Somatostatin for Injection
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Regulatory Mechanisms of Somatostatin Expression
International Journal of Molecular Sciences Review Regulatory Mechanisms of Somatostatin Expression Emmanuel Ampofo * , Lisa Nalbach, Michael D. Menger and Matthias W. Laschke Institute for Clinical & Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany; [email protected] (L.N.); [email protected] (M.D.M.); [email protected] (M.W.L.) * Correspondence: [email protected]; Tel.: +49-6841-162-6561; Fax: +49-6841-162-6553 Received: 25 May 2020; Accepted: 9 June 2020; Published: 11 June 2020 Abstract: Somatostatin is a peptide hormone, which most commonly is produced by endocrine cells and the central nervous system. In mammals, somatostatin originates from pre-prosomatostatin and is processed to a shorter form, i.e., somatostatin-14, and a longer form, i.e., somatostatin-28. The two peptides repress growth hormone secretion and are involved in the regulation of glucagon and insulin synthesis in the pancreas. In recent years, the processing and secretion of somatostatin have been studied intensively. However, little attention has been paid to the regulatory mechanisms that control its expression. This review provides an up-to-date overview of these mechanisms. In particular, it focuses on the role of enhancers and silencers within the promoter region as well as on the binding of modulatory transcription factors to these elements. Moreover, it addresses extracellular factors, which trigger key signaling pathways, leading to an enhanced somatostatin expression in health and disease. Keywords: somatostatin; pre-prosomatostatin; δ-cells; central nervous system (CNS); gut; hypothalamus; cAMP resonse element (CRE); pancreas/duodenum homeobox protein (PDX)1; paired box protein (PAX)6; growth hormone (GH); brain-derived neurotrophic factor (BDNF); glutamateric system; pancreas 1. -
Plasma Somatostatin and Cholecystokinin Levels in Preterm Infants and Their Mothers at Birth
0031-399819513706-0771$03.0010 PEDIATRIC RESEARCH Vol. 37, No. 6, 1995 Copyright O 1995 International Pediatric Research Foundation, Inc Printed in U.S.A. Plasma Somatostatin and Cholecystokinin Levels in Preterm Infants and Their Mothers at Birth C.-J. TORNHAGE, F. SERENIUS, K. UVNAS-MOBERG,AND T. LINDBERG Department of Pediatrics, UmeB University, UmeB [C.-J.T., F.S., T.L.] and Department of Pharmacology, Karolinska Institute, Stockholm, Sweden [K. U-M.] Regulatory gut peptides play an important role in regulating same. They were also independent of sex, birth weight, gesta- the gastrointestinal tract. Our knowledge about the pattern of tional age, umbilical cord blood pH, or glucose level. In mothers, secretion and function of these peptides is scanty in preterm but not in infants, plasma SS levels were higher after vaginal infants. Therefore, plasma somatostatin (SS) and cholecystokinin delivery than after cesarean section. After multiple birth, new- (CCK) levels were estimated just after birth in 65 mothers and 73 born plasma SS, but not plasma CCK, was significantly lower preterm infants (umbilical cord blood). The gestational age was than after single birth (9.1 + 7.7 versus 16.9 2 12.7 pmol/L). 32 (24-36 median ranges) wk and birth weight 1900 (475-3350) (Pediatr Res 37: 771-776, 1995) g. The umbilical cord blood pH was 7.32 + 0.10 (mean t- SD). After Sep-Pak-C,, semichromatography of plasma, SS and CCK Abbreviations were analyzed by RIA. Both plasma SS and CCK levels were SS, somatostatin significantly higher in infants than in mothers (SS = 14.5 i. -
Potential for Gut Peptide-Based Therapy in Postprandial Hypotension
nutrients Review Potential for Gut Peptide-Based Therapy in Postprandial Hypotension Malcolm J. Borg 1, Cong Xie 1 , Christopher K. Rayner 1, Michael Horowitz 1,2, Karen L. Jones 1,2 and Tongzhi Wu 1,2,* 1 Adelaide Medical School and Centre of Research Excellence in Translating Nutritional Science to Good Health, The University of Adelaide, Adelaide 5000, Australia; [email protected] (M.J.B.); [email protected] (C.X.); [email protected] (C.K.R.); [email protected] (M.H.); [email protected] (K.L.J.) 2 Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide 5000, Australia * Correspondence: [email protected]; Tel.: +61-8-8313-6535 Abstract: Postprandial hypotension (PPH) is an important and under-recognised disorder resulting from inadequate compensatory cardiovascular responses to meal-induced splanchnic blood pool- ing. Current approaches to management are suboptimal. Recent studies have established that the cardiovascular response to a meal is modulated profoundly by gastrointestinal factors, including the type and caloric content of ingested meals, rate of gastric emptying, and small intestinal transit and absorption of nutrients. The small intestine represents the major site of nutrient-gut interactions and associated neurohormonal responses, including secretion of glucagon-like peptide-1, glucose- dependent insulinotropic peptide and somatostatin, which exert pleotropic actions relevant to the postprandial haemodynamic profile. This review summarises knowledge relating to the role of these gut peptides in the cardiovascular response to a meal and their potential application to the management of PPH. Keywords: postprandial hypotension; glucagon-like peptide-1; glucose-dependent insulinotropic Citation: Borg, M.J.; Xie, C.; Rayner, polypeptide; somatostatin; diabetes mellitus; autonomic failure C.K.; Horowitz, M.; Jones, K.L.; Wu, T. -
Effect of the Natural Sweetener Xylitol on Gut Hormone Secretion and Gastric Emptying in Humans: a Pilot Dose-Ranging Study
nutrients Article Effect of the Natural Sweetener Xylitol on Gut Hormone Secretion and Gastric Emptying in Humans: A Pilot Dose-Ranging Study Anne Christin Meyer-Gerspach 1,2,* , Jürgen Drewe 3, Wout Verbeure 4 , Carel W. le Roux 5, Ludmilla Dellatorre-Teixeira 5, Jens F. Rehfeld 6, Jens J. Holst 7 , Bolette Hartmann 7, Jan Tack 4, Ralph Peterli 8, Christoph Beglinger 1,2 and Bettina K. Wölnerhanssen 1,2,* 1 St. Clara Research Ltd. at St. Claraspital, 4002 Basel, Switzerland; [email protected] 2 Faculty of Medicine, University of Basel, 4001 Basel, Switzerland 3 Department of Clinical Pharmacology and Toxicology, University Hospital of Basel, 4001 Basel, Switzerland; [email protected] 4 Translational Research Center for Gastrointestinal Disorders, Catholic University of Leuven, 3000 Leuven, Belgium; [email protected] (W.V.); [email protected] (J.T.) 5 Diabetes Complications Research Centre, Conway Institute University College Dublin, 3444 Dublin, Ireland; [email protected] (C.W.l.R.); [email protected] (L.D.-T.) 6 Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark; [email protected] 7 Department of Biomedical Sciences and Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark; [email protected] (J.J.H.); [email protected] (B.H.) 8 Department of Surgery, Clarunis, St. Claraspital, 4002 Basel, Switzerland; [email protected] * Correspondence: [email protected] (A.C.M.-G.); [email protected] (B.K.W.); Tel.: +41-61-685-85-85 (A.C.M.-G. -
Regulation of CRH-Induced Secretion of ACTH and Corticosterone By
European Journal of Endocrinology (2005) 153 R7–R10 ISSN 0804-4643 RAPID COMMUNICATION Regulation of CRH-induced secretion of ACTH and corticosterone by SOM230 in rats A P Silva, P Schoeffter, G Weckbecker, C Bruns and H A Schmid Novartis Institutes for BioMedical Research, Basel, Switzerland (Correspondence should be addressed to H Schmid; Email: [email protected]) Abstract Objective: Adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome is biochemically characterized by increased plasma concentrations of ACTH inducing hypersecretion of cortisol. Somatostatin is known to inhibit ACTH secretion, and in vitro data have shown the inhibition of ACTH secretion by agonists activating sst2 and sst5 receptors. The present study aimed to determine the inhibitory effect of the multireceptor ligand SOM230, compared with the sst2-preferring agonist octreotide, on corticotropin-releasing hormone (CRH)-stimulated secretion of ACTH and corticoster- one in rats. Methods: Secretion of ACTH and corticosterone was induced by i.v. application of CRH (0.5 mg/kg) in rats pretreated 1 h before by i.v. application of SOM230 (1, 3, or 10 mg/kg), octreotide (10 mg/kg) or NaCl 0.9%. Results: SOM230 (3 and 10 mg/kg) inhibited CRH-induced ACTH release by 45^3% and 51^2%, respectively, and corticosterone release by 43^5% and 27^16%, respectively. 10 mg/kg of octreotide tended to be less potent at inhibiting ACTH release (34^6% inhibition) and did not alter the secretion of corticosterone. Conclusion: SOM230 has a stronger inhibitory effect on ACTH and corticosterone secretion than octreotide in rats. This difference can be explained by its higher affinity to sst1, sst3 and especially sst5 receptors compared with octreotide. -
Plasma Hormones Facilitated the Hypermotility of the Colon in a Chronic Stress Rat Model
Plasma Hormones Facilitated the Hypermotility of the Colon in a Chronic Stress Rat Model Chengbai Liang, Hesheng Luo*, Ying Liu, Jiwang Cao, Hong Xia Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China Abstract Objective: To study the relationship between brain-gut peptides, gastrointestinal hormones and altered motility in a rat model of repetitive water avoidance stress (WAS), which mimics the irritable bowel syndrome (IBS). Methods: Male Wistar rats were submitted daily to 1-h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. Plasma hormones were determined using Enzyme Immunoassay Kits. Proximal colonic smooth muscle (PCSM) contractions were studied in an organ bath system. PCSM cells were isolated by enzymatic digestion and IKv and IBKca were recorded by the patch-clamp technique. Results: The number of fecal pellets during 1 h of acute restraint stress and the plasma hormones levels of substance P (SP), thyrotropin-releasing hormone (TRH), motilin (MTL), and cholecystokinin (CCK) in WAS rats were significantly increased compared with SWAS rats, whereas vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP) and corticotropin releasing hormone (CRH) in WAS rats were not significantly changed and peptide YY (PYY) in WAS rats was significantly decreased. Likewise, the amplitudes of spontaneous contractions of PCSM in WAS rats were significantly increased comparing with SWAS rats. The plasma of WAS rats (100 ml) decreased the amplitude of spontaneous contractions of controls. The IKv and IBKCa of PCSMs were significantly decreased in WAS rats compared with SWAS rats and the plasma of WAS rats (100 ml) increased the amplitude of IKv and IBKCa in normal rats. -
Inhibition of Gastrin Release by Secretin Is Mediated by Somatostatin in Cultured Rat Antral Mucosa
Inhibition of gastrin release by secretin is mediated by somatostatin in cultured rat antral mucosa. M M Wolfe, … , G M Reel, J E McGuigan J Clin Invest. 1983;72(5):1586-1593. https://doi.org/10.1172/JCI111117. Research Article Somatostatin-containing cells have been shown to be in close anatomic proximity to gastrin-producing cells in rat antral mucosa. The present studies were directed to examine the effect of secretin on carbachol-stimulated gastrin release and to assess the potential role of somatostatin in mediating this effect. Rat antral mucosa was cultured at 37 degrees C in Krebs-Henseleit buffer, pH 7.4, gassed with 95% O2-5% CO2. After 1 h the culture medium was decanted and mucosal gastrin and somatostatin were extracted. Carbachol (2.5 X 10(-6) M) in the culture medium increased gastrin level in the medium from 14.1 +/- 2.5 to 26.9 +/- 3.0 ng/mg tissue protein (P less than 0.02), and decreased somatostatin-like immunoreactivity in the medium from 1.91 +/- 0.28 to 0.62 +/- 0.12 ng/mg (P less than 0.01) and extracted mucosal somatostatin-like immunoreactivity from 2.60 +/- 0.30 to 1.52 +/- 0.16 ng/mg (P less than 0.001). Rat antral mucosa was then cultured in the presence of secretin to determine its effect on carbachol-stimulated gastrin release. Inclusion of secretin (10(-9)-10(-7) M) inhibited significantly carbachol-stimulated gastrin release into the medium, decreasing gastrin from 26.9 +/- 3.0 to 13.6 +/- 3.2 ng/mg (10(-9) M secretin) (P less than 0.05), to 11.9 +/- 1.7 ng/mg (10(-8) secretin) (P less than 0.02), and to 10.8 +/- 4.0 ng/mg (10(-7) M secretin) (P less than […] Find the latest version: https://jci.me/111117/pdf Inhibition of Gastrin Release by Secretin Is Mediated by Somatostatin in Cultured Rat Antral Mucosa M. -
The Gastrointestinal Cholecystokinin Receptors in Health and Diseases
Roczniki Akademii Medycznej w Białymstoku · Vol. 50, 2005 · TheAnnales gastrointestinal Academiae cholecystokinin Medicae Bialostocensis receptors in health and diseases 21 The gastrointestinal cholecystokinin receptors in health and diseases Morisset J* Service de Gastroentérologie, Université de Sherbrooke, Canada Key words: cholecystokinin, gastrin, cholecystokinin recep- gene in different species, their localization and the results of tors, pancreas. their specific occupation under normal and pathological states. Introduction Cholecystokinin Over the years, cholecystokinin (CCK) has been accepted as A. Molecular forms the gastrointestinal hormone mainly responsible for the control Shortly after his discovery of CCK-33 in pig intestine [1], of gallbladder contraction, pancreatic enzyme secretion, growth Mutt purified the slightly larger form CCK-39 from the same of the pancreatic gland and gut motility. On the contrary, its sis- species’ intestine [5]. Later on, smaller and larger molecules ter hormone gastrin is recognized to regulate gastric acid secre- were isolated from several species’ brain and intestine. CCK-58, tion and proliferation of the acid secreting portion of the gastric 8, 5 and 4 were found in porcine brain [6] whereas the molecular mucosae as well as that of the upper intestine and colon. forms 58, 39, 33, 25, 18, 8, 7 and 5 were all identified in dog These two hormones share the same carboxy-terminal pen- intestine [7,8]. Some of these same peptides were also identified tapeptide amide sequence but differ in their sulfation sites on in bovine intestine, 39 and 33, in rat intestine, 58, 22, 8 and in the active C-terminal portion of their molecule; indeed, gastrin guinea pig intestine, 22 and 8 [9-11]. -
Gastrointestinal Hormone Actions in the Central Regulation of Energy Metabolism: Potential Sensory Roles for the Circumventricular Organs
International Journal of Obesity (2009) 33, S16–S21 & 2009 Macmillan Publishers Limited All rights reserved 0307-0565/09 $32.00 www.nature.com/ijo REVIEW Gastrointestinal hormone actions in the central regulation of energy metabolism: potential sensory roles for the circumventricular organs TD Hoyda, PM Smith and AV Ferguson Department of Physiology, Queen’s University, Kingston, Ontario, Canada A variety of circulating signals provide essential information to the central nervous system (CNS) regarding nutritional status. The gastrointestinal system produces many such molecules that are now known to have profound effects on feeding behavior and the control of metabolism as a consequence of their ability to regulate the neural circuitry involved in metabolic homeostasis. Although many of these substances have been suggested to directly access such brain centers, their lipophobic characteristics suggest that alternative mechanisms should be considered. In this paper, we consider one such alternative, namely, that a specialized group of CNS structures collectively known as the sensory circumventricular organs (CVOs), which are not protected by the normal blood–brain barrier, may play important roles in such blood to brain communications. Specifically, we review a developing literature that shows receptors for, and functional actions of, gastrointestinal hormones such as amylin, cholecystokinin, ghrelin and peptide YY in the area postrema and subfornical organ. Collectively, these observations suggest potentially significant roles for the sensory CVOs in the regulation of energy balance. International Journal of Obesity (2009) 33, S16–S21; doi:10.1038/ijo.2009.11 Keywords: amylin; ghrelin; peptide YY; regulation of food intake; adipokines; circumventricular organs Introduction appreciation of the regulatory circuitry controlling the integration of feeding and metabolism. -
Distribution of the Gut Hormones in the Primate Intestinal Tract
Gut: first published as 10.1136/gut.20.8.653 on 1 August 1979. Downloaded from Gut, 1979, 20, 653-659 Distribution of the gut hormones in the primate intestinal tract M. G. BRYANT AND S. R. BLOOM From the Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London SUMMARY Reliable and specific radioimmunoassays have been developed for the gut hormones secretin, gastrin, cholecystokinin, pancreatic glucagon, VIP, GIP, motilin, and enteroglucagon. Using these assays, the relative pattern of distribution of the gut hormones has been determined using the same bowel extracts for all measurements. VIP occurred in high concentration in all regions of the bowel, whereas secretin, GIP, motilin, and CCK were predominantly localised in the proximal small intestine. Pancreatic glucagon was almost exclusively confined to the pancreas. Like VIP, enteroglucagon also exhibited a wide pattern of distribution but was maximal in the ileum. The acid ethanol extraction method that was used was found to be unsuitable for gastrin. On gel chromatography of the extracts, motilin and VIP eluted as single molecular species in identical position to the pure porcine peptides. CCK, pancreatic glucagon, enteroglucagon and GIP were all multiform. Over the last decade the development of radio- peptide throughout the primate intestinal tract immunoassays for the gut hormones has allowed using the same bowel extracts for all measurements. their quantitative measurement both in plasma and in tissue. Although this has prompted several investi- Methods http://gut.bmj.com/ gations to determine the normal distribution of these hormones in different species (Unger et al., 1961; EXTRACTION Bloom and Bryant, 1973; Reeder et al., 1973; The complete intestinal tract was removed after Rehfeld et al., 1975; Bloom et al., 1975; O'Dorisio brief anaesthesia from four healthy baboons and et al., 1976), no comprehensive study has been three monkeys (Macaca Iris) all of whom had been undertaken in the primate. -
The Role of Somatostatin in the Regulation of Gonadotropin Secretion in Sheep
Graduate Theses, Dissertations, and Problem Reports 2017 The Role of Somatostatin in the Regulation of Gonadotropin Secretion in Sheep Richard B. McCosh Follow this and additional works at: https://researchrepository.wvu.edu/etd Recommended Citation McCosh, Richard B., "The Role of Somatostatin in the Regulation of Gonadotropin Secretion in Sheep" (2017). Graduate Theses, Dissertations, and Problem Reports. 6194. https://researchrepository.wvu.edu/etd/6194 This Dissertation is protected by copyright and/or related rights. It has been brought to you by the The Research Repository @ WVU with permission from the rights-holder(s). You are free to use this Dissertation in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you must obtain permission from the rights-holder(s) directly, unless additional rights are indicated by a Creative Commons license in the record and/ or on the work itself. This Dissertation has been accepted for inclusion in WVU Graduate Theses, Dissertations, and Problem Reports collection by an authorized administrator of The Research Repository @ WVU. For more information, please contact [email protected]. The Role of Somatostatin in the Regulation of Gonadotropin Secretion in Sheep Richard B. McCosh Dissertation submitted to the School of Medicine at West Virginia University in partial fulfillment of the requirements for the degree of Doctor of Philosophy In Biomedical Science Cellular and Integrative Physiology Robert L. Goodman, PhD; Mentor Stanley M. Hileman, PhD; Chair Michael W. Vernon, PhD Steven L. Hardy, PhD Donal C. Skinner, PhD Department of Physiology and Pharmacology Morgantown, West Virginia 2017 Key Words: gonadotropin releasing hormone, luteinizing hormone, somatostatin, kisspeptin, sheep Copyright 2017 Richard B. -
Arginine Vasopressin and Somatostatin Receptors in Rat Astrocytes Nasser Syed Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 2006 Arginine vasopressin and somatostatin receptors in rat astrocytes Nasser Syed Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Animal Sciences Commons, Medical Toxicology Commons, Physiology Commons, Toxicology Commons, Veterinary Physiology Commons, and the Veterinary Toxicology and Pharmacology Commons Recommended Citation Syed, Nasser, "Arginine vasopressin and somatostatin receptors in rat astrocytes " (2006). Retrospective Theses and Dissertations. 883. https://lib.dr.iastate.edu/rtd/883 This Thesis is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. Arginine vasopressin and somatostatin receptors in rat astrocytes By Nasser Syed A thesis submitted to the graduate faculty in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Major: Toxicology Program of Study Committee: Walter H. Hsu, Major Professor Richard J. Martin Mary West Greenlee Arthi Kanthasamy Iowa State University Ames, Iowa 2006 Copyright © Nasser Syed, 2006. All rights reserved. UMI Number: 1439915 UMI ® UMI Microform 1439915 Copyright 2007 by ProQuest Information and Learning Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17, United States Code. ProQuest Information and Learning Company 300 North Zeeb Road P.O. Box 1346 Ann Arbor, Ml 48106-1346 11 DEDICATION THIS THESIS IS DEDICATED TO ALLMIGHTY ALLLAH, MY GRAND PARENTS, MY PARENTS, MY WIFE AND MY DAUGHTER Ill TABLE OF CONTENTS List of abbreviations v Abstract vi Chapter 1.