Gastric Inhibitory Polypeptide Release Research Articles

Metabolic effects of glucose, mannose, galactose, and fructose in man.

The effects of various hexoses upon immunoreactive insulin (IRI) secretion, glucose disposal, and gastric inhibitory polypeptide (GIP) release have been compared in 10 normal nonobese men. Rapid iv infusion (0.5 g/kg in 3 min) of D-mannose resulted in significant ITI release, the peak levels approaching those after D-glucose infusion. D-Galactose, however, was ineffective. The 60-min urine excretions of mannose, galactose, and glucose were 35 +/- 7%, 16 +/- 4%, and 5.5 +/- 0.7% (mean +/- SEM) of the administered dose, respectively. All subjects also received 50 g oral glucose, mannose, galactose, and fructose on different days, each followed by an iv glucose infusion 30 min later. The ingestion of glucose or galactose resulted in a similar increment of GIP (P less than 0.01), followed by a similar increment in the IRI response to iv glucose. Furthermore, the glucose disposal rate increased 2.5-fold compared to that after iv glucose alone (P less than 0.001). However, oral msnnose or oral fructose caused no significant GIP release, yet the IRI response to a subsequent iv glucose load was moderately augmented after oral mannose or oral fructose when compared to iv glucose alone. In addition, there was a similar enhancement of glucose disposal of the iv glucose load after both oral mannose and oral fructose (P less than 0.01). From these studies we conclude that 1) galactose does not elicit IRI secretion per se, yet, like glucose, potentiates GIP and IRI secretion; 2) mannose, despite weak transport across gut or kidney, evokes significant betacytotropic effects; and 3) mannose- and fructose-induced enhancement of glucose disposal might be mediated by a factor(s) other than GIP.

Glucose stimulated release of gastric inhibitory polypeptide from hamster small intestine: An in vitro model

A superfusion model was used to study in vitro gastric inhibitory polypeptide (GIP) release from hamster small intestinal mucosa. A 10% glucose solution, in both fed and fasted hamsters, produced a prompt, sustained, three-fold rise in mean GIP release. In contrast, superfusion of a solution of 10% mannitol did not alter release of the peptide. This model provides potential for elucidation of the mechanisms through which glucose and other agents release GIP and other gastrointestinal peptides.

Mechanisms of release of gastro-entero-pancreatic endocrine cells.

AbstractEndocrine cells of the gastro‐entero‐pancreatic (GEP) system release their hormones in response to nutrient stimulation. Gastro‐entero endocrine cells receive stimulation from the circulation and lumen and have the potential to secrete into the circulation and lumen. Pancreatic endocrine cells cannot receive stimulation from nor secrete into the lumen.Antral gastrin‐producing G cells released hormone in a biphasic manner in response to feeding; the initial plasma gastrin peak was absent after a 48‐hour fast. The increase of antral tissue gastrin detected was far more than that required for the major plasma gastrin response. Intravenous hyperalimentation (IVH) (30% dextrose, 12% amino acids) was used to assess the effect of the absence of luminal stimulation upon GEP hormone (gastrin, gastric inhibitory polypeptide, glucagon, and insulin) release. During the first 6 days of IVH, circulating insulin concentrations increased absolutely and in relationship to glucagon; gastrin concentrations decreased to undetectable levels. During the following 4 days of IVH, circulating insulin decreased and gastrin increased to their initial concentrations. The IVH responses reflect the abilities of the different cells to adapt to intravenous nutrients.GEP endocrine cells have distinct differences in their hormone turnover mechanisms in response to nutrient stimulation. These different cellular response mechanisms may provide a clue to the functional evolution and sophistication of GEP endocrine cells.

Release of Gastric Inhibitory Polypeptide (GIP) by Intraduodenal Acidification in Rats and Humans and Abolishment of the Incretin Effect of Acid by GIP-Antiserum in Rats

Intraduodenal infusion of 0.05-0.5 N hydrochloric acid dose-dependently increases serum levels of immunoreactive gastric inhibitory polypeptide (GIP) in rats. Immunoreactive GIP released by duodenal acidification is biologically active because it augments the glucose-induced release of immunoreactive insulin (IRI). This augmentation of glucose-induced IRI release by intraduodenal acid can be abolished for 30 min by simultaneous intravenous infusion of GIP-antiserum. From this it is concluded that the initial capacity to augment the glucose-induced insulin release (incretin activity) of hydrochloric acid is due to its ability to release GIP. Later on, other gut factors with incretin activity might be released by hydrochloric acid. Also, in humans, intraduodenal infusion of 0.1 N hydrochloric acid releases GIP without changing serum levels of glucose or insulin. The GIP release is a direct effect of intraduodenal acid and is not mediated via secretin release. Injection of secretin in supraphysiologic doses does not change serum levels of immunoreactive GIP. However, such secretin injections induce a short-term insulin release and a decrease in serum glucose concentration.

Mannitol and glucose: effects on gastric acid secretion and endogenous gastric inhibitory polypeptide (GIP).

Serum gastric inhibitory polypeptide was measured in dogs prepared with Heidenhain pouches and Mann-Bollman fistulae following the intraduodenal (ID) infusion of isotonic saline, 20% glucose, or 20% mannitol. Following ID 20% glucose, serum GIP concentrations rose significantly (P less than 0.05) between 30 and 120 min and there was a significant inhibition (P less than 0.05) of acid secretion in the Heidenhain pouches between 15 and 75 min. A good correlation (r = 0.925) was found between the rise in serum GIP and the inhibition of acid secretion. Although neither ID isotonic saline nor 20% mannitol stimulated GIP release, the latter produced a significant (P less than 0.05) inhibition of acid secretion between 60 and 105 min. We conclude: (1) the inhibitory effect of acid secretion following ID glucose is mediated in part by the release of endogenous GIP; (2) glucose and mannitol probably inhibit gastric acid secretion by different mechanisms.

Selective release of gastric inhibitory polypeptide by intraduodenal amino acid perfusion in man

Intraduodenal amino acids are known to stimulate the release of gastric inhibitory polypeptide and cholecystokinin. In order to separate and quantitate gastric inhibitory polypeptide secretion selectively, 12 normal subjects received an intraduodenal perfusion of a mixed amino acid solution (158 mM) containing either methionine, phenylalanine, tryptophan, and valine (perfusate 1), or an amino acid solution containing arginine, histidine, isoleucine, leucine, lysine, and threonine (perfusate 2). Serum concentrations of gastric inhibitory polypeptide and insulin were significantly greater in the group receiving perfusate 2 (P < 0.001). In contrast, after administration of amino acid perfusate 1, there was only a slight increase in serum gastric inhibitory polypeptide concentration and insulin secretion increased only slightly. Mean trypsin and bilirubin outputs in the group receiving perfusate 1 were nearly 3 times greater than the outputs of the group receiving the other amino acid mixture. This study expands the importance of intraduodenal amino acid mixtures in stimulating secretion of gastric inhibitory polypeptide and insulin and quantitatively separates gastric inhibitory polypeptide release from release of hormones that stimulate pancreatic enzyme secretion, such as cholecystokinin.

Abnormal gastric inhibitory polypeptide (GIP) and insulin release in duodenal ulcer (DU) patients

Abnormal gastric inhibitory polypeptide (GIP) and insulin release in duodenal ulcer (DU) patients

Glucose-stimulated gastric inhibitory polypeptide release from hamster small bowel mucosa: An in vitro model

Glucose-stimulated gastric inhibitory polypeptide release from hamster small bowel mucosa: An in vitro model

GUT-HORMONE PROFILE IN CŒLIAC DISEASE

Patients with cœliac disease have a highly significant reduction in the release of secretin and gastric inhibitory polypeptide from the upper small intestine, but a greatly increased release of enteroglucagon, and also of neurotensin, from the lower part of the small intestine. The release of gastrin and pancreatic polypeptide, from the antrum and pancreas respectively, is, however, normal. Thus the pattern of hormone release reflects the location of the mucosal lesion. The gut-hormone profile may also help to characterise other gastrointestinal diseases.

Effect of atropine on meal-stimulated gastrin and gastric inhibitory polypeptide (GIP) release.

The effect of atropine on meal-stimulated gastric inhibitory polypeptide (GIP) and gastrin release was studied in 5 purebred foxhounds and compared with control studies done in the same animals given a meal without atropine, peak incremental serum gastrin occurred between 5 and 15 min after the meal whereas the greatest increment in serum GIP occurred 60 min postcibal. Atropine had no effect on basal concentrations of gastrin or GIP. However, when atropine was given before feeding serum gastrin concentrations from 75 to 120 min postcibal were significantly higher (P less than 0.04) than after the meal alone. The normal meal-stimulated rise in serum GIP was almost completely inhibited by atropine. We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP.

Gastric inhibitory polypeptide (GIP) and insulin in obesity: Increased response to stimulation and defective feedback control of serum levels

To investigate the possibility that an abnormality of the entero-insular axis is responsible for the hyperinsulinaemia of obesity, serum immunoreactive gastric inhibitory polypeptide (IR-GIP) and insulin (IRI) were measured after the ingestion of a liquid mixed test meal, glucose or fat, in normal weight and obese subjects. The latter were divided into a group with normal oral glucose tolerance (nOGT) and a group with pathological glucose tolerance (pOGT). Fasting levels of IR-GIP were significantly elevated in the obese group with pOGT. After the mixed meal the overweight subjects showed a significantly greater response of IR-GIP than the controls, with highest levels in the pOGT group. Simultaneously, the IRI response was significantly greater in the obese subjects than in the controls. The increases of IR-GIP and IRI after an oral load of 100 g glucose were normal in the obese subjects, but showed a significantly greater integrated response in the obese patients with pOGT. The ingestion of 100 g fat induced no IRI release but a significantly greater release of IR-GIP in the obese subjects, irrespective of their glucose tolerance. It is concluded that fat is a stronger releaser of IR-GIP than glucose. The effect of a combined load of glucose (30 g) and fat (100 g) was also compared in obese and normal weight subjects with the effect of either alone. Fat but not glucose released significantly more IR-GIP in obese subjects. In normal weight controls, but not in obese subjects, the IR-GIP release after fat plus glucose became significantly smaller than after fat alone. Since only the combined ingestion of glucose and fat and not fat alone releases insulin it is suggested that endogenous insulin inhibits GIP release and that this feedback control between insulin and GIP is defective in patients with obesity.

Stimulation of Gastric Inhibitory Polypeptide in Normal and Duodenal Ulcer Patients

To investigate the role of gastric inhibitory polypeptide (GIP), a potent inhibitor of gastric acid secretion, in the hypersecretion associated with duodenal ulcer, we compared the serum GIP concentrations in 11 healthy subjects and 16 duodenal ulcer patients after the stimulation of GIP release by a mixed meal. Fasting and postprandial serum gastrin and GIP concentrations were measured by radioimmunoassay at frequent intervals after the ingestion of a test meal. The duodenal ulcer patients showed an augmented and significantly greater release of GIP as well as of gastrin compared to normal subjects. These results indicate that a defective GIP release cannot account for the gastric hypersecretion seen in patients with duodenal ulcer. The mechanism of the increased GIP response in patients with duodenal ulcer is not clear from these studies.

Localization of Gastric Inhibitory Polypeptide Release by Intestinal Glucose Perfusion in Man

To determine the site of endogenous release of gastric inhibitory polypeptide (GIP), glucose perfusions (556 mmoles per liter) of duodenum, proximal jejunum, midjejunum, and ileum were performed in human volunteers using an occluding balloon perfusion technique. Preperfusion GIP concentrations were below assay sensitivity (125 pg per ml) in all subjects. After glucose perfusion, maximal serum GIP concentrations for the four groups were: duodenum, 1383 +/- 152 pg per ml; proximal jejunum, 904 +/- 87 pg per ml; midjejunum, 545 +/- 91 pg per ml, and ileum 305 +/- 38 pg per ml. Integrated GIP secretion was significantly greater with duodenal perfusion (111 +/- 21 ng-min ml-1) d proximal jejunal perfusion (69 +/- 5 ng-min ml-1), as compared to either midjejunal (47 +/- 7 ng-min ml-1) or ileal (25 +/- 6 ng-min ml-1) perfusions. Peak serum insulin concentrations and integrated insulin secretion were also significantly greater with perfusion of the duodenum or proximal jejunum. Serum glucose concentrations, integrated serum glucose, and glucose absorption were similar for the four areas perfused. The results of this study indicate that the proximal small intestine is the primary site of endogenous GIP release in man, but that smaller quantities are also released by the distal small bowel.

Gastric inhibitory polypeptide (GIP)

Radioimmunoassayable gastric inhibitory polypeptide was measured in extracts of canine antrum, duodenum, jejunum, and ileum. The highest GIP concentrations were found in the duodenum (347 +/- 53 ng/g) and jejunum (300 +/- 68 ng/g). An immunochemical similarity was demonstrable between porcine GIP and canine GIP. Dogs prepared with Mann Bollman fistulae were given an amino acid (AA) mixture or medium-chain triglycerides (MTC) by intraduodenal perfusion. With AA, a peak mean serum concentration of 672 +/- 106 pg/ml was reached 15 min after starting the perfusion. MCT resulted in a peak mean serum GIP concentration of 504 +/- 55 pg/ml 30 min after beginning the perfusion. When compared to results previously reported from this laboratory, AA and MCT are not as potent as corn oil (long-chain triglyceride) or glucose in stimulating GIP release. We conclude: (1) Immunoassayable GIP concentrations are highest in the canine proximal small intestine. (2) AA and MCT are weak stimulants of GIP release in the dog.

Gastric inhibitory polypeptide (GIP), gastrin and insulin: response to test meal in coeliac disease and after duodeno-pancreatectomy.

The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.

The effect of somatostatin on release and insulinotropic action of gastric inhibitory polypeptide.

Studies were carried out in conscious dogs in which the effect of intravenous somatostatin on immunoreactive gastric inhibitory polypeptide (IR-GIP) release was investigated. In addition, the inhibitory action of somatostatin on the insulin response to pure porcine GIP was assessed. Intravenous administration of somatostatin resulted in a delayed IR-GIP and immunoreactive insulin (IRI) response to oral glucose. Somatostatin also delayed the IR-GIP response to the ingestion of fat. In both types of experiments, initial depression of IRI levels was followed by a sharp rise in IRI release. Intravenous infusion of somatostatin produced 80% inhibition of the IRI response to pure porcine GIP. It was concluded that somatostatin inhibits the physiological release of IR-GIP and the insulinotropic action of exogenous porcine GIP.

Release of immunoreactive gastric inhibitory polypeptide (IR-GIP) by oral ingestion of food substances

Release of immunoreactive gastric inhibitory polypeptide (IR-GIP) by oral ingestion of food substances

Gastric inhibitory polypeptide (GIP) stimulated by fat ingestion in man.

Ten normal volunteers ingested emulsified corn oil and the immunoreactive GIP, insulin (IRI) and nonesterified fatty acid (NEFA) responses were measured. Serum GIP levels increased after the ingestion of corn oil in all subjects, rising from a mean fasting level of 272 pg/ml to 856 +/- 272 pg/ml (P less than 0.05) by 30 minutes. The peak mean serum GIP concentration of 1,345 +/- 291 pg/ml occurred at 60 minutes; and mean serum GIP levels at 180 minutes remained significantly elevated over fasting values. Serum IRI, glucose and NEFA concentrations did not change during the 180 minutes of study. No changes in serum GIP concentrations occurred when, for control purposes, six volunteers ingested water on another day. We conclude: 1) Fat is a potent stimulus for the release of GIP in normal individuals. 2) Endogenously released GIP is not insulinotropic under the conditions of this study.

Gastric inhibitory polypeptide (GIP) stimulation by oral glucose in man.

ABSTRACT Gastric inhibitory polypeptide (GIP) was measured by a specific radioimmunoassay in 25 normal subjects who received 75 g of oral glucose or 25 g intravenously. Serum GIP levels increased in every subject after oral glucose ingestion. The mean fasting GIP was 319 ± 18 pg/ml and increased to a mean peak response of 747 ± 59 pg/ml between 15 and 60 min after oral glucose. In contrast, intravenous glucose did not significantly stimulate GIP release. We conclude that oral glucose is a potent stimulus for the enteric release of GIP.

Intestinal transport of 3-O-methyl-D-glucose in the normal and alloxan-diabetic rat.

ARTICLESIntestinal transport of 3-O-methyl-D-glucose in the normal and alloxan-diabetic ratP Flores, and HP SchedlP Flores, and HP SchedlPublished Online:01 Apr 1968https://doi.org/10.1152/ajplegacy.1968.214.4.725MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe effects of insulin on glucose and fluid transport in the isolated small intestine of normal ratsLife Sciences, Vol. 81, No. 1Alterations in intestinal morphology of streptozotocin-induced diabetic rats fed Jamaican bitter yam (Dioscorea polygonoides) steroidal sapogenin extractNutrition Research, Vol. 23, No. 11EFFECTS OF DIABETES ON CALCIUM UPTAKE BY RAT BRUSH BORDER MEMBRANE VESICLESClinical and Experimental Pharmacology and Physiology, Vol. 22, No. 4Experimental streptozotocin-induced diabetes and intestinal glucose metabolism in the rat, in vivo and in vitroActa Diabetologica, Vol. 32, No. 3Hypoglycaemic and antidiabetic effects in mice ofAloe arborescens Miller var.natalensis BergerPhytotherapy Research, Vol. 7, No. 7The role of insulin in the intestinal absorption of glucose in the ratInternational Journal of Biochemistry, Vol. 24, No. 4Variation of ileal taurocholate transport capacity in rats fed on high-fat diets and in alloxan-diabetic ratsNutrition Research, Vol. 11, No. 7Insulin regulates Na+/glucose cotransporter activity in rat small intestineBiochimica et Biophysica Acta (BBA) - 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Biomembranes, Vol. 367, No. 2Untersuchungen zum Einfluß des Insulins auf die intestinale Resorption beim MenschenResearch in Experimental Medicine, Vol. 161, No. 4Untersuchungen zum Einfluß von Glucagon und Insulin auf die Glucoseresorption beim MenschenSugar and electrolyte absorption in the rat intestine perfused ?in vivo?Pfl�gers Archiv European Journal of Physiology, Vol. 340, No. 4Increase of intestinal brush border hydrolases in mucosa of streptozotocin-diabetic ratsDiabetologia, Vol. 8, No. 6Untersuchungen zum Einfluß von Insulin auf die Glucoseresorption beim MenschenEffects of diabetes on intestinal growth in the ratJournal of Experimental Zoology, Vol. 176, No. 4Carbohydrate Digestion and AbsorptionGastroenterology, Vol. 58, No. 1 More from this issue > Volume 214Issue 4April 1968Pages 725-729 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.214.4.725PubMed5642932History Published online 1 April 1968 Published in print 1 April 1968 Metrics