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

With the structural characterization of the hypothalamic hormones, luteinizing hormone-releasing hormone (LH-RH), thyrotrophin-releasing (TRH), melanocyte-stimulating hormone release-inhibiting hormine (MIH), and growth hormone release-inhibiting hormone, (GH-RIH or somatostatin), it has been possible to investigate their enzymic inactivation by peptidases which are present at various sites in the body. Enzymes may play an important part in the control of polypeptide hormone levels and the peptidases acting on these four hypothalamic hormones may regulate the amount of TRH, LH-RH, MIH and somatostatin released from the hypothalamus, or their action at the level of the pituitary and their removal from the circulation. By studying the peptidase enzymes, further information may be obtained on the physiological mechanisms controlling the secretion and actions of hypothalamic hormones, as well as on the design of analogues with increased or competitive activity.
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PMID:Peptidase inactivation of hypothalamic releasing hormones. 1 75

The effects of various neurogenic peptides and neurotransmitter substances on the release of ACTH induced by hypothalamic corticotropin releasing factor (HY-CRF) were investigated using monolayer cultured anterior pituitary cells. Test substances were given in combination with 0.05-0.1 hypothalamic extract (HE)/ml, because HE evoked a significant ACTH release and a linear dose response relationship was demonstrated sequentially between 0.0165 HE/ml and 0.5 HE/ml. Relative high doses of lysine-vasopressin showed a slight additive effect on the release of ACTH induced by 0.1 HE/ml. Leu-enkephalin, dopamine, prostaglandin E1 and E2 slightly reduced the release of ACTH induced by HY-CRF, but the inhibitory effect of these substances were not dose-related. Other tested substances including luteinizing hormone releasing hormone, thyrotropin releasing hormone, somatostatin, melanocyte stimulating hormone release inhibiting factor, beta-endorphin, neurotensin, substance P, vasoactive intestinal polypeptide, angiotensin II, norepinephrine, serotonin, acetylcholine, histamine and gamma-amino butyric acid showed neither agonistic nor antagonistic effect on the release of ACTH induced by HY-CRF. These results indicate that the release of ACTH is controlled specifically by HY-CRF and corticosterone, and modified slightly by some other substances such as vasopressin and prostaglandins, and that the effect of most other neurogenic peptides and neurotransmitter substances is negligible or non-physiological at the pituitary level.
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PMID:ACTH release in pituitary cell cultures. Effect of neurogenic peptides and neurotransmitter substances on ACTH release induced by hypothalamic corticotropin releasing factor (CRF). 3 43

By applying at the ultrastructural level the silver methenamine impregnation method to glutaraldehyde-osmium fixed pancreatic tissue of Snell-Bagg mice it was found that two islet cell types show deposition of reduced silver on their secretory granules: B cells and another cell type. Histochemical analyses indicate that very likely the osmium dependent argentaffinity is due to S-S groups. After alkaline treatment the reactivity of B cells is lost, while that of the other cells remains unaffected. It is suggested that the third cell type stores the pancreatic somatostatin, an S-S containing polypeptide hormone.
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PMID:Osmium dependent argentaffin reaction in the pancreatic islet. 6 46

The mechanisms of enzymic inactivation of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone and somatostatin, the three fully-characterized hypothalamic regulatory hormones, and the possible physiological significance of the peptidases in neuroendocrine control has been reviewed. Application of the criteria of enzyme location (at the sites of biosynthesis, release, action, elimination and excretion), appropriate biochemical characteristics of the enzymes and changes in enzyme activity in physiological circumstances all suggest that the peptidases can contribute to the mechanisms controlling the hypothalamic hormones' release and actions. Besides their physiological function, the enzymes may also be directly involved in certain pathological conditions. There is evidence to indicate that the enzymes degrading the regulatory hormones may participate in the process of hormone activation as well as inactivation. A continuing investigation of the peptidases may lead to a better understanding of the established endocrine and other putative functions of these hypothalamic polypeptide hormones.
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PMID:Mechanisms of inactivation of hypothalamic regulatory hormones. 22 39

Subcellular fractionation of the rat cerebral cortex demonstrated the presence of immunoreactive cholecystokinin in the pellet identified by electron microscopy as containing a high proportion of synaptic vesicles. The recovery in this pellet of 40% of the total immunoreactivity in the initial cortical extract is quite comparable to the recovery of other peptides such as vasoactive intestinal polypeptide and somatostatin, which are also located in synaptosomes and for which roles as neuroregulators or transmitters have been suggested. The evidence of concentration of cholecystokinin-like peptides in the synaptosomal pellet is consistent with our earlier demonstration by immunohistochemical techniques of cholecystokinin's presence in rabbit cerebral cortical neurons. These observations and the evidence for diminished concentration of cholecystokinin-like peptides in the brains of hyperphagic mice are consistent with cholecystolinin's suggested role as a neuroregulator for appetite.
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PMID:Localization of cholecystokinin-like immunoreactivity in isolated nerve terminals. 28 49

Most of the somatostatin-like activity from pigeon pancreas was found to correspond to small species with an apparent molecular weight of 1500--2500. This species was isolated under conditions minimizing intermolecular interactions and protease activities. The isolated product was characterized by two somatostatin radioimmunoassays, a bioassay, endgroup determination, and amino acid analysis. The structure of the isolated compound was determined to be H-Ala-Gly-cyclo-(Cys-Lys-Asn-Phe-Phe-Trp-Lys-Thr-Phe-Thr-Ser-Cys)-OH. Additionally, small amounts of des-Ala1-somatostatin, a possible degradation product of pancreatic somatostatin, and a large somatostatin-like species with an apparent molecular weight of 11,000--12,500 were detected. It is concluded that the main somatostatin-like polypeptide isolated from pigeon pancreas is identical to the mammalian hypothalamic tetradecapeptide somatostatin.
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PMID:Isolation and characterization of somatostatin from pigeon pancreas. 28 81

The endocrine cells of the processus uncinatus in the dog pancreas were investigated with special reference to the formerly known F-cell. The F-cell was detected frequently in the periphery of pancreatic islets as well as among exocrine tissue. In both localizations the F-cell shows similar ultrastructural features. Membrane-bound irregularly shaped secretory granules of variable electron density were seen. The cell possesses all features of an endocrine polypeptide secreting cell. Using the immunofluorescence and immunoperoxidase technique in the uncinate processus of the dog, we could reveal that the anti-sera against bovine pancreatic polypeptide (BPP) reacts with the cell which is localized at the same sites as the F-cell. We therefore conclude that the pancreatic F-cell is identical to the pancreatic polypeptide-producing cell. The other endocrine cell types of the dog pancreas are glucagon-producing A-cells, insulin-producing B-cells, and somatostatin-producing D-cells, as well as serotonin-producing EC-cells which are regularly present in the dog pancreatic islets and also scattered among exocrine tissue and the duct epithelial cells.
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PMID:The identification of the F-cell in the dog pancreas as the pancreatic polypeptide producing cell. 31 86

We studied the pancreatic and enteric hormone profile of a 46-year-old woman who had hyperglycemia and a pancreatic tumor. Before operation, there was no evidence of overproduction of glucagon or insulin. The tumor's ultrastructure had a distinctive endocrine morphology, resembling D cells. Prompted by the recent demonstration of somatostatin in D cells of pancreatic islets, we analyzed the tumor and found a large quantity of immunoreactive somatostatin (301 ng per milligram of tissue). Insulin, glucagon, gastrin, vasoactive intestinal polypeptide and human pancreatic polypeptide were present in only trace quantities. The tumor cells were cultured in monolayers, which remained viable up to 51 days and released somatostatin into the culture medium. In seven insulinomas and two glucagonomas, we found the somatostatin content either much lower (less than 0.6 ng per milligram of tissue) or undetectable. After complete resection of the tumor, our patient became euglycemic and has remained so for the past 20 months.
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PMID:"Somatostatinoma": a somatostatin-containing tumor of the endocrine pancreas. 32 60

Steroid hormone concentrating cells in hypothalamic and extrahypothalamic regions are reviewed and the topographic relationship to the periventricular brain and the ventricular recess organs is discussed. Steroid hormone target cells in the brain are considered feedback sites and production sites of polypeptide hormones. The anatomical distribution of estrogen, androgen and progestin target neurons, as defined by autoradiography, is compared with the localization of antibodies to luteinizing hormone-releasing hormone and somatostatin in perikarya of neurons, as characterized by immunocytochemistry. Around the optic recess of the third ventricle in the lamina terminalis and the preoptic nucleus as well as in the periventricular nucleus of the hypothalamus, the steroid hormone target neurons and the assumed polypeptide hormone producing neurons occupy corresponding sites.
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PMID:Steroid hormone target cells in the periventricular brain: relationship to peptide hormone producing cells. 32 16

This is a review of current information concerning the role of hormones and the autonomic nervous system in the control of exocrine secretions of the pancreas. A greater emphasis has been placed on the role of hormones because of information accumulated during the last several years. With the development of radioimmunoassay techniques, it is now possible to correlate circulating hormone concentrations with biological function. The role of hormones has been discussed with the framework of the secretin-glucagon family, the cholecystokinin-gastrin family, and other proposed gastrointestinal hormones and related peptides. Gastrin, secretin and cholecystokinin-pancreozymin are three prime gut hormones that regulate pancreatic secretion. Other hormones that may have a role in pancreatic secretion include glucagon, vasoactive intestinal polypeptide, chymodenin, somatostatin, pancreatic polypeptide, motilin, and bombesin. Neural mechanisms play an important although not so succinct a role in the over-all control of exocrine secretion. A complex relationship exists between the parasympathetic nervous system and the release of the hormones and their effect on pancreatic acinar and duct cells.
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PMID:Neurohormonal control of pancreatic secretion. A review. 34 Mar 22


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