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At least 739 records · Page 41Linked to original sources
PubMed1975

Growth-hormone release-inhibiting hormone in gastrointestinal and pancreatic D cells.

The normal pancreatic D cell has been well recognised since 1931, but its secretory product has not been identified with certainty. Combined immunocytochemical methods, and histological methods for endocrine granules, have demonstrated that it contains a product with G.H.-R.I.H.-like immunoreactivity. G.H.-R.I.H. has also been localised in the upper gastrointestinal tract, tentatively in the morphologically similar D cell of the Wiesbaden classification. The potent actions of this peptide on pancreatic and gastrointestinal function suggest that it may play an important role in digestive physiology.

Animals↗
PubMed1998

Gastrointestinal complications of renal failure.

ESRD has well-documented effects on the esophagus, stomach, duodenum, and pancreas. Unless the supply of donor kidneys increases dramatically, these complications of ESRD will continue to be an important clinical issue for gastroenterologists given the large percentage of patients with symptoms. Further study of uremic retention products and abnormal gastrointestinal hormone profiles on the gastrointestinal tract should help provide additional insights into this complex group of patients.

Digestive System Diseases↗
PubMed2003

Bombesin-like peptides: candidates as diagnostic and therapeutic tools.

Bombesin (BBS) is proved to have a wide variety of the pharmacologic effects, including effects on the release of gastrointestinal hormones and control of gastrointestinal motility. More recently, the role of BBS in tumor growth, cellular proliferation and inflammation has attracted attention. There is evidence that increased BBS receptor expression may be considered as a specific marker for small-cell lung cancer, colorectal adenocarcinoma, gastric and pancreatic cancer, prostate, ovarian and breast cancer, neuroblastoma, renal cell carcinoma, malignant melanoma and thyroid carcinoma. BBS expression was found to be correlated with the histological grade of the tumor. Similarly, BBS treatment significantly improves the healing of chronic gastric ulcers and ameliorates the severity of burn- or colitis-induced gut injury. Although there is much complexity still to be elucidated to understand fully the physiologic and pathologic roles of BBS-like peptides several clinical or experimental trials have addressed that circulating or tissue levels of BBS-like peptides or their receptor expression may be used as diagnostic or prognostic markers of neoplastic disease, and incorporation of BBS receptor antagonists in the treatment of human cancer could provide substantial benefit to the cancer patients. Moreover, trophic, anti-ulcerogenic and anti-inflammatory actions of exogenous BBS make this peptide a potential supplement in minimizing or reversing tissue damage against several injurious challenges. In conclusion, based on the evidence summarized herein, related to the mitogenic and anti-inflammatory effects of BBS-like peptides, further investigations are needed to derive the benefit of BBS-like peptides in pharmacologic strategies.

Animals↗
PubMed1976

Gastrointestinal peptide hormone analogues.

All derivatives of the C-terminal tetrapeptide fragment of gastrins with 17 amino acids elicit every physiological effect of the gastrin. This recognation led to detailed studies on the structure-activity relationships. In the case of cholecystokinin-pancreozymin, a substance consisting of 33 amino acids, the smallest sequence which possesses biological activity is the C-terminal octapeptide fragment. Synthesis of analogous derivatives of this fragment allowed the determination of the structural elements necessary to evoke the biological action.

Amino Acid Sequence↗
PubMedDate not supplied

An unusual clinical course of a hormone-secreting gastrointestinal tumor: a case presentation from clinical practice.

The gastrinoma was first described in 1955 by the surgeons Zollinger and Ellison. The basic characteristic of this disease is an endocrine tumor of the gastrointestinal tract, which secretes gastrin. There is a hypersecretion of gastric juice and recurrent gastric, duodenal and jejunal ulcers. Herein, the case of a 49 year-old female is presented. In 1982, two liver tumors, sized 10 and 6 cm, were discovered in the right and left lobes of the liver, respectively. A duodenal ulcer was also found. During explorative laparotomy, a liver biopsy specimen was obtained and defined pathohistologically as a metastatic, small cell epithelial tumor with an organoid endocrine pattern, morphologically corresponding to tumors of the APUD (Amine Precursor Uptake and Decarboxylation) series. The gastrinoma was verified by immunohistochemical staining. Serum gastrin values exceeded normal values by 10 times. The patient refused further treatment at that time. In the following years, she was treated conservatively several times for sequelae of ulcer disease. For the past three years, she has been treated as an outpatient, mostly for chronic diarrhea.

Female↗
PubMed1992

Effects of peripheral hormones on memory and ingestive behaviors.

This article explores the mechanisms by which peripheral gastrointestinal hormones produce central nervous system effects on memory and feeding. Cholecystokinin produces its satiety effects and memory-enhancing effects by stimulating ascending vagal fibers. Hyperglycemia has been demonstrated to be a cause of memory dysfunction in persons with diabetes mellitus. A number of other hormones, such as amylin and bombesin, modulate both memory processing and feeding. The causes of the anorexia of aging are briefly reviewed.

Aging↗
PubMed1995

Nutrient intake is modulated by peripheral peptide administration.

Many peptides have been shown to modulate nutrient intake. In most cases, these peptides decrease food intake, but in a few cases they have been demonstrated to stimulate feeding. Infusion of insulin peripherally will decrease food intake unless hypoglycemia occurs where the reduced glucose is a stimulus to feeding. Other pancreatic hormones including glucagon, amylin, pancreatic polypeptide, and enterostatin reduce food intake. Of the gastrointestinal hormones, cholecystokinin has been the most widely studied and reduces food intake in a number of species, including human beings. Gastrin-releasing peptide and its relative bombesin have been shown to decrease food intake in experimental animals and man. Somatostatin reduces food intake in experimental animals, but no clinical studies are available. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte stimulating hormone (dMSH), growth hormone, and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides which modulate feeding. beta-casomorphin, a hepta peptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines, and thyrotropin-releasing hormone decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors which relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.

Animals↗
PubMed1986

Influence on plasma levels of somatostatin, gastrin, glucagon, insulin and VIP-like immunoreactivity in peripheral venous blood of anaesthetized cats induced by low intensity afferent stimulation of the sciatic nerve.

The objective of the present study was to investigate whether gastrointestinal hormones can be released in response to low intensity afferent activation of the sciatic nerve. Experiments were performed on anaesthetized cats in which the sciatic nerve was stimulated electrically at 3 Hz, to V and 0.2 ms. Blood samples were collected in a peripheral vein and the plasma levels of somatostatin, gastrin, glucagon, insulin and VIP-like immunoreactivity (below referred to as somatostatin, gastrin, glucagon, insulin and VIP) were recorded by radioimmunoassay. Afferent stimulation of the sciatic nerve caused immediate (approximately 15 min long) changes of the levels of all the above mentioned peptides. Somatostatin, gastrin and glucagon levels rose significantly, whereas in the case of insulin and VIP a significant relationship between the effect of sciatic nerve stimulation and basal levels was established. Thus, insulin and VIP levels decreased when basal levels were high and increased when basal levels were low. The secretion of gastrointestinal and pancreatic hormones is in part regulated by the autonomic nervous system. It is suggested that afferent stimulation of the sciatic nerve causes a reflex activation of the vagal and/or the splanchnic nerves, which in turn affects the release rate of the above-mentioned hormones. In conclusion, these data show that the release of gastrointestinal hormones can be influenced by low intensity stimulation of the sciatic nerve. The physiological trigger of these responses may be touching of the skin.

Afferent Pathways↗
PubMed1985

Pancreatic islet hormone response to oral glucose in morbidly obese patients.

Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.

Adult↗
PubMed1993

Abnormal plasma gut hormones in pathologic duodenogastric reflux and their response to surgery.

Fasting and postprandial plasma levels of the gut hormones gastrin, cholecystokinin (CCK), secretin, glucose-dependent insulinotropic polypeptide, motilin, neurotensin, peptide YY (PYY), enteroglucagon, glucagon, insulin, and pancreatic polypeptide were measured in 11 patients with alkaline gastritis associated with excessive duodenogastric reflux not related to previous gastric surgery (primary DGR), 12 primary DGR patients after pancreatico-biliary diversion ("duodenal switch" procedure), and in 10 age-matched healthy controls. Gastric emptying of a semisolid oatmeal was also measured in patients with primary DGR and in patients after bile diversion. Fasting plasma levels of the distal gut hormone neurotensin and the pancreatic islet hormone insulin were significantly greater in patients with primary DGR compared with controls. Neurotensin levels were normal in patients studied after bile diversion. Postprandial plasma levels, incremental integrated and total integrated responses for CCK, secretin, insulin, neurotensin, PYY, and enteroglucagon, were significantly greater in patients with primary DGR compared with controls. The majority of these responses normalized after bile diversion; however, the postprandial response for insulin and enteroglucagon remained elevated. Patients with primary DGR had a rapid early postprandial phase of gastric emptying of solids, which showed a significant correlation with plasma neurotensin levels. Bile diversion produced a significant delay in this lag-phase of gastric emptying. These abnormalities in gut regulatory hormones appear to be adaptive changes to rapid early postprandial gastric emptying, probably related to antropyloric dysmotility, which has been implicated in the pathogenesis of this condition. Measurement of these gastrointestinal hormones may become useful in the diagnosis of primary DGR.

Anastomosis, Roux-en-Y↗
PubMed1992

[The effect of hormones on the gastrointestinal mucosa].

Proliferative effects of hormones on the gastrointestinal mucosa are discussed according to literature data. There are presented the trophic effects of gastrin, cholecystokinin, secretin, enteroglucagon, somatostatin, growth hormone, thyroxine, peptide YY, epidermal growth factor and submaxillary growth factor.

Animals↗
PubMedDate not supplied

A centenary of gastrointestinal endocrinology.

Gastrointestinal hormones are peptides released to circulation from endocrine cells as well as neurons in the gastrointestinal tract. More than 30 hormone genes are currently known to be expressed in the stomach and intestines, which makes the gut the largest endocrine organ in the body. Moreover, cell and molecular biology now makes it feasible to conceive gastrointestinal endocrinology under five general headings: 1) The structural homology groups the hormones into eight families, each of which is assumed to originate from a common ancestral gene; 2) the individual hormone gene often have multiple phenotypes due to alternative splicing of the primary transcript, tandem organization of the translational product or differentiated maturation of the prohormone. By a combination of these mechanisms, more than 100 different hormonally active peptides are released from the gastrointestinal tract; 3) in addition, gut hormone genes are also widely expressed outside the gut, some only in neurons and/or in endocrine cells, but others also in other extraintestinal cell-types; 4) the different cell types may express different hormonally active fragments of the same prohormone by variation in the cell-specific posttranslational processing. Finally, 5) endocrine cells, neurons, and spermatozoa display different cell-specific release of gut peptides, so the same peptide may act as a metabolic blood-borne hormone, as a neurotransmitter, as a long-acting growth factor, and as an acute fertility factor.

Alternative Splicing↗
PubMed1982

Motilin stimulates growth hormone release in vitro.

Motilin, a twenty two amino acid polypeptide originally isolated from duodenal extracts, has been detected recently in the mammalian hypothalamus and pituitary. We have investigated the possibility that motilin might play a role in neuroendocrine events and report here the ability of synthetic porcine motilin (10(-6)M) to stimulate growth hormone release from rat hemipituitaries and dispersed anterior pituitary cells in vitro. No significant effects on luteinizing hormone, thyroid stimulating hormone or prolactin release were observed. Motilin may be added therefore to the growing list of gastrointestinal hormones which can act directly at the level of the anterior pituitary to alter hormone release.

Animals↗