. pylori was similar in mildly cobalamin-deficient subjects (54.2%) and in non-cobalamin-deficient subjects (44.4%) (chi2 = 0.5, P = 0.5). CONCLUSIONS: The high prevalence of mild cobalamin deficiency in healthy, free-living, older Dutch subjects could be explained by inadequate cobalamin intake or severe atrophic gastritis in only 28% of the study population. Other mechanisms explaining mild cobalamin deficiency in older people must be sought.

Aged↗

PubMed1998

Expression of somatostatin receptors in human pancreatic tumor.

Somatostatin (SST) and its analogues are candidates for use as endocrine agents in the treatment of pancreatic neoplasm. To determine whether the status of SST receptors in the human pancreatic tumors differs from that in the tumor-free pancreata of the human and whether pancreatic adenocarcinoma expresses the same subgroup of SST receptors as found in gastrinomas, this study visualized and characterized SST receptors in human control pancreata (n = 10) as well as pancreatic cancers (n = 12) and gastrinomas (n = 8) with storage phosphor autoradiography. Both pancreatic adenocarcinoma and gastrinoma expressed specific SST receptors. The binding capacity (Bmax, 35.4 +/- 7.6 fmol/mg protein) and the affinity (Kd, 0.32 +/- 0.27 nM) of SST receptors in gastrinomas were significantly higher than in pancreatic cancers (Bmax, 15 +/- 2.5 fmol/mg protein; Kd, 2.16 +/- 0.4 nM). No specific SST receptors were detected in the human control pancreata. Octreotide showed similarly high potencies of inhibition of 125I-SST-28 binding as SST-28 in gastrinomas. Unlike gastrinomas, little competitive binding of 125I-SST-28 was found with octreotide in pancreatic cancers. In conclusion, compared with the control pancreas, an up-regulation of SST receptors was present in both pancreatic cancer and gastrinoma. The subgroup of SST receptors in pancreatic cancers differs from that in gastrinomas.

Adenocarcinoma↗

PubMed1998

Effect of intragastric or intraduodenal administration of a polymeric diet on gallbladder motility, small-bowel transit time, and hormone release.

OBJECTIVE: During postpyloric tube feeding, GI intolerance is observed more frequently than during prepyloric feeding, possibly by evoking a stronger GI response. METHODS: We investigated the effect of intragastric and intraduodenal administration of a polymeric diet (125 kcal/h) on gallbladder motility (by ultrasonography), duodeno-cecal transit time (by lactulose H2 breath test), and GI hormone release (including cholecystokinin, pancreatic polypeptide, and gastrin). Six healthy subjects (two male, four female; mean age 22 yr, range 18-27 yr) were studied on two separate occasions in random order during 6 h of continuous administration of the diet through either the gastric or duodenal port of a two-lumen tube. RESULTS: Intraduodenal feeding resulted in a more rapid contraction of the gallbladder, from 32 +/- 4 to 23 +/- 4 cm3 at 10 min (p < 0.05), reaching a minimum of 6 +/- 1 cm3, in contrast to intragastric feeding (31 +/- 4 to 19 +/- 3 cm3 at 60 min, p < 0.05; minimum 14 +/- 1 cm3). The gallbladder remained contracted during the 6-h study period during both intraduodenal and intragastric feeding. Small-bowel transit time was significantly accelerated during intraduodenal compared with intragastric feeding (51 +/- 12 vs 81 +/- 9 min; p = 0.003). Plasma cholecystokinin secretion was significantly (p < 0.05) increased during intraduodenal compared with intragastric feeding (848 +/- 107 vs 279 +/- 89 pmol x L(-1) x 360 min). The same was true for pancreatic polypeptide secretion. However, gastrin release was significantly (p < 0.05) higher during intragastric feeding. CONCLUSIONS: Intraduodenal feeding elicited a stronger GI response than intragastric feeding, as demonstrated by accelerated small-bowel transit time, more rapid and stronger gallbladder contractions, and increased cholecystokinin and pancreatic polypeptide release. Gastrin release, on the other hand, was stronger during intragastric feeding.

Adolescent↗

PubMed1998

Effect of medium- and long-chain triglycerides on lower esophageal sphincter pressure: role of CCK.

Fat meals are known to decrease lower esophageal sphincter (LES) pressure, possibly through postprandial CCK release. Dietary fat consists mainly of long-chain triglycerides (LCT), which potently stimulate CCK secretion. This effect contrasts with that of medium-chain triglycerides (MCT), which do not induce CCK release. We recorded LES pressure and gallbladder volume in six healthy subjects on five separate occasions during intraduodenal administration of 1) saline control, 2) LCT, 3) MCT, 4) LCT during intravenous infusion of the CCK receptor antagonist loxiglumide, and 5) MCT together with loxiglumide. LES pressure decreased significantly during administration of both LCT and MCT. Loxiglumide completely prevented the reduction in LES pressure during intraduodenal LCT, but not during intraduodenal MCT. Gallbladder volume decreased during LCT, but not during MCT. It is concluded that intraduodenal administration of equimolar amounts of both LCT and MCT significantly reduces LES pressure. The effect of LCT on LES pressure is mediated by CCK. The effect of MCT is not dependent on CCK, since MCT does not release CCK and loxiglumide does not prevent the MCT-induced reduction in LES pressure.

Adult↗

PubMed1997

Expression of receptors for gut peptides in human pancreatic adenocarcinoma and tumour-free pancreas.

Gut hormones that modulate the growth of normal pancreas may also modulate the growth of cancers originating from pancreas. This study visualized and compared the receptors for cholecystokinin (CCK), bombesin (BBS), secretin and vasoactive intestinal peptide (VIP) in tumour-free tissue sections of human pancreas (n = 10) and pancreatic ductal adenocarcinomas (n = 12) with storage phosphor autoradiography using radioligands. CCK-B receptors, present in control pancreata, were not detected in any of the pancreatic cancers. BBS receptors were visualized in control pancreata, but they were absent in 10 of 12 pancreatic cancers. In 5 of 12 pancreatic cancers, receptors for secretin were visualized, while binding for secretin was present in all tumour-free pancreata. Conversely, no specific binding of VIP was detected in control pancreata but was identified in 3 of 12 pancreatic cancer specimens. It is concluded that the expression of gut peptide receptors in pancreatic cancer differs from that in tumour-free pancreas. Receptors for these peptides are present in only a minority of pancreatic cancer specimens.

Adenocarcinoma↗

PubMed1997

Expression of peptide receptors in human endocrine tumours of the pancreas.

BACKGROUND: Gut peptides are known to influence hormone release and growth of endocrine tumours of the pancreas. Although information on somatostatin receptors has been provided recently, little is known on the receptor status of other gastrointestinal hormones in such tumours. AIMS: To analyse the spectrum of gut hormone receptors on endocrine tumours of pancreas. SUBJECTS: Four types of endocrine tumours from eight patientS. METHODS: The receptors for bombesin, secretin, vasoactive intestinal peptide, cholecystokinin, and somatostatin have been visualised and quantified with storage phosphor autoradiography. RESULTS: Bombesin receptors were present in all five gastrinomas and two primary VIPomas. Secretin receptors were expressed in four primary gastrinomas and one primary VIPoma from pancreas. Vasoactive intestinal peptide receptors were identified in four primary gastrinomas and all VIPomas. Furthermore, all VIPomas expressed cholecystokinin-B (gastrin) receptors, whereas, gastrinomas did not contain cholecystokinin-B receptors. The receptors for somatostatin were detected in all gastrinomas and VIPomas. Both somatostatinoma and glucagonoma were negative for all five types of peptide receptors studied. CONCLUSIONS: Besides somatostatin receptors, most of gastrinomas and VIPomas also express receptors for bombesin, secretin, and vasoactive intestinal peptide.

Adenoma, Islet Cell↗