Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Standardized breakfasts with or without beet-fibre were given, in random order, to non-insulin-dependent diabetics. The blood glucose levels were monitored continuously and hormonal responses were determined at regular intervals for 3 hr. After the beet-fibre breakfast including 10.8 g dietary fibre from the sugar beet, the glucose plateau level and the area below the curve were lower than after the control meal. The rate of glucose decrease was also slower after the beet-fibre meal. There were no notable differences with regard to the plasma levels of insulin, C-peptide or glucagon. The gastric inhibitory polypeptide response was greater during the first part of the curve, while the somatostatin response after the beet-fibre meal displayed a significantly larger total area below the curve. The results suggest that the diminished glycemic response after the beet-fibre meal is associated with an increased response of somatostatin, giving a reduced glucose absorption and a delayed gastrointestinal transit time.
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PMID:Reduced glycemic response to beet-fibre meal in non-insulin-dependent diabetics and its relation to plasma levels of pancreatic and gastrointestinal hormones. 300 77

This is a survey of the results of recent investigations on gastrointestinal (GI) peptide hormones. In addition to the classical GI hormones (secretin, gastrin, and cholecystokinin-pancreozymin (CCK-PZ], there are at least nine other peptides whose structures and GI effects are known. These include vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), motilin, pancreatic polypeptide (PP), substance P, neurotensin, somatostatin, enkephalins, and a bombesin-like gastrin-releasing peptide. It is now obvious that the traditional distinctions between hormones, neurotransmitters, and paracrines are rapidly becoming obsolete, as the actions and interactions of these substances within the complex motor system of the GI tract are gradually revealed. The study of perturbed states and toxic effects on the motor function of the small intestine is complicated by the integration of the activity of the small intestine with the activities of the body as a whole. A contemporary approach for evaluating intestinal contractile activity is described that uses computer assistance to measure the intercontractile interval (ICI). This technique may prove useful in assessing the effects of toxicological agents on spontaneous intestinal motor activity in vitro when the agents are delivered to the target sites by physiological mechanisms, in contrast to adding them to the tissue bath.
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PMID:Gastrointestinal hormones and the quantitation of spontaneous duodenal motor activity. 305 20

The isolated perfused human pancreas was used as a model to assess factors mediating the pancreatic polypeptide cell response to glucose, insulin, gastric inhibitory polypeptide, and splanchnic nerve stimulation. Pancreases obtained from 18 cadaveric organ donors were isolated and perfused by way of the splenic artery utilizing a Krebs bicarbonate buffer in a single-pass perfusion system. Hormonal stimulation and inhibition of pancreatic polypeptide secretion were assessed, as was the influence of direct electrical stimulation of celiac neural fibers innervating the pancreas. In this in vitro human model, pancreatic polypeptide cell secretion was inhibited by hyperglycemia, although the presence of gastric inhibitory polypeptide augmented the pancreatic polypeptide cell response. Perfusion with low levels of insulin and splanchnic nerve stimulation augmented the response of the pancreatic polypeptide cell to hyperglycemia and gastric inhibitory polypeptide. Since the immunoreactive pancreatic polypeptide response was augmented when insulin and somatostatin release was inhibited by perfusion insulin or nerve stimulation, we conclude that the pancreatic polypeptide cell is regulated by the ambient degree of somatostatin release, insulin release, or both. These findings support a centrifugal pattern of intraislet blood flow.
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PMID:Regulation of pancreatic polypeptide secretion in the isolated perfused human pancreas. 327 67

Calcitonin gene-related peptide (CGRP) is a 37-amino acid peptide that is present in peripheral cells of islets and in nerves around and within islets. CGRP can inhibit insulin secretion in vitro and in vivo. Whether the inhibitory action of CGRP is mediated by somatostatin or by nerve terminals is, however, not known. The objective of this study was to examine the effect of CGRP on insulin secretion, using cultured newborn and adult rat islet cells which did not contain nerve terminals. In adult rat islet cells, CGRP (10(-10) to 10(-8) M) significantly inhibited glucose-stimulated and gastric inhibitory polypeptide (GIP)-potentiated insulin secretion, but in newborn rat islet cells, CGRP did not inhibit glucose-stimulated insulin secretion. Inhibition of glucose-stimulated and GIP-potentiated insulin release was dependent on the glucose concentration during the prestimulation period. CGRP did not stimulate release of somatostatin. These findings suggest that rat CGRP can act directly on beta-cells through a specific receptor that is absent in newborn rat beta-cells.
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PMID:Effect of calcitonin gene-related peptide on glucose and gastric inhibitory polypeptide-stimulated insulin release from cultured newborn and adult rat islet cells. 328 Nov 89

The endocrine cells in the gut of Mugil saliens Risso, 1810 (leaping grey mullet) were investigated by immunocytochemical and electron microscopic techniques. Gastrin-, glucagon-, and somatostatin-immunoreactive cells were identified in the cardiac and cecal stomach regions, located mainly in the lower part of the gastric folds and in the upper part of the glands. Substance P-, somatostatin-, and pancreatic polypeptide (PP)-immunoreactive cells were found between epithelial cells in the pyloric stomach region. Gastrin-, cholecystokinin (CCK)-, gastric inhibitory polypeptide (GIP)-, substance P-, Met-enkephalin- and PP-immunoreactive cells were observed throughout the intestine while only the last three of these appeared in the posterior intestine. Nine types of gastroenteroendocrine cells were ultrastructurally characterized; some of them were related to the cell types immunocytochemically identified.
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PMID:The endocrine cells in the gut of Mugil saliens Risso, 1810 (Teleostei): an immunocytochemical and ultrastructural study. 329 46

Recent data on the immunolocalization of regulatory peptides and related propeptide sequences in endocrine cells and tumors of the gastrointestinal tract, pancreas, lung, thyroid, pituitary (ACTH and opioids), adrenals and paraganglia have been revised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory polypeptide), neurotensin, glicentin/glucagon-37 and PYY (peptide tyrosine tyrosine) are the main products of gastrointestinal endocrine cells; glucagon, CRF (corticotropin releasing factor), somatostatin, PP (pancreatic polypeptide) and GRF (growth hormone releasing factor), in addition to insulin, are produced in pancreatic islet cells; bombesin-related peptides are the main markers of pulmonary endocrine cells; calcitonin and CGRP (calcitonin gene-related peptide) occur in thyroid and extrathyroid C cells; ACTH and endorphins in anterior and intermediate lobe pituitary cells, alpha-MSH and CLIP (corticotropin-like intermediate lobe peptide) in intermediate lobe cells; met- and leu-enkephalins and related peptides in adrenal medullary and paraganglionic cells as well as in some gut (enterochromaffin) cells; NPY (neuropeptide Y) in adrenaline-type adrenal medullary cells, etc.. Both tissue-appropriate and tissue-inappropriate regulatory peptides are produced by endocrine tumours, with inappropriate peptides mostly produced by malignant tumours.
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PMID:Endocrine cells producing regulatory peptides. 329 70

Diabetes, the most common metabolic disease, is responsible for the deaths of over 300,000 Americans annually. The incidence of the disease increases with age and since the U.S. population is graying, prevalence is also increasing. Obesity and family history are strong predictors of diabetes. The etiology of Type II diabetes is heterogeneous. The hyperglycemia of Type II diabetes can result from a variety of metabolic defects including impaired beta cell secretion, receptor deficiencies, or abnormal hepatic production or uptake of glucose. Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. Environmental factors including stress, diet, and exercise may also contribute to the disease. Since most diabetics are obese, weight loss should be the first priority in improving status. A variety of diet and exercise regimens may help achieve this goal or even improve glucose control without weight loss. Due to the heterogeneity of the disease individualized treatment must be used to improve status of patients with the various metabolic defects of Type II diabetes.
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PMID:Dietary sugars and carbohydrate metabolism in type II diabetes. 330 10

The gastroenteropancreatic (GEP) endocrine cells of the Japanese field vole were studied immunohistochemically. Somatostatin-, 5-hydroxytryptamine-, glicentin-, glucagon-, bovine pancreatic polypeptide-, gastrin-, gastric inhibitory polypeptide-, cholecystokinin-, substance P-, secretin-, neurotensin- and insulin-immunoreactive cells were revealed. The characteristic findings of the regional distribution and relative frequency of these immunoreactive cells in the GEP system of the vole were as follows. Somatostatin-immunoreactive cells were more numerous in the oxyntic glands than in the pyloric glands. Some somatostatin-immunoreactive cells were found in small clusters in the oxyntic glands. Gastrin-immunoreactive cells were detected not only in the pyloric glands and small intestine but also in the caecum and spiral colon. Gastric inhibitory polypeptide-immunoreactive cells were also detected in the pyloric glands and no motilin-immunoreactive cell was found in the gastroenteropancreatic system.
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PMID:Immunohistochemical study of gastroenteropancreatic endocrine cells of the herbivorous Japanese field vole, Microtus montebelli. 353 46

Clinical applications of analyses of hormones in amniotic fluid (AF) have recently been increased. In diabetic pregnancy, determinations of insulin and C-peptide in AF have been suggested as good indicators of the status of the foetus. We have investigated the pancreatic alpha and beta cell function by measuring insulin (IRI), C-peptide (CPR), glucagon (IRG), somatostatin (SLI), and gastric inhibitory polypeptide (GIP) in amniotic fluid collected during basal conditions or 2 h after an arginine test in 92 diabetic and 32 non-diabetic pregnant women. During basal conditions, in diabetic pregnant women, IRI, CPR and the insulin: glucagon molar ratio (I/G) were all significantly higher while amniotic fluid-IRG was significantly lower than in the controls. After arginine stimulation, IRI increased in AF of the diabetic pregnant women but not in AF of the controls while no differences were observed in AF-GIP and AF-SLI concentrations. Higher IRI and CPR, as well as lower IRG values were significantly related to poor maternal metabolic control. The occurrence of neonatal morbidity including macrosomia was significantly associated with increased AF, IRI and CPR concentrations after an arginine challenge and these factors were the most sensitive predictors of neonatal morbidity in infants of diabetic mothers. Increased AF glucose concentrations and I/G ratios were related to neonatal hypoglycaemia; jaundice and respiratory distress syndrome were associated to low concentrations of SF-IRG.
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PMID:Gastro-entero-pancreatic hormones in amniotic fluid from normal and diabetic pregnant women. 353 68

In cultured rat hepatocytes, the effects of gut hormones on bile acid uptake and release were studied. It was found that cultured hepatocytes continued to secrete bile acids into the culture medium and incorporated them effectively as a function of incubation time. Gut hormones such as secretin, glucagon, vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), gastric inhibitory polypeptide (GIP), tetragastrin, cholecystokinin-octapeptide (CCK-8), pancreatic polypeptide (PP), neurotensin substance P, beta-endorphin (beta-End), methionine-enkephalin (Met-enk), motilin, bombesin and somatostatin (SS) had no effect on bile acid uptake by cultured hepatocytes. In bile acid release studies, only secretin caused a dose-dependent stimulation of bile acid release, while other gut hormones had no effect on bile acid release into medium. These results indicate that secretin acts directly on cultured rat hepatocytes and/or bile canaliculi, besides its effect on the bile duct, and influences bile acid metabolism.
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PMID:Effects of gut hormones on bile acid uptake and release in cultured rat hepatocytes. 359 53


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