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)

Somatostatin, under physiological conditions, is a regulator of thyroid stimulating hormone, growth hormone, pancreatic islet-cell hormones and gastrin. In pharmacological dosage, gastric acid output, splanchnic blood flow and plasma renin levels, are influenced. A possible therapeutic effect on increased growth hormone secretion, disturbances of carbohydrate metabolism, gastroenteropathies and renal hypertension, is discussed. The clinical application is limited by the short biological half-life of the substance and the unspecific action on several organs.
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PMID:[Somatostatin]. 37 88

We found that renin and aldosterone values do not drop except when administering Carbenoxolone. The significant rise of sodium (11) in the serum and the drop of the serum-potassium values are probably responsible for the undesirable Carbenoxolone side effects; they occur following the administration of deglycyrrhizinized succus. The rise of post-prandial gastrin in the serum of the above as compared to the values obtained from untreated controls is common to both.
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PMID:[Behavior of gastrin, renin, aldosterone and electrolytes after administration of deglycyrrhizinized liquorice and carbenoxolone in healthy subjects]. 80 22

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients. 145 6

Eleven hemodialyzed patients with uremia were examined for the effect of erythropoietin (EP) treatment carried out for 3 months on functions of different endocrine organs. EP treatment resulted in a decrease of the initial plasma levels of somatotropin, prolactin, follicle-stimulating and luteinizing hormones. EP treatment being over, there was a decrease in the plasma content of ACTH, cortisol and aldosterone. The treatment with EP was also associated with an insignificant rise of the plasma levels of parathyroid hormone and testosterone. EP treatment did not influence the plasma concentration of calcitonin and 25-OH-D. EP was found to exert no significant effect on the pituitary-thyroid reverse relationship. The 3-month treatment with EP eventuated in plasma renin activity inhibition as well as in an increase of the atrial level of natriuretic peptide in the plasma. EP treatment stimulated insulin secretion and reduced glucagon secretion. Finally, EP decreased the gastrin level and to a less degree the plasma level of pancreatic polypeptide.
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PMID:[The effect of erythropoietin treatment on endocrine organ function in patients with terminal-stage kidney failure on hemodialysis]. 194 56

A housewife, 40 years of age, was admitted with dysesthesia of the extremities, muscle weakness, and attacks of adynamia and thirst. She had been taking a laxative for more than 20 years. On physical examination, blood pressure was 94/56 mmHg. Laboratory tests revealed thrombocytosis, low serum K and marked increases in both plasma renin activity and serum aldosterone. Serum TBG was increased. Serum gastrin was also markedly increased and could not be enhanced by exogenous secretin. Both angiotensin 11 loading test and noradrenalin loading test failed to increase blood pressure. Ammonium chloride loading to examine the disturbance of urinary acidification was abnormal in the short term test and borderline in the long term test. Following a diagnosis of pseudo-Bartter's syndrome induced by long term intake of laxative and repeated diarrhea, the administration of laxative was interrupted and potassium, indomethacin and spironolactone were administered. However, serum K remained low. Hypergastrinemia, thrombocytosis and a high serum TBG level also persisted, the causes of which remain unknown. This is the first reported case of pseudo-Bartter's syndrome associated with hypergastrinemia, thrombocytosis and increased serum TBG.
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PMID:A case of pseudo-Bartter's syndrome associated with hypergastrinemia, thrombocytosis and increased serum thyroxine-binding globulin. 212

Several factors are involved in the persistence of endocrine alterations after renal transplantation, among which the following are to be mentioned: (1) duration of chronic uraemia before renal transplantation; (2) residual function of the patients' native kidneys; (3) quality of function of the renal graft; (4) modulation of secretion, transport, and degradation of hormones, and/or (5) altered target organ responsiveness to hormones induced by immunosuppressive drugs (glucocorticoids, azathioprine, cyclosporin A) or altered internal environment. In kidney transplant patients the following endocrine abnormalities are to be mentioned: dissociation of the physiological relationship between aldosterone synthesis and function of the renin-angiotensin system, abnormal volumetric regulation of arginine vasopressin secretion, suppressed responsiveness of cortisol secretion to stimulatory manoeuvres, persistent secondary hyperparathyroidism, relative deficiency of insulin (induced by glucocorticoid therapy), with consequent carbohydrate intolerance or even diabetes mellitus, suppressed response of gastrin and pancreatic hormone secretion to a test meal, and reduced responsiveness of atrial natriuretic peptide secretion to central hypervolaemia. Episodes of acute graft rejection are characterized by endocrine alterations similar to those seen in patients with acute or chronic renal failure.
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PMID:Endocrine alterations in kidney transplant patients. 219 17

Twenty-two different humoral parameters including stress-, gastrointestinal- and volume-regulating hormones were measured before and within 45 min after parabolic flight maneuvers of twenty healthy adult subjects. We compared hormonal data of motion sickness-affected participants with those unaffected. Changes in cortisol and vasoactive intestinal peptide plasma levels were significantly different (p less than 0.002 and p less than 0.004) between the two groups with increasing plasma levels of both hormones during motion sickness but decreasing levels within the control group. Growth hormone and prolactin plasma levels increased by 400% and 115% within the motion sickness-affected group and to a smaller degree (120% and 40% increases, respectively) within the control group, while ACTH levels were almost unchanged within both groups. Pancreatic polypeptide and gastrin plasma levels as well as plasma levels of insulin and C-peptide were significantly decreased within both groups after the parabolic flight. Plasma renin, aldosterone, atrial natriuretic peptide and cyclic GMP levels were unchanged within the control group. Within the motion sickness-affected group, plasma renin and aldosterone levels were decreased and atrial natriuretic peptide levels increased after the flight. Humoral parameters of the thyroid gland were neither changed within the groups nor different between the groups. The present data confirm previous results that increases in plasma levels of certain stress hormones participate in motion sickness. Furthermore, increases in vasoactive intestinal peptide levels participate in motion sickness. These increases could explain some of the gastrointestinal symptoms in motion sickness and might serve as markers for a discrimination between regular stress and motion sickness.
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PMID:Hormonal changes after parabolic flight: implications on the development of motion sickness. 224 48

In nine splenectomized male dogs a splenic artery, -splenic vein shunt was made. Before splenectomy and 3, 6 and 18 months after arterialization of portal blood, different metabolic and endocrine parameters were estimated. Long-term arterialization of portal blood was followed by only insignificant increase of portal vein pressure but a significant drop of pCO2 and increase of pO2 in portal blood was recorded. Simultaneously, a significant decrease of the erythrocyte count, hematocrit value, serum cholesterol and uric acid levels, and a shortening of the T1/2 of insulin and glucagon were found. In contrast, long-term arterialization of portal blood was followed by a significant increase of serum triglycerides, alpha2-globulins, plasma renin activity, cortisol, gastrin and 25-hydroxyvitamin D, and by slight carbohydrate intolerance. No morphological abnormalities in the liver and kidney tissue were found. Data presented in this paper suggest usefulness of a splenic artery-splenic vein shunt in the treatment of some metabolic disorders and of the failing hepatocytes.
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PMID:Metabolic effects of long-term arterialization of portal blood. 309 52

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

Decapeptide ceruletide (CRL), chemically related to cholecystokinin and gastrin, proved to have remarkable analgesic properties when administered to a group of 22 burned patients, 15 patients with acute myocardial infarction, and 8 patients suffering from pain caused by malignant tumours with metastases. Its effect was such, that many of the patients required no other analgesics (opiates) even after a prolonged administration (up to 10 days) of CRL. In some of the patients a marked euphoria developed. There were no substantial changes in EEG records during CRL administration in 15 controls, among them 4 epileptics. It is probable that CRL helps to activate the internal analgesic system. In the burned patients cortisol, testosterone, renin, prolactin and tri-iodothyronine (T3) levels in serum (plasma) were measured (radio-immunoassays). CRL did not block the stress response (no drop of increased cortisol levels, no increase in low T3 levels), but it modified (influenced) it (drop of the high renin levels, and a tendency to increase the very low testosterone levels). CRL appears to act as an endorphin releaser, as evidenced by the plasma levels of beta-endorphins (quotations). CRL and similar drugs may represent a new, more physiological and probably safer approach to the management of pain.
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PMID:Endorphin releasers: a new possible approach to the treatment of pain after burns--a preliminary report. 631 91


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