Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of carcinoma of the stomach associated with severe hypoglycemia is reported. Diagnosis of insulinoma was excluded on the basis of history as well as laboratory tests. Postmortem examination revealed widespread small metastases to various organs; no metastasis was found in the pancreas; the histology of this gland did not show any pathological finding. No impairment in pituitary, thyroid, adrenal and liver function was detected. Fasting blood sugar ranged from 18 to 56 mg/100 ml. An oral glucose tolerance test showed a diabetic pattern with low insulin. Tolbutamide, glucagon and glucose injected i.v. gave only a moderate rise in plasma insulin levels; plasma glucagon response to arginine was subnormal. The determination of NSILA-s and gastrin in the serum of this patient gave normal values. Diazoxide infusion induced an increase in blood glucose and subsequent treatment with diazoxide relieved hypoglycemia for some months. The occasional detection of an islet cell antibody by immunofluorescence in this case is not easily understandable, but it might partly account for the carbohydrate intolerance. An impairment in gluconeogenesis dependent upon some substrate deficiency might account for the hypoglycemia in this patient.
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PMID:Gastric carcinoma associated with severe hypoglycemia sensitive to diazoxide. 39 98

The direct effect of insulin on the secretion of insulin (as measured by C-peptide), glucagon, gastric inhibitory polypeptide, and gastrin was studied in normal subjects by infusing insulin while the plasma level of glucose was maintained in the normal fasting range (euglycemic clamp). Insulin-induced hypoglycemia resulted in increases in circulating glucagon and gastric inhibitory polypeptide, a decrease in C-peptide, and no change in gastrin levels. In contrast, during the euglycemic clamp, insulin was found to behave a direct suppressive effect on the secretion of glucagon, C-peptide, and gastrin, but no effect on levels of gastric inhibitory polypeptide.
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PMID:Direct effect of insulin on secretion of insulin, glucagon, gastric inhibitory polypeptide, and gastrin during maintenance of normoglycemia. 40 Jul 22

The gastrointestinal contribution to carbohydrate metabolism includes carbohydrate absorption and the release of gastrointestinal hormones that interact with the endocrine pancreas. To learn the contributions to the enteroinsular axis from different levels of the gastrointestinal tract and different nutrients in chyme, we determined serum concentrations of glucose, gastric inhibitory peptide (GIP), insulin, and glucagon postprandially in six normal subjects who underwent diversion of chyme just proximal to an occlusive balloon at the ligament of Treitz and jejunal infusion of saline or chyme carbohydrate, protein, and lipid, separately or in combination. Postprandial elevations of serum glucose, GIP, and insulin and decrease of serum glucagon were elicited predominantly from the bowel and its contents distal to the ligament of Treitz. In this segment, each chyme nutrient (but especially carbohydrate) significantly stimulated factors affecting carbohydrate metabolism. Protein and lipid were able to block carbohydrate-induced glucagon inhibition. The gastroduodenal segment, although containing several proposed insulinotropic hormones (gastrin, secretin, and cholecystokinin), had no effect on serum glucose of glucagon and stimulated only small insulin and GIP responses.
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PMID:Intestinal nutrient influence on the enteroinsular axis. 40 Jul 36

Little is known on the enteral stimuli for gastro-intestinal hormone release in newborn infants. We have compared the effect of the first feed of human breast milk (5 ml/kg) or 10% dextrose (5 ml/kg) on blood glucose and plasma gastrin, enteroglucagon, Gastric Inhibitory polypeptide (GIP), pancreatic glucagon, and insulin in 21 full-term infants at 4--6 hours of age. The first feed of human milk caused a rise in blood glucose and plasma insulin, gastrin and enteroglucagon, but no change occurred in GIP or pancreatic glucagon. The 10% dextrose feed did not stimulate enteroglucagon release, although similar changes occurred in blood glucose and plasma insulin and gastrin. We conclude that the composition of the feed influences the pattern of gastro-intestinal hormone release during the first hours of life and that the entero-insular responses to feeding differ in the neonate and the adult.
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PMID:The effect of feeds of differing composition on entero-insular hormone secretion in the first hours of life in human neonates. 41 93

The responses of plasma gastro-entero-pancreatic (GEP) hormones and free fatty acids (FFA) to a standard mixed meal before and after starvation have been measured. Raised insulin, glucose and FFA levels were found following refeeding after starvation and levels of secretin and C-terminal glucagon-like-immunoreactivity (C-GLI), raised by starvation, were rapidly suppressed on refeeding. The responses of gastrin and N-terminal glucagon-like-immunoreactivity (N-GLI) to a standard mixed meal were not altered by starvation. Although this study does not directly support that secretin and glucagon are responsible for the hyperglycaemia or hyperinsulinaemia of starvation diabetes, a role for both hormones in the raised FFA levels is proposed, as well as a role for glucagon in the initial hyperglycaemic response to a meal after starvation.
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PMID:The gastro-entero-pancreatic hormone secretion after a mixed meal in normal subjects before and after a 72 hour period of starvation. 44 30

The blood serum levels of gastrin and insulin and arterial blood levels of glucose were determined immediately before intravenous injection of 1 mg of glucagon, and 10, 20, 40 and 60 minutes later in 12 gastric ulcer patients, 14 duodenal ulcer patients and 12 controls using the radioimmunological and orthotoluidine methods respectively. Following glucagon administration the gastrin levels dropped in the controls and the gastrin patients, and increased in the duodenal patients by an average of 30%. Insulin levels increased in all three groups, but the increase was statistically significant in the two patients groups. Glucose levels in the blood also increased with no significant differences between the groups. It is suggested that the different effect of glucagon on gastrin levels may be due to gastrin-insulin interaction; the levels of the two hormones in the blood of duodenal patients were higher than in the other two groups studied.
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PMID:The effect of glucagon on the blood levels of gastrin, insulin and glucose in patients with gastric and duodenal ulcers. 52 17

The aim of the present study was to investigate the effect of somatostatin (growth-hormone release-inhibiting hormone) on ulcer formation during immobilisation stress. This was done in male Albino-rats to study the effect of somatostatin on number and size of ulcers, to calculate ulcer index, to measure pH-value of gastric juice as well as plasma levels of gastrointestinal hormones. Rats treated with somatostatin before and during stress exposition had only the third part of the ulcers compared with the untreated animals. Total ulceration area was less than the tenth of the untreated rats. Normal corticoid plasma levels during stress exposition were found in the lower range of normal values in somatostatin treated rats. Decrease of plasma gastrin during stress exposition exceeded the gastrin decrease of somatostatin treated rats. Rise of plasma glucagon was completely inhibited during somatostatin application. Results of serum glucose paralleled those seen in glucagon.
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PMID:Prophylactic effect of somatostatin on stress ulcer formation in rats. 60 21

Serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG), and insulin (IRI) were estimated in 41 normal weight patients with duodenal ulcer (DU) and 25 age-matched controls in response to a high calorie liquid test meal. 28 out of 41 DU patients had a hyperglycaemic glucose response during the test meal, and 15 had a pathological oral glucose tolerance test. Fasting and food-stimulated IR-GIP and IRG levels were significantly elevated in the DU patients. Serum IRI also increased to significantly higher levels in DU patients after the test meal. The degree of the greater hormone response was dependent on the glucose increase after the test meal in the case of insulin and GIP, but not in the case of gastrin. It is concluded: firstly, that a faster glucose absorption (possibly due to rapid initial gastric emptying or increased intestinal motility) is responsible for the high and short-lasting glucose peak and the increased GIP and insulin secretion; secondly, that the GIP response could well be causally related to the insulin response; thirdly, that hyposcretion of GIP is ruled out as a possible factor in the pathogenesis of gastric acid hypersecretion of duodenal ulcer patients.
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PMID:Serum gastric inhibitory polypeptide (GIP) in duodenal ulcer disease: relationship to glucose tolerance, insulin, and gastrin release. 63 45

The release of pancreatic polypeptide (PP) by gut hormones, acetyl choline and adrenaline was investigated in an isolated perfused pancreas preparation. PP was potently released by 1 nmol/1 caerulein (186 +/- 12%, p is less than 0.001) and gastric inhibitory peptide (GIP) (211 +/- 31%, p is less than 0.005) as well as by 1 mumol/1 acetyl choline (1097 +/- 59%, p is less than 0.001). A significant two-fold release of PP was also evoked by 1 nmol/1 vasoactive intestinal peptide (VIP) (129 +/- 38%, p is less than 0.02 and gastrin (108 +/- 25% p is less than 0.01). Insulin release, induced by high glucose concentration was enhanced by both GIP (210 +/- 38%, p is less than (0.01) and VIP (48 +/- 5%, p is less than 0.001). In addition GIP enhanced the release of glucagon by 179 +/- 18% (p is less 0.001) at 1.4 mmol/1 glucose and by 127 +/- 24% (p is less than 0.005) at 8.3 mmol/1 glucose. Thus no simple inter-relationship appears to exist between the control of the three circulating islet hormones.
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PMID:Pancreatic polypeptide, glucagon and insulin secretion from the isolated perfused canine pancreas. 66 4

1. Pancreatic endocrine responses to ingestion of milk have been investigated in conscious unweaned calves, 3-5 weeks after birth. Passage of gastric content from abomasum to small intestine was prevented by means of a cannula placed in the duodenum adjacent to the pylorus and food was witheld for at least 22 h in order to deplete liver glycogen. 2. Under these conditions ingestion of milk was followed by a prompt rise in the concentrations of pancreatic glucagon, PP and gastrin in the arterial plasma but the usual rises in plasma glucose and insulin concentration were absent. 3. Evidence was obtained to show that absorption of glucose from the small intestine occurs sufficiently rapidly to account for the initial rise in plasma glucose concentration after feeding in normal animals. However, the rise in plasma glucagon concentration was sufficient to contribute to alimentary hyperglycaemia by promoting hepatic glycogenolysis in calves with abundant liver glycogen. 4. None of the neuroendocrine responses to ingestion of milk was affected by prior section of the splanchnic nerves whereas each was blocked by atropine (0.2 mg/kg), showing that all depend upon muscarinic, parasympathetic rather than sympathetic activity, in the absence of extraneous stress.
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PMID:The role of the autonomic nervous system in the control of pancreatic endocrine responses to milk ingestion in the calf. 69 Aug 86


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