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Results for “Gastric Inhibitory Polypeptide”

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At least 19 recordsLinked to original sources
PubMed1992

Are ionic fluxes of pancreatic beta cells a target for gastric inhibitory polypeptide?

Gastric inhibitory polypeptide (GIP), an incretin candidate, is suggested to amplify the glucose-induced insulin secretion. To evaluate its mode of action we examined whether GIP affects 86Rb+ efflux, 45Ca2+ uptake or efflux, and intracellularly recorded electrical activity of mouse pancreatic islets. GIP (5 nM) neither inhibited 86Rb+ efflux at 3 mM glucose nor modulated 86Rb+ efflux that was inhibited by 5.6 mM glucose or stimulated by the calcium ionophore A23187. 45Ca2+ uptake was increased by GIP in the presence of 16.7 mM which was not observed at 3 or 11 mM glucose. GIP elevated 45Ca2+ efflux from islets, but did not modify 45Ca2+ efflux when a virtually Ca2+ free medium was used. Electrical activity of beta cells induced by 16.7 mM glucose was significantly increased by 5 nM GIP. It is concluded that the amplification of insulin release by GIP is based on the effect of GIP on Ca2+ uptake.

Action Potentials↗
PubMed1979

The effect of a test meal on plasma vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), and secretin in man.

In six fasting healthy young male students a 15-min test meal consisting of 160 ml milk, 200 ml coffee, 70 g bread, 3.5 g butter, 35 g cheese, and 30 g ham (45 g carbohydrates, 30 g proteins, and 25 g fat) caused a late but significant elevation in plasma vasoactive intestinal polypeptide (VIP), an early and sustained significant rise in plasma gastric inhibitory polypeptide (GIP), but no significant change in plasma secretin.

Adult↗
PubMed1978

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.

Animals↗
PubMed1976

Inhibition of actions of glucagon in adipocytes by gastric inhibitory polypeptide.

Possible interactions between gastric inhibitory polypeptide (GIP) and glucagon were investigated in rat adipocytes. GIP was nonlipolytic and inhibited lipolysis stimulated by glucagon but not that stimulated by secretin or vasoactive intestinal polypeptide (VIP). GIP competed with 125I-glucagon for binding to adipocyte receptors, and at physiologic concentrations inhibited the stimulation of AMP produced by glucagon. Thus GIP acts as an inhibitor of actions of glucagon on adipocytes and may be a physiologic modulator of effects of glucagon.

Adipose Tissue↗
PubMed1979

Fat-induced jejunal inhibition of gastric acid secretion and release of pancreatic glucagon, enteroglucagon, gastric inhibitory polypeptide, and vasoactive intestinal polypeptide in man.

The effect of intrajejunal (i.j.) infusion of fat on meal-stimulated gastric acid secretion and release of pancreatic glucagon (PG), enteroglucagon (EG), gastric inhibitory polypeptide (GIP), and vasoactive intestinal polypeptide (VIP) was studied in seven healthy volunteers. I.j. fat markedly inhibited meal-stimulated acid secretion as compared to a control study with i.j. saline infusion. The acid inhibition was accompanied by augmental plasma concentrations of EG, GIP, and VIP but not of PG, suggesting that EG, GIP, and VIP may be among mediators of fat-induced jejunal inhibition of acid secretion. Concentration-time relationship makes it unlikely that the observed inhibition could be ascribed to any single peptide studied.

Adult↗
PubMed1978

[Gastric inhibitory polypeptide (GIP) (author's transl].

Gastric inhibitory polypeptide (GIP) is released from the duodenum and jejunum following the ingestion of glucose, fat and amino acids. This hormone potentiates the glucose-induced insulin release from the beta-cells of the pancreas. The role of GIP as "incretin" is discussed. The method of the radioimmunoassay for the determination of GIP in serum samples is described. The lower limit of sensitivity of the GIP radioimmunoassay is in the range of 30-50 pg per ml serum. The described radioimmunoassay is sensitive enough to determine fasting levels of GIP in normal subjects (287 +/- 59 pg/ml). The clinical and pathophysiological importance of GIP is discussed by means of various diseases (obesity, maturity-onset diabetes mellitus, duodenal ulcer disease).

Administration, Oral↗
PubMed1977

Hypersecretion of gastric inhibitory polypeptide following oral glucose in diabetes mellitus.

Gastric inhibitory polypeptide (GIP) is insulinotropic and is released after ingestion of glucose in normal man. Changes in plasma immunoreactive gastric inhibitory polypeptide (IRGIP) were therefore studied during a 50-gm. oral glucose tolerance test in 10 normal subjects and 20 subjects with maturity-onset diabetes mellitus. The diabetics were nonobese and treated by diet alone; they exhibited exaggerated increments of plasma IRGIP in association with delayed and diminished peak increases in plasma immunoreactive insulin, suggesting relative failure of the beta-cell response to GIP. The diabetic subjects also showed a paradoxic rise in mean plasma immunoreactive glucagon, with a peak coinciding with that of plasma IRGIP. It is suggested that the defective beta-cell response may lead to diminished feedback inhibition of GIP secretion by insulin in diabetes mellitus and that the glucagonotropic action of GIP may be expressed under these conditions.

Adolescent↗
PubMed1978

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 less than 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.

Adult↗
PubMed1975

The insulinotropic action of gastric inhibitory polypeptide.

The effect of highly purified gastric inhibitory polypeptide (GIP) on immunoreactive insulin (IRI) secretion in the conscious fasted dog was investigated. Significant increases in IRI release were observed with intravenous administration of three different doses of GIP. These were accompanied by depression in fasting serum-glucose levels. Preliminary studies were undertaken to determine whether this insulinotropic action of GIP could be attributed to a particular segment of the GIP molecule. GIP fragments produced by cleavage with cyanogen bromide and trypsin showed no significant stimulation of IRI release. The possibility that GIP might itself enhance glucose uptake or potentiate insulin-induced glucose uptake was studied with the rat hemidiaphragm preparation. No such effect was observed. In the light of this and other recent work, it is concluded that GIP is a strong candidate for an active principle in the enteroinsular axis.

Animals↗
PubMed1978

Radioimmunoassay of gastric inhibitory polypeptide.

A radioimmunoassay for the measurement of gastric inhibitory polypeptide (GIP) in unextracted plasma in man has been developed using a rabbit antiserum raised against porcine GIP. Porcine GIP was employed also as standard and to produce a 125I-labelled tracer. The assay was able to distinguish 110 pg/ml GIP from zero in plasma samples. Negligible cross-reactivity was demonstrated with cholecystokinin, insulin, pancreatic polypeptide, glucagon, secretin, and vasoactive intestinal polypeptide. The mean overnight fasting plasma GIP level in 28 normal subjects was 203 pg/ml (range: undetectable--420 pg/ml). Plasma GIP levels rose, within 45 minutes of eating a mixed meal, to a mean level of 1573 pg/ml.

Animals↗
PubMed1978

Oral glucose augmentation of insulin secretion. Interactions of gastric inhibitory polypeptide with ambient glucose and insulin levels.

Gastric inhibitory polypeptide, or GIP, has been postulated as the major enteric hormonal mediator of insulin release. The release of immuno-reactive GIP (IR-GIP) after oral glucose and its role in insulin release was studied in normal men by the glucose clamp technique. In 24 subjects studied with the hyperglycemic clamp, blood glucose was maintained at 125 mg/dl above basal for 2 h via a primed-continuous IV glucose infusion coupled to a servo-controlled negative feedback system. 40 g glucose per m(2) surface area was ingested at 60 min, and the blood glucose was maintained at the steady-state hyperglycemic level. Plasma IR-GIP and insulin (IRI) levels were measured throughout the 2-h period. IR-GIP levels changed little when IV glucose alone was given; the mean basal value was 305+/-34 (SEM) pg/ml. After oral glucose, IR-GIP levels began to rise within 10 min and reached a peak within 40 min of 752+/-105 pg/ml. Plasma IRI responded initially to the square wave of hyperglycemia in the typical biphasic pattern. After oral glucose, plasma IRI levels rose strikingly above the elevated levels produced by hyperglycemia alone, reaching a peak of 170+/-15 muU/ml within 45 min. The time course of the rise in IR-GIP and IRI was nearly identical. To assess whether the maintenance of euglycemia would affect this process, the euglycemic clamp was employed in 11 subjects to maintain basal blood glucose levels during a similar 2-h study. A primed-continuous insulin infusion, with a constant rate of 120 mU/m(2) per min was given together with a servo-controlled glucose infusion. This resulted in hyper-insulinemia of approximately 300 muU/ml. Glucose was ingested by six subjects at 60 min. Plasma IR-GIP responded to oral glucose similarly to the effect seen in the hyperglycemic studies. No increase in endogenous insulin release was seen despite the increase in IR-GIP when euglycemia was maintained. However, in five of seven subjects given insulin whose blood glucose concentration rose by 20 mg/dl or more after oral glucose, there was an increase in plasma insulin concentration associated with the elevation in IR-GIP. Thus, the effect of glucose-released IR-GIP on insulin secretion is dependent upon the presence of some degree of hyper-glycemia and is not inhibited in the presence of marked hyperinsulinemia.

Adolescent↗
PubMed1976

The insulinotropic action of gastric inhibitory polypeptide in the perfused isolated rat pancreas.

Gastric inhibitory polypeptide (GIP) produced a dose-related increase in immunoreactive insulin (IRI) from the perfused isolated rat pancreas. The doses employed were within physiological limits. This effect was glucose-concentration-dependent in that there existed a threshold concentration of glucose above which GIP exerted the insulinotropic action, and that, at a fixed concentration of GIP, increased glucose concentrations stimulated IRI release in more than an additive manner. A biologically active fragment of the GIP molecule was isolated and purified. All criteria have been satisfied that GIP is an insulinotropic hormone.

Animals↗
PubMed1976

Gastric inhibitory polypeptide (GIP) in chronic pancreatitis.

The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Patients with pancreatitis also have a paradoxical rise in PGLI and an exaggerated rise in GGLI concentration following oral glucose.

Adult↗
PubMed1977

Renal effects on serum gastric inhibitory polypeptide (GIP).

Fasting and meal-stimulated serum immunoreactive gastric inhibitory polypeptide (GIP) concentrations were measured in normal subjects and in uremic patients undergoing chronic hemodialysis. Mean fasting GIP was higher in the uremic patients (1006 +/- 145 (SE) pg/ml) than in the normal control subjects (132 +/- 31 pg/ml, p less than 0.001). Also, postcibal absolute and incremental serum GIP concentrations between 15 and 180 min were greater (p less than 0.05) in the uremic patients than in the control subjects; in the former they failed to return to fasting levels 180 min after the meal. In a second study, using anesthetized normal dogs, simultaneous renal arterial and venous serum GIP concentrations were measured during an intraduodenal perfusion of glucose. The renal arterial-venous (A-V) GIP gradient became greater as serum arterial GIP concentrations increased. The correlation between renal A-V GIP gradient and renal arterial GIP concentration was quite good (r = 0.85), with a 39% maximum mean A-V reduction in serum GIP concentrations observed across the kidney. This large renal A-V GIP gradient observed under nonsteady conditions suggests that the kidney may be an important site for the removal of GIP from the circulation. Thus, the higher than normal fasting and stimulated serum GIP concentrations observed in uremic patients can be attributed, at least in part, to a loss of the renal extraction mechanism for GIP.

Adult↗
PubMed1992

Gastric inhibitory polypeptide (GIP) response in diabetes using a highly specific antiserum.

Gastric inhibitory polypeptide (GIP), a hormone secreted from the proximal small gut, is recognized as a major component of the enteroinsular axis. However, circulating levels of GIP in diabetes have been reported to be exaggerated, normal or decreased following glucose ingestion, which may be due to the presence of variable crossreacting immunoreactive GIP forms in the circulation. We have raised an antibody (S705) which recognizes only 5 kDa GIP. Using this antiserum we have measured circulating GIP levels in 18 healthy volunteers, and 13 Type 2 diabetic and 9 Type 1 diabetic patients following ingestion of 75 g glucose. As expected, blood glucose levels and blood insulin levels are significantly abnormal in the diabetic groups. On the other hand, circulating GIP levels at all time-points and integrated incremental GIP over 120 min were not different from the control group. However, we cannot exclude the possibility that apparently normal immunoreactive GIP levels in diabetes might conceal subtle alterations in biological activity which could play a role in the pathogenesis of the disease.

Adult↗
PubMed1977

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.

Adult↗