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)

Post-natal malnutrition was induced in rats using the expanded litter model. Pepsinogen secretion of isolated gastric glands in response to several secretagogues was measured. Malnourished 19-day-old pups showed no response to carbachol, CCK-8, gastrin, secretin and ionophore A23187 compared to well-nourished animals, but showed comparable secretion of pepsinogen after stimulation with dibutyryl cAMP (DiBcAMP). Hydrocortisone treatment for 48 h caused increased pepsinogen accumulation and elevated pepsinogen secretory responsiveness to carbachol and secretin of gastric glands isolated from post-natal malnourished pups. Our results indicate that isolated gastric glands obtained from well-nourished rat possess two functionally distinct receptors for gastrin and C-terminal fragment of CCK. Our study supports the concept that in malnourished rats there is a decreased number of binding sites or/and some post-receptor defects. Pepsinogen release mechanisms remain unaffected.
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PMID:The effect of post-natal malnutrition on pepsinogen secretion receptors in weanling rats. 235 49

The effect of chronic administration of hydrocortisone during pregnancy on growth and maturation of the foetal gut and pancreas was investigated. Groups of 10- to 11-day pregnant rats were injected with saline or hydrocortisone (50 mg/kg) once a day for 10 days. The pancreas, antrum, and small intestine of newborns (8-10 h after birth) were analysed for various determinants of growth and maturation. The small-intestinal weight and DNA, RNA, and protein were significantly higher in newborns from hydrocortisone-treated animals than those of saline-treated controls. Hydrocortisone treatment resulted in an induction of sucrase and significantly stimulated total lactase activity. After the steroid treatment during pregnancy, the weight of the pancreas and its DNA content in newborns were also significantly elevated when compared with those from saline-treated controls. However, neither pancreatic RNA nor protein content differed significantly between the groups. Antral gastrin content in newborns from hydrocortisone-treated mothers was significantly higher than that from saline-treated controls. Pancreatic gastrin content in newborns was slightly but not significantly reduced after the steroid administration to mothers. It is concluded that glucocorticoids induce growth and maturation of foetal gut and pancreas.
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PMID:Influence of glucocorticoids on prenatal development of the gut and pancreas in rats. 258 7

In experimentally hyperthyroid rats an increased amount of gastrin-producing (G) and histamine-producing (ECl) cells was noted by means of immunofluorescent biochemical methods and electron microscopically. Increased amount of the ECl cells was combined with a rise in histamine contents in the gastric mucosa. Hydrocortisone injections resulted in degranulation of the G- and ECl-cells. After hydrocortisone injection, the amount of histamine decreased more than two-fold. It was demonstrated that not only parietal glandulocytes, but also the gastric endocrine cells participated in disorders of a complex acid-producing mechanism.
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PMID:[Structuro-metabolic integration of gastric endocrine cells in the presence of a disruption in hormone balance]. 611 27

Intravenous application of 100 micrograms synthetic ovine corticotropin releasing factor (CRF) led to stimulation of ACTH-secretion in nine normal controls, with a maximum 30 min after CRF. Cortisol, corticosterone, cortisone and 11-deoxycortisol increased with a maximum at 60 min after CRF, whereas no rise was seen in aldosterone, 11-deoxycorticosterone, 17-alpha-hydroxyprogesterone, progesterone, DHEA-S and testosterone. The specificity of CRF-stimulation was also shown by unchanged TSH, LH, FSH, hGH, prolactin and thyroid hormone levels, als well as unchanged insulin and gastrin levels. No serious side-effects were observed during the test period and afterwards. CRF-tests were performed in ten patients with disturbances of the hypothalamo pituitary adrenal axis (HPAA). Preliminary findings show hyperresponsiveness of ACTH in all situations of ACTH-hypersecretion (two patients with Cushing's disease, one patient with Nelson's syndrome, and one with Addison's disease). In contrast, one patient with successful microadenomectomy showed no response of ACTH to CRF, whereas in another patient with a macroadenoma ACTH and cortisol-levels still increased postoperatively. Divergent patterns in ACTH-responsiveness to CRF were seen in four patients with secondary adrenal insufficiency, allowing the localization of the defect. These data point to the possible importance of the "CRF-test" as a differential diagnostic tool and prognostic factor in diseases of the HPAA.
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PMID:Corticotropin releasing factor (CRF)-stimulation test in normal controls and patients with disturbances of the hypothalamo-pituitary-adrenal axis. 630 May 9

The effect of hydrocortisone (75 mg/kg) on antral, duodenal and pancreatic gastrin concentrations and on intestinal lactase, sucrase, maltase and alkaline phosphatase activities was investigated in suckling rats. Antral and pancreatic gastrin levels in normal 4- to 22-day-old rats were also determined. Hydrocortisone was injected daily to 7- and 10-day-old rats for 6 days. At the end of the experimental period the animals were 12 and 15 days old. Control groups were injected with saline. Hydrocortisone administration caused a profound induction in sucrase activity and markedly stimulated maltase and alkaline phosphatase activities in both age groups. After hydrocortisone administration 12-day-old rats showed a slight (28%) but significant stimulation in lactase activity, whereas in 15-day-old rats the enzyme activity was significantly decreased by 23%, compared to the respective saline control. Gastrin concentration in the antrum increased steadily between 4 and 22 days of age, whereas in the pancreas it decreased sharply from a relatively high level in 4-day-old rats to an essentially undetectable level in 22-day-old rats. Following hydrocortisone administration gastrin concentration in the antrum of 12- and 15-day-old rats was found to be significantly increased by 104 and 47%, respectively, but in the pancreas it decreased by 44 and 57%, when compared with the corresponding saline control. Hydrocortisone caused no apparent change in duodenal gastrin concentration in 12-day-old rats but produced a nonsignificant 35% increment in 15-day-old animals. The observed changes after hydrocortisone treatment are thought to be the result of an early maturation of the gastrointestinal mucosa and pancreas by the steroid.
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PMID:Effect of hydrocortisone on gastrin cell function in various tissues of suckling rats. 641 68

Strenuous training in women has been shown to cause menstrual dysfunction and decreased bone mineral density. These endocrine and metabolic complications are associated with an insufficient dietary intake and decreased body fat content in female athletes. The present investigation was undertaken to study serum levels of cholecystokinin (CCK), insulin, gastrin, and cortisol in 14 female long-distance runners and 15 sex- and age-matched control subjects during intake of a standardized meal (500 kcal). The athletes showed a decreased response of the "satiety peptide" CCK to the meal and reported increased hunger compared with the control group. Meal-related insulin response was also decreased in the athletes, whereas gastrin levels were comparable to those of controls. Basal levels of glucose were increased in the athletes, but there was no difference in postprandial levels between the groups. Cortisol levels were clearly elevated in the female runners. We conclude that insufficient food intake in female athletes cannot be explained by increased CCK secretion and satiety. Since the athletes reported a larger caloric intake of a normal daily breakfast than the control subjects, the decreased CCK response may instead be explained by an adaptation to increased food intake. The decreased meal-related insulin response may be a reflection of increased insulin sensitivity as an adaptation to physical exercise. However, an impaired peptide secretion cannot be excluded. The role of elevated cortisol levels in the gastrointestinal hormone response needs further investigation.
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PMID:Reduced serum cholecystokinin response to food intake in female athletes. 812 5

Human gastric mucosa contains aspartic proteinases that can be separated electrophoretically on the basis of their physical properties into two major groups: Pepsinogen I (PGA, PGI); and Pepsinogen II (PGC, PGII). Pepsinogens consist of a single polypeptide chain with molecular weight of approximately 42,000 Da. Pepsinogens are mainly synthesized and secreted by the gastric chief cells of the human stomach before being converted into the proteolytic enzyme pepsin, which is crucial for the digestive processes in the stomach. Pepsinogen synthesis and secretion are regulated by positive and negative feed-back mechanisms. In the resting state pepsinogens are stored in granules, which inhibit further synthesis. After appropriate physiological or external chemical stimuli, pepsinogens are secreted in the stomach lumen where hydrochloric acid, secreted by the parietal cells, converts them into the corresponding active enzyme pepsins. The stimulus-secreting coupling mechanisms of pepsinogens appear to include at least two major pathways: one involving cAMP as a mediator, the other involving modification of intracellular Ca(2+)concentration. Physiological or external chemical stimuli acting through the intracellular metabolic adenyl cyclase are more effective in inducing ' de novo ' pepsinogen synthesis than those acting through intracellular Ca(2+). The activation of protein kinase C (PK-C) would appear to be involved in regulatory processes. The measurement of pepsinogens A and C in the serum is considered to be one of the non-invasive biochemical markers for monitoring peptic secretion and obtaining information on the gastric mucosa status of healthy subjects. Recently, pepsinogen measurements have been used as an effective biochemical method for evaluating and monitoring patients with gastrointestinal diseases and for checking the effects of drug treatment. The level of PGA in the serum is always high in normal gastritis, while in atrophic gastritis it is always low. In both cases the PGC level in the serum is high. In most gastrointestinal pathologies the ratio between the PGA/PGC decreases. Various reports concerning hormone and/or enzyme modification as well as gastrointestinal distress in the case of long distance exercise have been reported. It has been suggested that the origin of the gastrointestinal distress experienced by long distance runners is a transient ischaemia of the gastric mucosa; it is also suggested that a hypobaric-hypoxic environment could contribute to induce gastric mucosa necrosis. Interrelation between gastrointestinal distress, hypobaric-hypoxic environment and modifications of PGA and PGC, gastrin and cortisol was evaluated in 13 athletes after a marathon performed at 4300 m. Gastrointestinal symptoms occurred in approximately 40% of the athletes. After the race the athletes showed a significant increase of gastrin and cortisol, while the ratio between PGA/PGC decreased. No relationship was observed between gastrointestinal symptoms and hormonal changes after the race. A control group of five subjects, who had been exposed to the same environmental conditions, showed no gastrointestinal or hormonal alteration. Conversely, control subjects presented a significant decrease of cortisol related to the circadian rhythm. The same incidence of gastrointestinal symptoms at high altitude and at sea level and the absence of pathological alteration of PGA and PGC in the serum of the athletes indicates that running a marathon and living for 6 days at 4300 m does not induce gastric mucosa necrosis. Cortisol and gastrin alteration observed in the athletes at this altitude would seem to be related to an activation of the mesopontine and forebrain structures involved in the behavioural and metabolic integration of the autonomic control and arousal and psychophysical-exercise stress. 2000 Academic Press@p$hr
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PMID:Pepsinogens: physiology, pharmacology pathophysiology and exercise. 1067 78

Ectopic Cushing's syndrome due to various malignancies is not uncommon. However, a few cases of ectopic Cushing's syndrome caused by corticotropin-releasing hormone (CRH), or CRH with adrenocorticotropic hormone (ACTH) have been reported. A 28-year-old woman presented with acute upper gastrointestinal bleeding caused by an active ulcer, located atypically in the 2nd portion of duodenum. Further work-up revealed high gastrin levels and abdominal computed tomography (CT) scans showed a large pancreatic head mass with multiple liver metastases. The serum cortisol and ACTH levels were checked due to hypokalemia with metabolic alkalosis and recent amenorrhea. Cortisol and ACTH were both highly elevated with pituitary hyperplasia and elevated CRH. The existence of ectopic ACTH and CRH in the liver biopsy was also demonstrated immunohistochemically. Since an operation was not feasible, chemotherapy was conducted using paclitaxel and etoposide. These two drugs were chosen according to the IN VITRO chemotherapy response assay to maximize the treatment. This report demonstrates concurrent ACTH- and CRH-related ectopic Cushing's syndrome caused by malignant gastrinoma with multiple liver metastases that was treated with marginal success using a multidisciplinary medical approach.
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PMID:Ectopic Cushing's syndrome due to concurrent corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) secreted by malignant gastrinoma. 1728 28