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

The concentrations of testosterone, cortisone, gastrin, GIP, somatomedin B, insulin, HGH, and TSH have been determined in the plasma and the ultrafiltrate of five uremic patients undergoing intermittent hemofiltration treatment. There was a considerable loss of gastrin, GIP, somatomedin B, and insulin by hemofiltration treatment; the plasma concentrations, however, did not decrease. Cortisone, HGH, and TSH were not detectable in the ultrafiltrate. Our results therefore indicate that hemofiltration does not cause a hormone deficiency syndrome. On the contrary, the loss of degradation products of hormones with disturbing biological activity may be a favourable effect of the hemofiltration treatment.
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PMID:Elimination of hormones through hemofiltration. 60 73

Serum gastrin, serum-GIP and serum insulin levels were measured before and after interposition operation (Henley-Soupault) in 10 patients with severe dumping-syndrome (PGS). The results were compared to those obtained in 10 normal subjects without any gastrointestinal disease. In the PGS pre-operative group there was a significantly lower serum gastrin concentration compared to normals, while the serum-GIP-concentration was significantly higher. After interposition operation all serum-hormone-levels tended towards normal values. There was no difference between the basal serum insulin levels of the three groups. The change in postprandial insulin release was parallel to the serum-GIP-levels. It is concluded that there is a close connection between disturbed release of gastrointestinal hormones and the dumping syndrome.
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PMID:[Gastrointestinal hormone release in dumping symdrome before and after reconstruction of duodenal passage]. 61 6

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

1. In duodenal ulcer patients SPV results in an increase of basal and postprandial serum gastrin levels. There is no decrease of hypergastrinemia even five years after SPV. 2. After SPV there is a significant increase in basal serum GIP levels; postprandial GIP concentrations show a faster increase after food intake. 3. Serum insulin and blood glucose concentrations are not altered by SPV.
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PMID:[The effect of selective proximal vagotomy on gastrin, GIP and insulin blood levels in patients with duodenal ulcer]. 75 95

The effect of intravenous glucagon infusion on serum levels of immunoreactive GIP (IR-GIP), insulin (IRI), gastrin (IRG), and on blood glucose has been investigated in six healthy volunteers in the fasting state and during ingestion of a mixed standard meal. Glucagon (500 ng/kg/min) lowered significantly serum levels of IR-GIP and IRG below the fasting values and increased the levels of IRI and blood glucose. Glucagon (50 ng/kg/min) infused 30 minutes before and continued 90 minutes after ingestion of a test meal abolished the IR-GIP response, suppressed significantly the IRG response, and left the IRI response unchanged. The same glucagon dose infused 60 minutes after ingestion of the test meal decreased significantly the raised levels of IR-GIP and IRG to fasting levels without changing IRI values. It is concluded that exogenous glucagon inhibits Gip release at the level of the GIP-producing cells.
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PMID:Lowering of fasting and food stimulated serum immunoreactive gastric inhibitory polypeptide (GIP) by glucagon. 85 72

Five dogs prepared with Heidenhain pouches received infusions of saline, GIP and VIP before and after a standard meat meal. Blood samples were obtained under basal conditions and at subsequent intervals for measurement of gastrin, insulin, GIP and VIP by radioimmunoassay. GIP and VIP infusions had no effect on basal levels of gastrin. GIP and VIP (in common with secretin and glucagon) were found to suppress food-stimulated release of gastrin and gastrin-stimulated acid secretion from the Heidenhain pouch. Insulin levels were significantly elevated during GIP and VIP infusions. Food released GIP (and perhaps VIP.
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PMID:Suppression of gastrin release and gastric secretion by gastric inhibitory polypeptide (GIP) and vasoactive intestinal polypeptide (VIP). 93 20

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.
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PMID:Gastric inhibitory polypeptide (GIP), gastrin and insulin: response to test meal in coeliac disease and after duodeno-pancreatectomy. 95 38

Gastrointestinal hormones are considered to be those that are formed in the gastrointestinal tract and there, in physiological concentrations, develop their effects on motility, secretion, trophism, bloodflow and absorption. Structural analysis, synthesis or a high degree of purity after extraction, and its exact demonstration by means of a useful radioimmunoassay, form the basis for the establishment of a polypeptide as a gastrointestinal hormone. To this category belong, at the present time, gastrin, cholecystokinin-pancreozymin (CCK-PZ) and secretin. GIP, VIP, motilin, glucagon and somatostatin are considered likely candidates. The substances gastrin and CCK-PZ, which are structurally related and have a predominantly stimulating effect, and the structurally dissimilar motilin, contrast with the partially or totally inhibiting hormones of the glucagon family, namely, secretin, VIP, glucagon-enteroglucagon, GIP and somatostatin. By the combined action of these hormones with one another and with the autonomic nervous system, the digestive processes are regulated. Disturbances in the formation of these hormones, in particular an overproduction, give rise to disease syndromes that can now be diagnosed and, in part, treated by surgery. The therapeutic application of gastrointestinal hormones has now also become a possibility.
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PMID:[Gastrointestinal hormones]. 96 Sep 54

Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.
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PMID:Response of gastric inhibitory polypeptide (GIP) to test meal in chronic pancreatitis--relationship to endocrine and exocrine insufficiency. 100 49

Somatostatin, a peptide isolated from ovine hypothalami, prevents growth hormone secretion in vivo and in vitro. Moreover, somatostatin interferes with the secretion of various other hormones: TSH insulin, glucagon, gastrin, VIP and GIP. Under certain conditions a blunting effect on the secretion of prolactin and ACTH can be demonstrated.
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PMID:[Somatostatin -- a review (author's transl)]. 126 5


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