PORCINE SECRETIN for Injection Label
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Cholecystokinin Expression in the Developing and Regenerating Pancreas and Intestine
233 Cholecystokinin expression in the developing and regenerating pancreas and intestine G Liu, S V Pakala, D Gu, T Krahl, L Mocnik and N Sarvetnick Department of Immunology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA (Requests for offprints should be addressed to N Sarvetnick; Email: [email protected]) Abstract In developmental terms, the endocrine system of neither NOD mice continued this pattern. By contrast, in IFN- the gut nor the pancreatic islets has been characterized transgenic mice, CCK expression was suppressed from fully. Little is known about the involvement of cholecysto- birth to 3 months of age in the pancreata but not intestines. kinin (CCK), a gut hormone, involved in regulating the However, by 5 months of age, CCK expression appeared secretion of pancreatic hormones, and pancreatic growth. in the regenerating pancreatic ductal region of IFN- Here, we tracked CCK-expressing cells in the intestines transgenic mice. In the intestine, CCK expression per- and pancreata of normal mice (BALB/c), Non Obese sisted from fetus to adulthood and was not influenced Diabetic (NOD) mice and interferon (IFN)- transgenic by IFN-. Intestinal cells expressing CCK did not mice, which exhibit pancreatic regeneration, during em- co-express glucagon, suggesting that these cells are bryonic development, the postnatal period and adulthood. phenotypically distinct from CCK-expressing cells in We also questioned whether IFN- influences the expres- the pancreatic islets, and the effect of IFN- on sion of CCK. The results from embryonic day 16 showed CCK varies depending upon the cytokine’s specific that all three strains had CCK in the acinar region of microenvironment. -
Secretin and Autism: a Clue but Not a Cure
SCIENCE & MEDICINE Secretin and Autism: A Clue But Not a Cure by Clarence E. Schutt, Ph.D. he world of autism has been shaken by NBC’s broadcast connections could not be found. on Dateline of a film segment documenting the effect of Tsecretin on restoring speech and sociability to autistic chil- The answer was provided nearly one hundred years ago by dren. At first blush, it seems unlikely that an intestinal hormone Bayless and Starling, who discovered that it is not nerve signals, regulating bicarbonate levels in the stomach in response to a but rather a novel substance that stimulates secretion from the good meal might influence the language centers of the brain so cells forming the intestinal mucosa. They called this substance profoundly. However, recent discoveries in neurobiology sug- “secretin.” They suggested that there could be many such cir- gest several ways of thinking about the secretin-autism connec- culating substances, or molecules, and they named them “hor- tion that could lead to the breakthroughs we dream about. mones” based on the Greek verb meaning “to excite”. As a parent with more than a decade of experience in consider- A simple analogy might help. If the body is regarded as a commu- ing a steady stream of claims of successful treatments, and as a nity of mutual service providers—the heart and muscles are the pri- scientist who believes that autism is a neurobiological disorder, I mary engines of movement, the stomach breaks down foods for have learned to temper my hopes about specific treatments by distribution, the liver detoxifies, and so on—then the need for a sys- seeing if I could construct plausible neurobiological mechanisms tem of messages conveyed by the blood becomes clear. -
Endocrine Pancreatic Tumors: Ultrastructure
ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 10, No. 1 Copyright© 1980, Institute for Clinical Science, Inc. Endocrine Pancreatic Tumors: Ultrastructure MERY KOSTIANOVSKY, M.D. Department of Pathology, Thomas Jefferson University, Philadelphia, PA 19107 ABSTRACT Endocrine pancreatic tumors are frequently multicellular and produce several hormones and peptides. A review of the basic concepts of hormone secretion, pancreatic islet cell composition and ultrastructural make-up of tumors is presented. The importance of correlating ultrastructural, immuno- cytochemical and biochemical studies of these tumors is emphasized. Introduction Morphofunctional Aspects of Pancreatic Islets During the last few years a great amount of information was accumulated regarding At the present time four different types the mechanisms of synthesis, storage and of cells have been described in the pan release of hormones.14,28,31 The use of ex creatic islets,17,33 each having a specific perimental in vitro m odels21,25,26,28 was secretory product (table I). A variety of very helpful in clarifying the participation other cells possibly exists, although of different organelles in the biosynthesis, further identification is awaited. By light cellular “packaging” and emyocytosis of microscopy, it is not possible to distin the secretory products. In a review, Lacy31 guish one type of cell from the other. has proposed a working model for hor Histochemical procedures are of help, mone secretion, describing the sim however, and B cells are easily stained ilarities between different endocrine with aldehyde fuchsin. The dicferent pro glands. Some of this information was ob cedures and empiric nature oi the silver tained through the studies of endocrine stain22 added confusion in the nomen pancreatic tumors as in the case of the clature of the cells (as seen in table I) discovery of pro-insulin in a beta cell where the same cell has been described adenoma.62 The purpose of this paper is to by different names. -
Reference ID: 4125998
HIGHLIGHTS OF PRESCRIBING INFORMATION • Determine the number of vials to be reconstituted based on the patient’s These highlights do not include all the information needed to use weight and prescribed dose (2.2) ® CHIRHOSTIM safely and effectively. See full prescribing information for • ChiRhoStim® must be reconstituted with 0.9% Sodium Chloride CHIRHOSTIM®. Injection prior to administration (2.2) • See full prescribing information for complete information on exocrine ® CHIRHOSTIM (human secretin) for injection, for intravenous use test methods (2.3) Initial U.S. Approval: 2004 -------------------------RECENT MAJOR CHANGES---------------------------- ---------------------DOSAGE FORMS AND STRENGTHS--------------------- Dosage and Administration (2.1) 07/2017 For injection: 16 mcg or 40 mcg of human secretin as a lyophilized powder in Contraindications, removed (4) 07/2017 single-dose vial for reconstitution (3) Warnings and Precautions (5.1, 5.2) 07/2017 -------------------------------CONTRAINDICATIONS----------------------------- -------------------------INDICATIONS AND USAGE----------------------------- None (4) ChiRhoStim® is a secretin class hormone indicated for stimulation of: • pancreatic secretions, including bicarbonate, to aid in the diagnosis of -----------------------WARNINGS AND PRECAUTIONS----------------------- exocrine pancreas dysfunction (1) • Hyporesponse to Secretin Stimulation Testing in Patients with • gastrin secretion to aid in the diagnosis of gastrinoma (1) Vagotomy, Inflammatory Bowel Disease or Receiving -
Digestive System Physiology of the Pancreas
Digestive System Physiology of the pancreas Dr. Hana Alzamil Objectives Pancreatic acini Pancreatic secretion Pancreatic enzymes Control of pancreatic secretion ◦ Neural ◦ Hormonal Secretin Cholecystokinin What are the types of glands? Anatomy of pancreas Objectives Pancreatic acini Pancreatic secretion Pancreatic enzymes Control of pancreatic secretion ◦ Neural ◦ Hormonal Secretin Cholecystokinin Histology of the Pancreas Acini ◦ Exocrine ◦ 99% of gland Islets of Langerhans ◦ Endocrine ◦ 1% of gland Secretory function of pancreas Acinar and ductal cells in the exocrine pancreas form a close functional unit. Pancreatic acini secrete the pancreatic digestive enzymes. The ductal cells secrete large volumes of sodium bicarbonate solution The combined product of enzymes and sodium bicarbonate solution then flows through a long pancreatic duct Pancreatic duct joins the common hepatic duct to form hepatopancreatic ampulla The ampulla empties its content through papilla of vater which is surrounded by sphincter of oddi Objectives Pancreatic acini Pancreatic secretion Pancreatic enzymes Control of pancreatic secretion ◦ Neural ◦ Hormonal Secretin Cholecystokinin Composition of Pancreatic Juice Contains ◦ Water ◦ Sodium bicarbonate ◦ Digestive enzymes Pancreatic amylase pancreatic lipase Pancreatic nucleases Pancreatic proteases Functions of pancreatic secretion Fluid (pH from 7.6 to 9.0) ◦ acts as a vehicle to carry inactive proteolytic enzymes to the duodenal lumen ◦ Neutralizes acidic gastric secretion Enzymes ◦ -
Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease
cells Review Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease Chongxu Zhang 1, Tengjiao Cui 1, Renzhi Cai 1, Medhi Wangpaichitr 1, Mehdi Mirsaeidi 1,2 , Andrew V. Schally 1,2,3 and Robert M. Jackson 1,2,* 1 Research Service, Miami VAHS, Miami, FL 33125, USA; [email protected] (C.Z.); [email protected] (T.C.); [email protected] (R.C.); [email protected] (M.W.); [email protected] (M.M.); [email protected] (A.V.S.) 2 Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33101, USA 3 Department of Pathology and Sylvester Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33101, USA * Correspondence: [email protected]; Tel.: +305-575-3548 or +305-632-2687 Received: 25 August 2020; Accepted: 17 October 2020; Published: 21 October 2020 Abstract: Growth hormone-releasing hormone (GHRH) is secreted primarily from the hypothalamus, but other tissues, including the lungs, produce it locally. GHRH stimulates the release and secretion of growth hormone (GH) by the pituitary and regulates the production of GH and hepatic insulin-like growth factor-1 (IGF-1). Pituitary-type GHRH-receptors (GHRH-R) are expressed in human lungs, indicating that GHRH or GH could participate in lung development, growth, and repair. GHRH-R antagonists (i.e., synthetic peptides), which we have tested in various models, exert growth-inhibitory effects in lung cancer cells in vitro and in vivo in addition to having anti-inflammatory, anti-oxidative, and pro-apoptotic effects. One antagonist of the GHRH-R used in recent studies reviewed here, MIA-602, lessens both inflammation and fibrosis in a mouse model of bleomycin lung injury. -
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. -
Normal Pancreatic Function 1. What Are the Functions of the Pancreas?
Normal Pancreatic Function Stephen J. Pandol Cedars-Sinai Medical Center and Department of Veterans Affairs Los Angeles, California USA [email protected] Version 1.0, June 13, 2015 [DOI: 10.3998/panc.2015.17] 1. What are the functions of the This chapter presents processes underlying the functions of the exocrine pancreas with pancreas? references to how specific abnormalities of the The pancreas has both exocrine and endocrine pancreas can lead to disease states. function. This chapter is devoted to the exocrine functions of the pancreas. The exocrine function 2. Where is the pancreas located? is devoted to secretion of digestive enzymes, ions and water into the intestine of the gastrointestinal The illustration in Figure 1 demonstrates the (GI) tract. The digestive enzymes are necessary anatomical relationships between the pancreas for converting a meal into molecules that can be and organs surrounding it in the abdomen. The absorbed across the surface lining of the GI tract regions of the pancreas are the head, body, tail into the body. Of note, there are digestive and uncinate process (Figure 2). The distal end enzymes secreted by our salivary glands, of the common bile duct passes through the head stomach and surface epithelium of the GI tract of the pancreas and joins the pancreatic duct as it that also contribute to digestion of a meal. enters the intestine (Figure 2). Because the bile However, the exocrine pancreas is necessary for duct passes through the pancreas before entering most of the digestion of a meal and without it the intestine, diseases of the pancreas such as a there is a substantial loss of digestion that results cancer at the head of the pancreas or swelling in malnutrition. -
Secretin/Vasoactive Intestinal Peptide-Stimulated Secretion of Bombesin/ Gastrin Releasing Peptide from Human Small Cell Carcinoma of the Lung1
ICANCER RESEARCH 46, 1214-1218, March 1986] Secretin/Vasoactive Intestinal Peptide-stimulated Secretion of Bombesin/ Gastrin Releasing Peptide from Human Small Cell Carcinoma of the Lung1 Louis Y. Korman,2 Desmond N. Carney, Marc L. Citron, and Terry W. Moody Medica/ Service (151W), Veterans Administration Medical Center, Washington, DC 20422 [L. Y.K., M.L.C.]; Department of Medicine and Biochemistry George Washington University School of Medicine, Washington, DC 20037 [T. W. M.¡;and National Cancer Institute-Navy Medical Oncology Branch National Cancer Institute and National Naval Medical Center, Bethesda, Maryland [D. N. C.¡ ABSTRACT autocrine factor for SCCL (12) growth. We studied the mecha nism of BLI secretion in several SCCL cell lines by examining Bombesin/gastrin releasing peptide-like immunoreactivity (BLI) the action of agents that increase intracellular cAMP. is found in the majority of small cell carcinoma of the lung (SCCL) Because of the results of these in vitro studies and the fact cell lines examined. Because BLI is present in high concentration that secretin stimulates hormone release in patients with gastrin in SCCL we studied the mechanism of BLI secretion from several producing tumors (Zollinger-Ellison syndrome), we examined the SCCL cell lines and in patients with SCCL. In cell line NCI-H345 action of i.v. secretin infusion on plasma BLI levels in several the structurally related polypeptide hormones secretin, vasoac- patients with SCCL, non-SCCL lung tumors, and patients with tive intestinal peptide, and peptide histidine isoleucine as well as theophylline, a phosphodiesterase inhibitor, N6,O2'-dibutyryl out any cancer. cyclic adenosine 3':5'-monophosphate, a cyclic nucleotide ana logue, increased BLI release by 16-120% and cyclic adenosine MATERIALS AND METHODS 3':5'-monophosphate by 36-350%. -
The Role of Corticotropin-Releasing Hormone at Peripheral Nociceptors: Implications for Pain Modulation
biomedicines Review The Role of Corticotropin-Releasing Hormone at Peripheral Nociceptors: Implications for Pain Modulation Haiyan Zheng 1, Ji Yeon Lim 1, Jae Young Seong 1 and Sun Wook Hwang 1,2,* 1 Department of Biomedical Sciences, College of Medicine, Korea University, Seoul 02841, Korea; [email protected] (H.Z.); [email protected] (J.Y.L.); [email protected] (J.Y.S.) 2 Department of Physiology, College of Medicine, Korea University, Seoul 02841, Korea * Correspondence: [email protected]; Tel.: +82-2-2286-1204; Fax: +82-2-925-5492 Received: 12 November 2020; Accepted: 15 December 2020; Published: 17 December 2020 Abstract: Peripheral nociceptors and their synaptic partners utilize neuropeptides for signal transmission. Such communication tunes the excitatory and inhibitory function of nociceptor-based circuits, eventually contributing to pain modulation. Corticotropin-releasing hormone (CRH) is the initiator hormone for the conventional hypothalamic-pituitary-adrenal axis, preparing our body for stress insults. Although knowledge of the expression and functional profiles of CRH and its receptors and the outcomes of their interactions has been actively accumulating for many brain regions, those for nociceptors are still under gradual investigation. Currently, based on the evidence of their expressions in nociceptors and their neighboring components, several hypotheses for possible pain modulations are emerging. Here we overview the historical attention to CRH and its receptors on the peripheral nociception and the recent increases in information regarding their roles in tuning pain signals. We also briefly contemplate the possibility that the stress-response paradigm can be locally intrapolated into intercellular communication that is driven by nociceptor neurons. -
Interactions Between Two Different G Protein-Coupled Receptors in Reproductive Hormone-Producing Cells: the Role of PACAP and Its Receptor PAC1R
International Journal of Molecular Sciences Review Interactions between Two Different G Protein-Coupled Receptors in Reproductive Hormone-Producing Cells: The Role of PACAP and Its Receptor PAC1R Haruhiko Kanasaki *, Aki Oride, Tomomi Hara, Tselmeg Mijiddorj, Unurjargal Sukhbaatar and Satoru Kyo Department of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya-cho, Izumo, Shimane 693-8501, Japan; [email protected] (A.O.); [email protected] (T.H.); [email protected] (T.M.); [email protected] (U.S.); [email protected] (S.K.) * Correspondence: [email protected]; Tel.: +81-853-20-2268; Fax: +81-853-20-2264 Academic Editor: Kathleen Van Craenenbroeck Received: 18 August 2016; Accepted: 19 September 2016; Published: 26 September 2016 Abstract: Gonadotropin-releasing hormone (GnRH) and gonadotropins are indispensable hormones for maintaining female reproductive functions. In a similar manner to other endocrine hormones, GnRH and gonadotropins are controlled by their principle regulators. Although it has been previously established that GnRH regulates the synthesis and secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH)—both gonadotropins—from pituitary gonadotrophs, it has recently become clear that hypothalamic GnRH is under the control of hypothalamic kisspeptin. Prolactin, which is also known as luteotropic hormone and is released from pituitary lactotrophs, stimulates milk production in mammals. Prolactin is also regulated by hypothalamic factors, and it is thought that prolactin synthesis and release are principally under inhibitory control by dopamine through the dopamine D2 receptor. In addition, although it remains unknown whether it is a physiological regulator, thyrotropin-releasing hormone (TRH) is a strong secretagogue for prolactin. -
Secretin/Secretin Receptors
JKVTAMand others Secretin and secretin receptor 52:3 T1–T14 Thematic Review evolution MOLECULAR EVOLUTION OF GPCRS Secretin/secretin receptors Correspondence Janice K V Tam, Leo T O Lee, Jun Jin and Billy K C Chow should be addressed to B K C Chow School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Hong Kong, Hong Kong Email [email protected] Abstract In mammals, secretin is a 27-amino acid peptide that was first studied in 1902 by Bayliss and Key Words Starling from the extracts of the jejunal mucosa for its ability to stimulate pancreatic " secretin secretion. To date, secretin has only been identified in tetrapods, with the earliest diverged " secretin receptor secretin found in frogs. Despite being the first hormone discovered, secretin’s evolutionary " evolution origin remains enigmatic, it shows moderate sequence identity in nonmammalian tetrapods " origin but is highly conserved in mammals. Current hypotheses suggest that although secretin has " divergence already emerged before the divergence of osteichthyans, it was lost in fish and retained only in land vertebrates. Nevertheless, the cognate receptor of secretin has been identified in both actinopterygian fish (zebrafish) and sarcopterygian fish (lungfish). However, the zebrafish secretin receptor was shown to be nonbioactive. Based on the present information that the earliest diverged bioactive secretin receptor was found in lungfish, and its ability to interact with both vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide potently suggested that secretin receptor was descended from a VPAC-like receptor gene before the Actinopterygii–Sarcopterygii split in the vertebrate lineage. Hence, Journal of Molecular Endocrinology secretin and secretin receptor have gone through independent evolutionary trajectories despite their concurrent emergence post-2R.