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)

Many alterations in metabolic and endocrine function occur in end-stage renal disease. Glucose intolerance is almost always present with uremia; it improves shortly after institution of regular hemodialysis. Hyperlipidemia (type IV) is prevalent, and atherosclerotic cardiovascular disease causes death in about 50% of patients receiving long-term hemodialysis. Although plasma levels of growth hormone usually are elevated, children with chronic renal failure show growth retardation. The occurrence of thyroid disorders is difficult to determine, since many clinical features of uremia are similar to those of hyperthyroidism and hypothyroidism. The incidence of duodenal ulcer is high, possibly due to high gastrin levels. Sex hormone disturbances are common. Anemia is a constant feature of chronic renal failure; patients usually tolerate it well.
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PMID:Metabolic and endocrine alterations in end-stage renal failure. 71 39

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

The authors carried out a self-controlled study using 11, non-obese patients with impaired glucose tolerance. The first day an oral glucose tolerance test was performed as a control. This was repeated the next day with a simultaneous intake of 20 g natural wheat bran. On both days blood samples were taken at 30 minute intervals (for three hours period) after glucose or glucose plus bran ingestion to measure the plasma sugar, insulin, C-peptid, gastrin and glucagon levels. It has been found that: 1. With simultaneous bran intake the blood glucose levels were decreased as compared to the control values. 2. The serum insulin, and C-peptid levels were similar in both tests. 3. The glucagon response curve fell below that of the control. 4. The serum gastrin levels did not show any change following either glucose or glucose plus bran intake. It has been concluded, that the dietary fibres are able to decrease of glucagon release, beside their direct inhibitory effect on the level of sugar absorption from gastrointestinal tract.
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PMID:[Hormonal changes during administration of dietary fibers in patients with decreased glucose tolerance]. 215 75

A somatostatin analog (SMS 201-995) was used to treat symptomatic patients with a residual tumor burden of gastrinoma or medullary thyroid carcinoma and pathologic elevations of circulating marker peptides associated with these neuroendocrine tumors. Possible inhibitory effects of the analog on marker peptides, patients' symptoms, or tumor progression were studied in a dose-response protocol and during several months of self-injection of SMS 201-995. Both patients reported remarkable relief of secretory diarrhea and other symptoms, and serum gastrin was successfully suppressed by increasing doses of the analog. However, no effect was seen in reduction of hypercalcitoninemia. Morphologic imaging of residual tumor showed no progression of medullary thyroid carcinoma during treatment and, in the case of hepatic gastrinoma metastases, remarkable tumor regression was confirmed. No toxicity or glucose intolerance was experienced. Somatostatin analog shows promise for palliative management of endocrinologic symptoms due to neuroendocrine tumors, and an inhibitory effect can be measured in some but not all peptide markers. Further evidence of its negative trophic effect on tumor blood flow may suggest an antineoplastic potential, as well as palliative use of this new treatment.
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PMID:Somatostatin analog: effects on hypergastrinemia and hypercalcitoninemia. 243 92

The purpose of the study was to evaluate some of the hormones in 20 patients with alcoholic cirrhosis. We investigated the diurnal rhythmicity of some of the hormones (cortisol, follicle-stimulating hormone-FSH, luteinizing hormone-LH, growth hormone-LH, prolactin-PRL) and basal serum concentrations of thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4) and testosterone, as well as gastrin and insulin, using provocative tests. Statistical analysis of the results obtained from the observed patients compared with controls, showed significantly lower concentrations of T3 (p less than 0.05), cortisol (p less than 0.05), testosterone (p less than 0.05) and FSH (p less than 0.05), and significantly higher (p less than 0.01) serum concentration of prolactin. Then, in the cirrhotic group the serum concentrations of gastrin and insulin increased significantly (p less than 0.01), together with the disorders of carbohydrate metabolism (impaired glucose tolerance and diabetes mellitus. The described disturbances of some of the observed hormones are complex, particularly in their relationship by which the clinical picture of the cirrhotic patients can be explained.
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PMID:[Hormone levels in patients with alcoholic liver cirrhosis]. 249 Sep 94

A study was undertaken of fasting and post-prandial blood levels of glucose and a number of gastrointestinal hormones in patients with anorexia nervosa. After an overnight fast their blood levels of glucose, insulin and pancreatic glucagon were significantly lower than those of age-sex matched healthy volunteers. There were no significant differences in the levels of gastrin, total glucagon-like immunoreactivity, vasoactive intestinal polypeptide, pancreatic polypeptide, secretin and gastric inhibitory polypeptide. Serial blood samples were taken for up to two hours after the ingestion of a standard mixed meal (450 kcal) and these showed a significant glucose intolerance, a reduced and delayed insulin response, and a reduced release of gastric inhibitory polypeptide, as compared with the controls. There was an increased release of pancreatic polypeptide but the difference in the post-prandial hormone profile between patients and controls for gastrin did not reach statistical significance.
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PMID:Gastrointestinal hormones in anorexia nervosa. 390 Mar 60

At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. We have measured their different molecular forms in plasma of six female controls, six normal pregnant (NP) women and six gestational diabetic (GD) women under basal conditions and 30 min after an oral glucose load (100 g) and a liquid mixed meal in order to study if their alteration could contribute to the impaired glucose tolerance in GD. Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. Neurotensin-1-13 was the main molecular form of all neurotensins at basal time in the three groups studied, being higher in GD in comparison with controls and NP. Somatostatin-1-14 was the predominant molecular form in controls and GD under basal conditions and did not show any change any change after stimuli. In NP, somatostatin-1-14 showed a significant increase following both kinds of stimuli. Total gastrin concentrations in NP and GD showed a significant increase after the glucose load, which was not observed in controls. Gastrin-17 was the main molecular form at basal time and 30 min post-stimuli in GD but not in NP and controls. We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. 810 15

Blood glucose level was estimated in 18 h fasted albino rabbits following acute feeding of graded doses of mianserin. Mianserin (6.0 mg/kg) produced a gradually increasing hyperglycemic effect which became significant (P < 0.01) at 10 h and onwards. This appears to be due to increased turnover and release of noradrenaline by the drug. The same dose of mianserin also produced glucose intolerance during early hours probably by interfering with gastrin functions.
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PMID:Effect of mianserin on blood glucose level in rabbits. 822 48

Effect of single graded doses of amitriptyline (4, 8 and 16, mg/kg, p.o.) were observed on blood glucose level in 18 h fasted albino rabbits. All the doses of Amitriptyline produced significant hyperglycemia at 4 h, which attained a peak at 24 h with 16 mg/kg dose and appears to be due to blockade of the uptake of monominergic transmitters across the axoplasmic membrane, It (16 mg/kg) also produced glucose intolerance during early hours probably due to interference with gastrin function.
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PMID:Effect of amitriptyline on blood glucose level in rabbits. 855 Jan 26

Cisplatin (9 mg/kg) or taxol (20 mg/kg) treatment of Wistar rats produced a sharp decrease in inducible nitric oxide synthase (iNOS) and gastrin in the pyloric region of the stomach, and an increase in iNOS and somatostatin in the pancreatic islets. Nitric oxide (NO) functions as a relaxation factor in the smooth muscle of the muscularis mucosa while gastrin plays an important role in the gastroprotection of the mucosa through NO. It is proposed that a decline of the iNOS and gastrin after cisplatin or taxol treatments is related to distention of the stomach, and possibly nausea and vomiting. Hyperglycemia and glucose intolerance after cisplatin treatment may be caused by increases of somatostatin and iNOS in the pancreatic islets. Combination therapy with cisplatin and taxol seems to ameliorate various toxicities due to these two individual drugs.
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PMID:Effects of cisplatin and taxol on inducible nitric oxide synthase, gastrin and somatostatin in gastrointestinal toxicity. 940 12


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