Hormones gastrin

Using peptides of the gastrin hormone family as model antigens these uncontrolled effects were fully confirmed in our laboratory (48,52). In fact, gastrin/BSA conjugates prepared in conventional manner by the water-soluble carbodiimide led in animal-dependent manner to antibodies of differentiated specificity in full agreement with results from other laboratories where immunization experiments were usually performed on a larger number of animals to obtain in a "trial and error" manner antisera of the desired specificity (53-55). 

Neoplasias that arise from the endocrine portion of the pancreas can be classified as secretory or non-secretory (Gouya et al. 2003). When secretory, the endocrine tumor will be subclassified according to the type of hormone produced (insulin hormone, gastrin hormone, or active peptides). Insulinomas are the most common endocrine tumors, while glucagonomas or somatostatinomas have not been reported in children. 

Zollinger-Ellison syndrome (ZES) is characterized by the development of a tumor (gastrinoma) or tumors that secrete excessive levels of gastrin, a hormone that stimulates production of acid by the stomach. In most cases, the tumor or tumors arise within the pancreas and/or the upper region of the small intestine (duodenum). 

Antrectomy Surgical excision of the wall of the antrum, the region of the stomach that produces the hormone gastrin. 

The major gastric factor that affects motility and the rate of emptying is the volume of chyme in the stomach. As the volume of chyme increases, the wall of the stomach becomes distended and mechanoreceptors are stimulated. This elicits reflexes that enhance gastric motility by way of the intrinsic and vagus nerves. The release of the hormone gastrin from the antral region of the stomach further contributes to enhanced motility. 

Gastrin is a hormone produced by gastric endocrine tissue — specifically, the G cells in the pyloric gland area. It is released into the blood and carried back to the stomach. The major function of gastrin is to enhance acid secretion by directly stimulating parietal cells (HC1) and chief cells (pepsinogen). Gastrin also stimulates the local release of histamine from enterochromaf-fin-like cells in the wall of the stomach. Histamine stimulates parietal cells to release HC1. 

The scope of applicability of radioimmunoassay is rapidly expanding with the dawn of each day as RIA is being developed for newer pharmaceutical substances. It has attained wide recognition and application both in vitro and in vivo measurements of compounds of interest like insulin, gastrin, glucagon, and growth hormones on one hand whereas drugs like ... 

Growth-Arrest-Specific protein 2 Domain Gastrin/cholecystokinin/caerulein family Dynamin GTPase effector domain Gelsolin homology domain G protein y subunit-like motifs Glycoprotein hormone a chain homologs... 

Gastrin A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]... 

Specific hormones Insulin, glucagon, somatostatin, gastrin, pancreatic polypeptide, serotonin, vasoactive intestinal peptide, cholecystokinin... 

Prostaglandins inhibit the secretion of protons by the parietal cells in the stomach, which is normally increased in response to food and the hormone gastrin. Consequently, inhibition of prostaglandin synthesis by aspirin or other similar drugs results in increased secretion of protons by the stomach, which can result in considerable gastric discomfort and can, if chronic, lead to the development of a peptic ulcer. Consequently, there is some conflict between the use of such inhibitors to relieve chronic pain (see below), in diseases such as arthritis, and the risk of development of ulcers. 

Gastrin release peptide. Melanocyte stimulating hormone. 

Ib. Inhibitors of add production. Acting on their respective receptors, the transmitter acetylcholine, the hormone gastrin, and histamine released intra-mucosally stimulate the parietal cells of the gastric mucosa to increase output of HCl. Histamine comes from entero-chromaffin-like (ECL) cells its release is stimulated by the vagus nerve (via Mi receptors) and hormonally by gastria The effects of acetylcholine and histamine can be abolished by orally applied antagonists that reach parietal cells via the blood. 

The gastric acid secretion can be stimulated by the transmitters acetylcholine, histamine and the hormone gastrin. Histamine, acting via H2-receptors,... 

Gastric acid secretion is inhibited in the presence of acid itself. A negative feedback occurs when the pH approaches 2.5 such that further secretion of gastrin is inhibited until the pH rises. Ingested carbohydrates and fat also inhibit acid secretion after they reach the intestines several hormonal mediators for this effect have been proposed. The secretion of pepsinogen appears to parallel the secretion of H+, while the patterns of secretion of mucus and bicarbonate have not been well characterized. 

The regulation of calcitonin synthesis and release from the parafollicular C cells of the thyroid gland is calcium dependent. Rising serum calcium is the principal stimulus responsible for calcitonin synthesis and release. Other hormones, such as glucagon, gastrin, and serotonin, also stimulate calcitonin release. Calcitonin has been isolated in tissues other than the parafollicular C cells (parathyroid, pancreas, thymus, adrenal), but it is not known whether this material is biologically active. 

A counterpart of evidence that CCK agonists are anxiogenic is to answer the question of whether the CCK system is functionally implicated in non-provoked symptoms of panic or anxiety. It is conceivable that endogenous variations of central and/or peripheral CCK activity may be a neurochemical concomitant of anxiety. It is interesting to mention that serum concentrations of gastrin, a CCK-B agonist, fluctuate in correlation with self-reported tension, conflict, and anxiety in psychiatrically healthy men (M. Feldman et al. 1992). Plasma CCK levels were markedly elevated in sportsmen before a competitive marathon run, as compared with CCK levels under control conditions (Phillip et al. 1992). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, and noradrenaline were also elevated and increased extensively after the running performance. However, CCK levels re-... 

Stimulation of gastric acid secretion is the most important response it is blocked only by Hj antagonists. As mentioned before, the hormone gastrin may be involved in histamine release, because Hj antagonists block gastrin-induced acid secretion. 

---