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Biomedical subjects

M M Wolfe

Publications and source records attributed to M M Wolfe.

At least 91 records · Page 5Linked to original sources
PubMed1985

Cimetidine interaction with amitriptyline.

The interaction of cimetidine with amitriptyline was assessed by means of amitriptyline and nortriptyline plasma concentration measurements, standing blood pressure and pulse rate, digit symbol substitution, and visual analogue scales. Cimetidine increased plasma amitriptyline concentrations and decreased plasma nortriptyline concentrations, apparently by inhibiting presystemic metabolism. The changes in blood pressure, pulse rate and digit symbol substitution correlated with changes in concentrations of amitriptyline in plasma and expected changes based on a dose ranging preliminary experiment. Changes in subjective ratings of effects correlated with changes in nortriptyline concentrations in plasma.

Adult↗
PubMed1985

Functional and anatomical relationships between antral gastrin cells and gastrin-releasing peptide neurons.

The present studies were directed to examine the effect of gastrin-releasing peptide (GRP) on beta-adrenergic stimulated gastrin release by cultured rat antral mucosa and to assess the anatomical relationship between gastrin cells and GRP nerves in rat and human antrum. Peptide-containing cells were identified by application of an avidin-biotin-peroxidase immunocytochemical double staining method utilizing antibodies to GRP and gastrin prepared in rabbits. Rat antral mucosa was cultured for 60 min and gastrin released into the culture medium was measured by radioimmunoassay. Inclusion of antibodies to GRP in culture medium did not affect carbachol-stimulated gastrin release, whereas isoproterenol-stimulated gastrin release into the medium was inhibited significantly by addition of GRP antiserum to the culture medium. GRP-containing neurons and axonal fibers were stained immunocytochemically with diaminobenzidine (reddish-brown specific staining) and were located in the lamina propria adjacent to and surrounding the main lobules of antral glands. After double staining utilizing 4-Cl-1-Naphthol as substrate, blue stained gastrin-containing cells were identified in the middle and deeper regions of antral glands in close proximity to GRP neuronal elements. These studies suggest that beta-adrenergic, but not cholinergic, stimulation of gastrin release is mediated, at least in part, through GRP. They also demonstrate intimate anatomical, as well as functional, relationships between gastrin cells and GRP-containing neurons.

Animals↗
PubMed1985

Effect of antibodies to somatostatin on acid secretion and gastrin release by the isolated perfused rat stomach.

The present studies were directed toward examining the effect of somatostatin on gastrin release and acid secretion by the isolated vascularly perfused rat stomach. Rat stomachs were perfused in situ with Krebs-Ringer bicarbonate buffer containing 10% ovine erythrocytes and gassed with 95% O2-5% CO2. Inclusion of pentagastrin in the perfusion buffer increased acid output from 2.2 +/- 0.4 microEq H+/h during control perfusion to 18.8 +/- 1.8 microEq H+/h (p less than 0.01). In order to determine the effect of somatostatin on acid secretion and gastrin release, specific antibodies to somatostatin were included in the perfusate. Inclusion of antibodies to somatostatin in the buffer without pentagastrin did not significantly enhance acid output; however, gastrin concentration in the portal venous effluent increased from 15.1 +/- 2.0 to 25.2 +/- 5.2 pg/ml at 45 min (p less than 0.05). When antibodies to somatostatin were perfused in the presence of pentagastrin, acid output increased by 32% to 24.9 +/- 1.2 microEq H+/h (p less than 0.05); however, no change in gastrin concentration over basal was detected in the portal effluent. Results of these studies indicate that the capacity of the isolated rat stomach to secrete acid permits direct assessment of factors involved in the regulation of acid secretion. Under the conditions of these experiments, gastric somatostatin inhibits basal gastrin release and directly inhibits pentagastrin-stimulated acid secretion without affecting gastrin release.

Animals↗
PubMed1985

Preferential binding of vasoactive intestinal peptide to hepatic nonparenchymal cells.

The binding of 125I-vasoactive intestinal peptide (125I-VIP) and 125I-insulin has been examined in highly enriched populations of rat hepatocytes and hepatic nonparenchymal cells. 125I-VIP bound to high-affinity sites (Ka = 1.7 X 10(9) M-1) in nonparenchymal cells. Specific binding in these cells was nearly fivefold greater than in hepatocytes (15.0 +/- 0.6% vs. 3.6 +/- 0.7% radioactivity bound per 4 X 10(5) cells). In contrast, 125I-insulin binding was similar in both cell populations (18.2 +/- 2.4% per 4 X 10(5) cells in hepatocytes vs. 17.1 +/- 1.0% in nonparenchymal cells). Glucagon and insulin had no effect on 125I-VIP binding in nonparenchymal cells. Secretin inhibited 125I-VIP binding but was only about 1% as potent as unlabeled VIP. VIP had no apparent effect on cAMP levels in either cell population, whereas glucagon increased cAMP levels in both cell types. Our findings suggest that VIP binds preferentially to hepatic nonparenchymal cells and that these cells are primarily responsible for the clearance of VIP from the portal circulation.

Animals↗
PubMed1985

Effect of GRP on beta-adrenergic-stimulated gastrin and somatostatin release in the isolated rat stomach.

The present studies were directed toward examining the effects of gastrin-releasing peptide (GRP) on acid secretion and on beta-adrenergic-stimulated gastrin and somatostatin release using the isolated vascularly perfused rat stomach. Including pentagastrin in perfusion buffer increased acid output from 2.2 +/- 0.4 mueq H+/h during control perfusion to 18.8 +/- 1.8 mueq H+/h (P less than 0.01). No significant changes in acid secretion were detected when either GRP or specific antibodies to GRP were included in perfusate in the absence or presence of pentagastrin. Inclusion of 10(-9) M isoproterenol in the perfusate did not change acid output with respect to control; however, gastrin and somatostatin release into the portal venous effluent was significantly enhanced. Peak gastrin and somatostatin concentrations observed at 15 min were 753 +/- 43% (P less than 0.001) and 345 +/- 43% (P less than 0.01), respectively, of basal levels. When antibodies to GRP were included in perfusate containing isoproterenol, gastrin and somatostatin release into the portal venous effluent was significantly inhibited. The results of these studies indicate that GRP does not affect basal or pentagastrin-stimulated gastric acid secretion in the isolated perfused rat stomach. However, under the conditions of these experiments, beta-adrenergic stimulation of gastrin and somatostatin release appears to be mediated, at least in part, through GRP.

Animals↗
PubMed1985

Zollinger-Ellison syndrome associated with persistently normal fasting serum gastrin concentrations.

A 63-year-old man with a 2-year history of upper gastrointestinal ulcers was found to have the Zollinger-Ellison syndrome. Despite histologic verification of gastrinoma, several fasting serum gastrin concentrations were normal. However, in response to intravenous secretin infusion, a paradoxical increase in serum gastrin levels indicative of gastrinoma was seen. Although serum gastrin concentrations in patients with suspected gastrinoma may be persistently normal, provocative testing may be necessary to establish the diagnosis of the Zollinger-Ellison syndrome.

Fasting↗
PubMed1985

Elevated fasting cholecystokinin levels in pancreatic exocrine impairment: evidence to support feedback regulation.

Previous studies have suggested that intraduodenal protease suppression of pancreatic exocrine secretion may be mediated through cholecystokinin (CCK) release. Our study compares basal plasma immunoreactive CCK concentrations in normal human subjects with those obtained in patients with chronic pancreatitis. Fasting plasma samples were collected from 18 normal subjects and from 18 patients with chronic pancreatitis. Eight patients had mild to moderate pancreatic exocrine impairment, and 10 had severe exocrine insufficiency. Venous plasma immunoreactive CCK concentrations were measured with two distinct peptide region-specific antibodies. Basal plasma CCK concentration in controls was 14.3 +/- 1.3 fmol/ml (mean +/- SEM), a value significantly less than that obtained in all patients with chronic pancreatitis, 30.1 +/- 4.0 fmol/ml (p less than 0.001). Patients with mild to moderate impairment had a fasting plasma CCK concentration of 32.8 +/- 7.9 fmol/ml (vs. control p less than 0.01), and those with severe disease 27.9 +/- 3.6 fmol/ml (vs. control p less than 0.001). In five patients with mild to moderate impairment of exocrine function and pancreatic extract-responsive abdominal pain, there was a 39 +/- 11% decrease in basal CCK levels during extract therapy (p less than 0.05). Results of this study indicate that pancreatic exocrine impairment is associated with elevated basal CCK levels, which may reflect a failure to provide feedback downmodulation of CCK release.

Adult↗
PubMed1985

Specificity of commercially available antibodies used for gastrin measurement.

We examined the specificity of commercially available antibodies used in measurement of serum gastrin. Antibodies were obtained from five commercial laboratories, and antibody immunoreactivity with gastrin and cross-reactivity with cholecystokinin (CCK) were determined. All antibodies were equally immunoreactive with gastrin, and cross-reactivity of three antibodies with CCK was minimal (less than 5%). In contrast, substantial cross-reactivity with CCK was found with two antibodies. To determine the clinical significance of cross-reactivity with CCK, secretin injection tests were performed in 24 individuals: seven in normal health, four with Zollinger-Ellison syndrome, three with antral gastrin cell hyperfunction, six with ordinary duodenal ulcer disease, and four with atrophic gastritis. Serum gastrin levels were measured with all five gastrin antibodies. The response to secretin was negative in all normal subjects and in those with duodenal ulcer and antral gastrin cell hyperfunction. The response to secretin was positive in all four patients with gastrinoma with use of the five antisera. All four patients with atrophic gastritis had normal responses to secretin when antibodies with minimal CCK cross-reactivity were used; however, two of four had false positive secretin test results when serum gastrin levels were measured with the two antibodies with a high degree of cross-reactivity with CCK. These studies indicate that significant cross-reactivity of gastrin antibodies with CCK can result in false positive secretin injection test results and can lead potentially to the erroneous diagnosis of Zollinger-Ellison syndrome.

Antibodies↗
PubMed1984

Pentagastrin-stimulated gastric acid secretion by the isolated perfused rat stomach.

The purpose of this present study was to develop a method for stimulation of acid secretion by the isolated perfused rat stomach. Rat stomachs were perfused in situ via the abdominal aorta and celiac axis with Krebs-Ringer bicarbonate buffer in the presence or absence of 10% ovine erythrocytes. The gastric lumen was perfused with distilled water and gastric contents were collected at frequent intervals through a catheter at the pylorus. Sixty minute gastric acid output in response to various concentrations of pentagastrin was determined by titration of gastric contents with 0.01 N NaOH to pH 7.0. During arterial perfusion with Krebs-Ringer bicarbonate buffer in the absence of ovine erythrocytes gastric acid output was 2.50 +/- 0.58 SEM microEq H+/h, which did not increase in response to perfusion with Krebs-Ringer bicarbonate buffer containing pentagastrin. However, inclusion of 10% ovine erythrocytes in the arterial perfusate resulted in substantial stimulation of gastric acid by pentagastrin: maximal acid output, achieved with a pentagastrin dose of 0.6 microgram/kg/h, was 23.5 +/- 3.73 microEq H+/h (p less than 0.01). The results of the present study demonstrate the capacity of the isolated vascularly perfused rat stomach to secrete acid and provide a model for studying interactions of gastrointestinal regulatory peptides and their physiologic roles in the regulation of gastric acid secretion.

Animals↗
PubMed1984

Alterations in motor function of the small intestine from intravenous and intraluminal cholecystokinin.

Cholecystokinin has been found within the lumen of the gastrointestinal tract; however, its effect on intestinal motility has not been studied. We examined the effect of intraluminal and intravenous infusion of the octapeptide of cholecystokinin (CCK-OP) on myoelectric activity in the intestine of rabbits. CCK-OP was infused intraluminally at 1,000 ng X kg-1 X h-1, and portal venous blood samples were obtained hourly for plasma immunoreactive CCK. CCK-OP was also infused intravenously at a similar rate, and hourly peripheral venous blood samples were obtained for plasma immunoreactive CCK. Myoelectric activity was monitored in a 12-cm ligated ileal segment and the proximal adjacent small intestine after the infusion of intraluminal or intravenous CCK-OP. Intraluminal infusion of CCK-OP caused a significant increase (P less than 0.01) in both migrating action potential complexes (MAPC) and repetitive bursts of action potentials (RBAP) (3.1 +/- 0.8 MAPC/h and 4.6 +/- 1.3 RBAP/h). In contrast, intravenous CCK-OP induced only repetitive bursts of action potentials (8.3 +/- 1.7 RBAP/h, P less than 0.01). In summary, alterations in intestinal motility may vary according to the route of administration of the individual peptide. Furthermore, results from these studies suggest that intraluminal release of regulatory peptides may be important in the modulation of intestinal motility.

Action Potentials↗
PubMed1984

Effects of carbachol on gastrin and somatostatin release in rat antral tissue culture.

Recent studies have demonstrated that somatostatin-containing cells are in close anatomic proximity to gastrin-producing cells in antral mucosa, suggesting a potential local regulatory role for somatostatin. The purpose of this study was to examine further the relationships between gastrin and somatostatin and the effects of the cholinergic agonist carbachol on content and release of gastrin and somatostatin using rat antral mucosa in tissue culture. Antral mucosa was cultured at 37 degrees C in Krebs-Henseleit buffer, pH 7.4, gassed with 95% O2-5% CO2. After 1 h, the culture medium was decanted and the tissue was boiled to extract mucosal gastrin and somatostatin. Inclusion of carbachol 2.5 X 10(-6) M in the culture medium decreased medium somatostatin from 1.91 +/- 0.28 (SEM) ng/mg tissue protein to 0.62 +/- 0.12 ng/mg (p less than 0.01), extracted mucosal somatostatin from 2.60 +/- 0.30 to 1.52 +/- 0.16 ng/mg (p less than 0.001), and percentage of somatostatin released from 42% +/- 2.6% to 27% +/- 2.2% (p less than 0.01). Carbachol also increased culture media gastrin from 14 +/- 2.5 to 27 +/- 3.0 ng/mg protein (p less than 0.01). Tissue content and release of gastrin and somatostatin were also examined during culture of rat antral mucosa in culture media containing antibodies to somatostatin in the presence and in the absence of carbachol. Incubation with somatostatin antisera, both with and without carbachol, markedly increased culture media concentrations of somatostatin, all of which was effectively bound by antibodies present in the media. Antibody binding of somatostatin was accompanied by significant increases in culture media gastrin concentrations, both in the presence and in the absence of carbachol. Results of these studies support the hypothesis that antral somatostatin exerts a local regulatory effect on gastrin release and that cholinergic stimulation of gastrin release is mediated, at least in part, through inhibition of somatostatin synthesis and release.

Animals↗
PubMed1984

Immunochemical characterization of gastrinlike and cholecystokininlike peptides released in dogs in response to a peptone meal.

This study was designed to examine and compare the nature of gastrinlike and cholecystokininlike peptides released into the portal and peripheral venous circulation in response to a peptone meal. Six dogs were prepared with portal venous catheters and gastric fistulas. Portal and peripheral venous sera were obtained before and after gastric infusion of a 10% peptone meal. Serum levels of gastrin and cholecystokinin immunoreactive peptides were determined by radioimmunoassay using two distinct peptide region-specific antibody preparations. These separate antibody preparations demonstrated specificity for (a) C-terminal tetradecapeptide gastrin (4-17hG17), heptadecapeptide gastrin (G17), and big gastrin (G34) (gastrin antibody); and (b) all biologically active forms of gastrin and cholecystokinin (gastrin-cholecystokinin antibody). Using the antibody preparation with specificity for gastrin and not cholecystokinin, the mean basal immunoreactive gastrin from portal (8.33 +/- 2.4 fmol/ml, mean +/- SEM) and from peripheral (6.19 +/- 0.9 fmol/ml) venous sera both increased after peptone infusion, with an early peak (2 min in portal and 4 min in peripheral serum) and a second peak at 30 min in both circulations. Measurements using antibodies with specificity for both cholecystokinin and gastrin yielded strikingly different results. The portal venous serum peptide concentration (49 +/- 10 fmol/ml) increased sharply within 30 s after peptone infusion to a single peak at 2 min (139 +/- 37 fmol/ml). The basal peripheral venous serum peptide concentration (43 +/- 8.8 fmol/ml) increased more gradually to a single peak at 8 min (78 +/- 14 fmol/ml). Studies with Sephadex (G-50 superfine) gel chromatography indicated that gastrin released in response to the peptone meal was primarily G17. However, of the peptides released in response to the peptone meal that were recognized by the gastrin-cholecystokinin antibody, greater than 80% were shown to be distinct from gastrin. Gel chromatographic studies demonstrated that peptone meal-stimulated immunoreactive cholecystokinin release consisted of two major peaks, eluting in positions identical to those of intact cholecystokinin (CCK33) and the octapeptide of cholecystokinin (CCK8).

Animals↗
PubMed1984

Hepatic clearance of gastrin and cholecystokinin peptides.

The purpose of this study was to examine and quantify hepatic uptake and degradation of gastrin and cholecystokinin peptides. Rat livers were perfused in situ, without recirculation, with Krebs-Ringer bicarbonate (pH 7.4) containing 10% bovine erythrocytes, gassed with 95% O2-5% CO2. Gastrin and cholecystokinin peptide fragments of various lengths were injected into a portal vein via a sidearm syringe for over 1 min, and hepatic venous effluent was collected every minute for 20 min. After injection of 125I-labeled gastrin peptides more than eight amino acids in length, greater than 95% radioactivity appeared in the hepatic venous effluent, all of which was intact peptide, as determined by immunoprecipitation, trichloroacetic acid precipitation, and Sephadex gel chromatography. Decreasing the chain length to eight or less amino acids resulted in progressive increases in hepatic uptake and degradation of gastrin fragments. Injected cholecystokinin peptides greater than seven amino acids in length traversed the liver intact, whereas smaller cholecystokinin peptides were cleared by the liver. The liver eliminated greater than 90% of the biologically active carboxyl-terminal tetrapeptide amide common to gastrin and cholecystokinin. The results of this study indicate that gastrin and cholecystokinin peptides longer than seven amino acids traverse the liver without significant degradation, however, smaller peptides are progressively cleared during hepatic transit. Therefore, if small gastrin and cholecystokinin peptides from antral and intestinal mucosa are released and reach the portal venous circulation, hepatic inactivation would appear to prevent them from reaching the systemic circulation, precluding their significant contribution to gastric acid secretion and other physiologic functions.

Animals↗
PubMed1983

Enteric release of vasoactive intestinal peptide after a peptone meal in the dog.

Vasoactive intestinal peptide (VIP) concentrations were measured by radioimmunoassay in plasma from portal and peripheral venous blood obtained from six alert, non-anesthetized dogs before and after gastric infusion of a 10% peptone meal. Mean basal portal and cephalic vein plasma VIP concentrations were 42 +/- 11.7 and 42 +/- 8.0 (S.E.M.) pg/ml, respectively. No significant changes in peripheral venous plasma VIP concentrations were noted after the peptone meal throughout the duration of the collection period. In contrast, however, the mean VIP concentration in portal plasma increased promptly after the peptone meal with a peak of 79 +/- 8.2 pg/ml (P less than 0.02) occurring 8 min after infusion of the meal. This was followed by a gradual decline in portal plasma VIP levels, with a return to prefeeding concentrations at 60 min (44 +/- 6.3 pg/ml). Results of these studies demonstrate that following gastric infusion of a peptone meal in the dog, portal, but not peripheral, plasma VIP concentrations increase significantly. Failure to detect augmentation of peripheral vein VIP levels after the meal is probably due to hepatic clearance of VIP.

Animals↗
PubMed1983

Myoelectric effects of vasoactive intestinal peptide on rabbit small intestine.

Myoelectric recording techniques were used to study the motility of rabbit ileum during infusions of vasoactive intestinal peptide (VIP). VIP was infused intravenously at a rate of 300 pmol X kg-1 X h-1, and peripheral venous blood samples were obtained hourly for VIP assay. VIP was also infused intraluminally at a similar rate, and hourly portal vein blood samples were obtained for VIP assay. Alterations in motility were observed after both intravenous and intraluminal infusions of VIP. These alterations in motility consisted of the migrating action potential complex and repetitive bursts of action potentials. The VIP infusion rate used and the mean peripheral plasma VIP level of 267 +/- 29 pg/ml attained during intravenous VIP infusion were similar to those that induced intestinal secretion in other animal species. Portal venous VIP levels (93 +/- 21 pg/ml) were unchanged during the intraluminal infusion of VIP. These studies show that intravenous infusion of VIP causes alterations in motility of rabbit ileum. These alterations in motility with concomitant secretion of water and electrolytes may contribute to the diarrhea induced by VIP infusion. In addition, intraluminal infusion of VIP also induced alterations in myoelectric activity, which suggested that this peptide has a luminal effect as well as a hormonal effect.

Action Potentials↗
PubMed1983

Inhibition of gastrin release by secretin is mediated by somatostatin in cultured rat antral mucosa.

Somatostatin-containing cells have been shown to be in close anatomic proximity to gastrin-producing cells in rat antral mucosa. The present studies were directed to examine the effect of secretin on carbachol-stimulated gastrin release and to assess the potential role of somatostatin in mediating this effect. Rat antral mucosa was cultured at 37 degrees C in Krebs-Henseleit buffer, pH 7.4, gassed with 95% O2-5% CO2. After 1 h the culture medium was decanted and mucosal gastrin and somatostatin were extracted. Carbachol (2.5 X 10(-6) M) in the culture medium increased gastrin level in the medium from 14.1 +/- 2.5 to 26.9 +/- 3.0 ng/mg tissue protein (P less than 0.02), and decreased somatostatin-like immunoreactivity in the medium from 1.91 +/- 0.28 to 0.62 +/- 0.12 ng/mg (P less than 0.01) and extracted mucosal somatostatin-like immunoreactivity from 2.60 +/- 0.30 to 1.52 +/- 0.16 ng/mg (P less than 0.001). Rat antral mucosa was then cultured in the presence of secretin to determine its effect on carbachol-stimulated gastrin release. Inclusion of secretin (10(-9)-10(-7) M) inhibited significantly carbachol-stimulated gastrin release into the medium, decreasing gastrin from 26.9 +/- 3.0 to 13.6 +/- 3.2 ng/mg (10(-9) M secretin) (P less than 0.05), to 11.9 +/- 1.7 ng/mg (10(-8) secretin) (P less than 0.02), and to 10.8 +/- 4.0 ng/mg (10(-7) M secretin) (P less than 0.02). Secretin (10(-7) and 10(-8) M) also increased concomitantly culture medium somatostatin concentration. To determine whether secretion inhibition of carbachol-stimulated gastrin release was mediated by somatostatin, antral mucosa was cultured with carbachol, secretin (10(-9)-10(-7) M), and antibodies to somatostatin. Inclusion of somatostatin antibodies in the culture medium abolished the capacity of secretin (10(-7) and 10(-8) M) to inhibit carbachol-stimulated gastrin release. Results of these studies indicate (a) that secretin inhibits carbachol-stimulated gastrin release and (b) that under the conditions of these experiments secretin inhibition of gastrin release is mediated, at least in part, locally through release of antral somatostatin.

Animals↗
PubMed1983

Effects of antibodies to gastric inhibitory peptide on gastric acid secretion and gastrin release in the dog.

Previous studies have questioned the physiological role of gastric inhibitory peptide in inhibiting gastric acid secretion. The present study was designed to examine and compare peptone meal-stimulated gastric acid secretion in dogs after intravenous infusion of rabbit serum containing antibodies to gastric inhibitory peptide or normal rabbit serum (as control). Five dogs were prepared with gastric fistulas. Basal acid output was collected for 90 min through the gastric fistula. After 30 min of basal acid output collection, either rabbit serum containing antibodies to gastric inhibitory peptide or normal control rabbit serum (0.1 ml/kg) was infused intravenously over 1 min. After the basal acid output collection, a 10% peptone meal was infused into the stomach. Gastric acid output was measured by intragastric titration (pH 5.0) for 60 min. Peripheral venous plasma was collected for measurement of gastrin and gastric inhibitory peptide and for binding of endogenous plasma gastric inhibitory peptide by administered antibodies to gastric inhibitory peptide before and at 2, 5, 10, 15, 30, 60, 90, and 120 min after the meal. After intravenous administration of antibodies to gastric inhibitory peptide, 98% +/- 3% (SEM) of endogenous plasma gastric inhibitory peptide was bound by administered antibodies to gastric inhibitory peptide. No binding of endogenous plasma gastric inhibitory peptide was detected after infusion of normal rabbit serum. In dogs receiving intravenous antibodies to gastric inhibitory peptide, both peptone-stimulated gastric acid output and integrated gastrin release responses were increased when compared with dogs receiving normal rabbit serum. With infusion of antibodies to gastric inhibitory peptide, there was a high degree of correlation between the increase in gastric acid output and the increase in integrated gastrin response (r = 0.900, p less than 0.04) that followed the peptone meal. This study, using antibodies to bind endogenous gastric inhibitory peptide, demonstrates the capacity of circulating gastric inhibitory peptide to inhibit meal-stimulated gastric acid secretion. Furthermore, these results support the conclusion that this enterogastrone effect of gastric inhibitory peptide is due, at least in part, to inhibition of gastrin release.

Animals↗