Thyroid Gland
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Hemodynamic and Renal Effects of Atrial Natriurectic Peptide in Normal
European Journal of Clinical Investigation The Journal of the European Society for Clinical Investigation Editors-in-Chief R. Arnold, M. Brandis, M. Kern Editorial Board 0. L. M. Bijvoet, A. B. Boneu, G. B. Bolli, J. Brodehl, P. van Brummelen, U. Fölsch, E. Harms, R. D. Hesch, D. R. Higgs, K. Hierholzer, U. Keller, G. Klöppel, K. Kühn, S. Lamberts, H. Löffler, S. Matern, F. R. Matthias, K. H. Meyer z. Büschenfelde, S. Moncada, K. J. Netter, C. Nissen, G. Paumgartner, B. A. Peskar, L. B. A. van de Putte, M. J. Rennie, C. Reiger, E. O. Riecken, H. -D. Roher, H. H. Ropers, P. Schauder, G. Schernthaner, H. Scholz, K. Schrör, V. Schusdziarra, M. Sheppard, K. Sikora, M. V. Singer, E. Steiness, B. E. Strauer, K. Unsicker, G. Utermann, P. Verroust, P. v. Wiehert, R. Ziegler, R. Zinkernagel Volume 18,1988 Published for the European Society for Clinical Investigation by Blackwell Scientific Publications, Oxford London Edinburgh Boston Palo Alto Melbourne Published by Blackwell Scientific Publications Ltd, Osney Mead, Oxford OX2 OEL, U.K. © 1988 Blackwell Scientific Publications Ltd. Authorization of photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Blackwell Scientific Publications Ltd for libraries and other users registered with the Copyright Clearance Center (CCC) Transactional Reporting Service, provided that the base fee of $3-00 per copy is paid directly to CCC, 27 Congress Street, Salem, MA 01970, U.S.A. Special requests should be addressed to the Editor. 0014-2972/88 $3 00. The use of registered names, trade marks, etc., in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulation and therefore free for general use. -
Discovery, Characterization, and Clinical Development of the Glucagon-Like Peptides
Discovery, characterization, and clinical development of the glucagon-like peptides Daniel J. Drucker, … , Joel F. Habener, Jens Juul Holst J Clin Invest. 2017;127(12):4217-4227. https://doi.org/10.1172/JCI97233. Harrington Prize Essay Endocrinology Gastroenterology The discovery, characterization, and clinical development of glucagon-like-peptide-1 (GLP-1) spans more than 30 years and includes contributions from multiple investigators, science recognized by the 2017 Harrington Award Prize for Innovation in Medicine. Herein, we provide perspectives on the historical events and key experimental findings establishing the biology of GLP-1 as an insulin-stimulating glucoregulatory hormone. Important attributes of GLP-1 action and enteroendocrine science are reviewed, with emphasis on mechanistic advances and clinical proof-of-concept studies. The discovery that GLP-2 promotes mucosal growth in the intestine is described, and key findings from both preclinical studies and the GLP-2 clinical development program for short bowel syndrome (SBS) are reviewed. Finally, we summarize recent progress in GLP biology, highlighting emerging concepts and scientific insights with translational relevance. Find the latest version: https://jci.me/97233/pdf The Journal of Clinical Investigation HARRINGTON PRIZE ESSAY Discovery, characterization, and clinical development of the glucagon-like peptides Daniel J. Drucker,1 Joel F. Habener,2 and Jens Juul Holst3 1Lunenfeld-Tanenbaum Research Institute, Mt. Sinai Hospital, University of Toronto, Toronto, Ontario, Canada. 2Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Harvard University, Boston, Massachusetts, USA. 3Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark. sequences of cloned recombinant cDNA copies of messenger RNAs. -
Beyond the Fixed Setpoint of the Hypothalamus–Pituitary–Thyroid Axis
E Fliers and others Hypothalamus–pituitary– 171:5 R197–R208 Review thyroid axis MECHANISMS IN ENDOCRINOLOGY Beyond the fixed setpoint of the hypothalamus–pituitary–thyroid axis Eric Fliers1, Andries Kalsbeek1,2 and Anita Boelen1 Correspondence should be addressed 1Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, 1105 AZ to E Fliers Amsterdam, The Netherlands and 2Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Email Amsterdam, The Netherlands e.fl[email protected] Abstract The hypothalamus–pituitary–thyroid (HPT) axis represents a classical example of an endocrine feedback loop. This review discusses dynamic changes in HPT axis setpoint regulation, identifying their molecular and cellular determinants, and speculates about their functional role. Hypothalamic thyrotropin-releasing hormone neurons were identified as key components of thyroid hormone (TH) setpoint regulation already in the 1980s, and this was followed by the demonstration of a pivotal role for the thyroid hormone receptor beta in negative feedback of TH on the hypothalamic and pituitary level. Gradually, the concept emerged of the HPT axis setpoint as a fixed entity, aiming at a particular TH serum concentration. However, TH serum concentrations appear to be variable and highly responsive to physiological and pathophysiological environmental factors, including the availability or absence of food, inflammation and clock time. During food deprivation and inflammation, TH serum concentrations decrease without a concomitant rise in serum TSH, reflecting a deviation from negative feedback regulation in the HPT axis. Surprisingly, TH action in peripheral organs in these conditions cannot be simply predicted by decreased serum TH concentrations. Instead, diverse environmental stimuli have differential effects on local TH metabolism, e.g. -
Study Guide Medical Terminology by Thea Liza Batan About the Author
Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails proficiencyincommunicatingwithhealthcareprofessionalssuchasphysicians,nurses, or dentists. -
1 to the Stomach Inhibits Gut-Brain Signalling by the Satiety Hormone Cholecystokinin (CCK)
Targeted Expression of Plasminogen Activator Inhibitor (PAI)-1 to the Stomach Inhibits Gut-Brain Signalling by the Satiety Hormone Cholecystokinin (CCK) Thesis submitted in accordance with the requirements of the University of Liverpool for the degree of Doctor in Philosophy By Joanne Gamble October 2013 I For Lily, you are the sunshine in my life…. II Table of Contents Figures and tables VII Acknowledgements XI Publications XIII Abstract XIV Chapter 1 ................................................................................................................................ 1 1.1 Overview ........................................................................................................................... 2 1.2 The Gastrointestinal Tract and Digestive Function ...................................................... 4 1.2.1 Distribution, Structure and Biology of Enteroendocrine (EEC) Cells ........................ 5 1.2.2 Luminal Sensing ......................................................................................................... 6 1.3 Energy Homeostasis ......................................................................................................... 7 1.3.1 Gut Hormones ........................................................................................................... 10 1.3.1.1 The Gastrin Family ............................................................................................ 11 1.3.2 PP-fold Family ......................................................................................................... -
Defects in Α-Cell Function in Patients with Diabetes Due to Chronic
Diabetes Care 1 Lena Mumme,1 Thomas G.K. Breuer,1 Defects in -Cell Function in CLIN CARE/EDUCATION/NUTRITION/PSYCHOSOCIAL a Stephan Rohrer,1 Nina Schenker,1 Patients With Diabetes Due to Bjorn¨ A. Menge,1 Jens J. Holst,2 Michael A. Nauck,1 and Juris J. Meier1 Chronic Pancreatitis Compared With Patients With Type 2 Diabetes and Healthy Individuals https://doi.org/10.2337/dc17-0792 OBJECTIVE Diabetes frequently develops in patients with chronic pancreatitis. We examined the alterations in the glucagon response to hypoglycemia and to oral glucose adminis- tration in patients with diabetes due to chronic pancreatitis. RESEARCH DESIGN AND METHODS Ten patients with diabetes secondary to chronic pancreatitis were compared with 13 patients with type 2 diabetes and 10 healthy control subjects. A stepwise hypo- glycemic clamp and an oral glucose tolerance test (OGTT) were performed. RESULTS Glucose levels during the OGTT were higher in patients with diabetes and chronic pancreatitis and lower in control subjects (P < 0.0001). Insulin and C-peptide levels were reduced, and the glucose-induced suppression of glucagon was impaired in both groups with diabetes (all P < 0.0001 vs. control subjects). During hypoglycemia, glucagon concentrations were reduced in patients with chronic pancreatitis and with type 2 diabetes (P < 0.05). The increase in glucagon during the clamp was inversely related to the glucose-induced glucagon suppression and positively related to b-cell function. Growth hormone responses to hypoglycemia were lower in patients with type 2 diabetes (P = 0.0002) but not in patients with chronic pancreatitis. 1Diabetes Division, Department of Medicine I, CONCLUSIONS St. -
Hormonal Control of Glucose Homoeostasis in Ruminants
PYOC.Nutr. SOC.(1983), 42, 149 '49 Hormonal control of glucose homoeostasis in ruminants By G. H. MCDOWELL,Dairy Research Unit, Department of Animal Husbandry, University of Syndey, Camden, NSW, 2570, Australia Little, if any, glucose is absorbed from the alimentary tract of the grazing ruminant and it appears that significant absorption of glucose only occurs in ruminants consuming relatively large amounts of grain (Bergman, 1973; Lindsay, 1978). In spite of this, ruminants have an absolute requirement for glucose which is similar to that of nonruminants. Certainly glucose is an essential metabolite for the brain as there is no oxidation of ketones in the brain of the ruminant (Lindsay, 1980). Moreover, glucose is required for turnover and synthesis of fat, as a precursor of muscle glycogen and in pregnant and lactating ruminants, glucose is an essential metabolite. Indeed the glucose requirements of late-pregnant and lactating ruminants increase dramatically beyond that required for maintenance (Bergman, 1973, see also Table 2, p. 164). It is not surprising that volatile fatty acids derived from rumen fermentation of carbohydrate provide some 70% of the energy requirements of the ruminant (Bergman, 1973). Even so, gluconeogenesis and the maintenance of glucose homoeostasis are critical processes in view of the absolute requirements for glucose. Unlike the situation in monogastric species, gluconeogenesis is maximal after feed ingestion and decreases during food restriction. The major factor influencing the rate of gluconeogenesis is the availability of substrates (Lindsay, 1978). In fed ruminants the principal precursors are propionate and amino acids, with lactate and glycerol making minor contributions to glucose production. -
Gut Hormones
259 PROCEEDINGS OF THE NUTRITION SOCIETY The Three Hundred and Eighteenth Scktajk Meeting was held in the Medical and Biological Sciences Building, University of Southampton, on 20 and 21 July I978 SYMPOSIUM ON ‘HORMONES AND FOOD UTILIZATION’ Gut hormones By S. R. BLOOM, Department of Medicine and J. M. POLAK,Department of Pathology, The Royal Postgraduate Medical School, Hamwsmith Hospital, Du Cane Road, London W12 oHS History At the end of the last century Pavlov proposed that the control of alimentary function was by nervous reflex. His explanation was intellectually satisfying and a great advance on previous extremely woolly theories. Histologically fine nerve fibres which could be seen running in the gut w& and sectioning the main nerve trunks undoubtedly affected gastrointestinal function. Meanwhile, however, Brown Sequard, attempting to rejuvenate his ageing body, was able to show that extracts of testes greatly increased his prowess in several directions. His findings, published in 1889, caught the public imagination and by the end of the century extracts of numerous organs were available for the purpose of treating real and imagined ailments. Thus when Bayliss & Starling were investigating the influence of the duodenum on the exocrine pancreas, the idea of making duodenal extracts came readily. They were astonished to find that such an extract had all the effects on the exocrine pancreas that had been previously attributed to Pavlov’s nervous reflexes. They proposed that there must be a chemical messenger released from the duodenum which acted via the circulation and proposed the term hormone. Nature of the gut endocrine system Although the first substance to be named hormone, secretin, was from the alimentary tract, progress in the understanding of gut endocrinology was very slow. -
Thyroid and Polycystic Ovary Syndrome
S Gabersˇcˇek and others Thyroid and PCOS 172:1 R9–R21 Review MECHANISMS IN ENDOCRINOLOGY Thyroid and polycystic ovary syndrome Simona Gabersˇcˇek1,2, Katja Zaletel1, Verena Schwetz3, Thomas Pieber3, Barbara Obermayer-Pietsch3 and Elisabeth Lerchbaum3 Correspondence should be addressed to 1Department of Nuclear Medicine, University Medical Centre Ljubljana, Zalosˇka 7, 1525 Ljubljana, Slovenia, B Obermayer-Pietsch 2Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1104 Ljubljana, Slovenia and 3Division of Endocrinology Email and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, barbara.obermayer@ 8036 Graz, Austria medunigraz.at Abstract Thyroid disorders, especially Hashimoto’s thyroiditis (HT), and polycystic ovary syndrome (PCOS) are closely associated, based on a number of studies showing a significantly higher prevalence of HT in women with PCOS than in controls. However, the mechanisms of this association are not as clear. Certainly, genetic susceptibility contributes an important part to the development of HT and PCOS. However, a common genetic background has not yet been established. Polymorphisms of the PCOS-related gene for fibrillin 3 (FBN3) could be involved in the pathogenesis of HT and PCOS. Fibrillins influence the activity of transforming growth factor beta (TGFb). Multifunctional TGFb is also a key regulator of immune tolerance by stimulating regulatory T cells (Tregs), which are known to inhibit excessive immune response. With lower TGFb and Treg levels, the autoimmune processes, well known in HT and assumed in PCOS, might develop. In fact, lower levels of TGFb1 were found in HT as well as in PCOS women carrying allele 8 of D19S884 in the FBN3 gene. -
Hedonic Interruption of the Physiological Controls of Eating: Sites and Mechanisms
Dissertation der Graduate School of Systemic Neurosciences der Ludwig-Maximillians-Universität München Hedonic interruption of the physiological controls of eating: sites and mechanisms ESTE LEIDMAA PhD Thesis 5th of Febuary 2016 Thesis Advisory Committee Professor Osborne Almeida (Supervisor) Professor Christophe Magnan (2nd reviewer) Professor Heidrun Potschka Dr. Susanne E La Fleur (External reviewer) Prof. Harald Luksch (Reviewer from GSN) Date of the thesis defence: 22.06.2016 Pühendusega minu perele Table of Contents Table of Contents ........................................................................................................................... List of Abbreviations ...................................................................................................................... i Abstract ............................................................................................................................................ 5 Chapter 1. General Introduction ...................................................................................................... 7 1.1. Feeding – an essential behaviour .................................................................................... 8 1.1.1. Meeting the energy demands of brain and body ....................................................... 8 1.1.2. Overeating and obesity ............................................................................................. 10 1.1.3. Pathological consequences of obesity ..................................................................... -
Endocrine Pathology Crines… Molecular Signaling Endocrine Pathology Endocrine Pathology
Endocrine Pathology Crines… Molecular signaling Autocrine Paracrine Endocrine Endocrine Pathology Endocrine Pathology Cell signaling system Too much hormone activity Surface receptors Too little hormone activity cAMP and tyrosine kinase system Autoimmune destruction Cytoplasmic receptors Inflammatory destruction Penetrate cell membrane Tumor or vascular destruction Gene activation -> transcription -> translation Space occupying lesions (tumors) Intranuclear receptors Malignant Gene activation -> transcription -> translation Benign 1 Endocrine Pathology Endocrine Pathology All parts of the endocrine system interconnect. All parts of the endocrine system interconnect Pituitary Pathology Too much Too little Especially space occupying lesions The Basics Pituitary Vascular Signaling proteins Anterior are release in hypothalmus. Comes from GI Travel by blood to Controlled by hypothalmus anterior pituitary Cause release of Posterior many activating Hormones orginate hormones further up. System of amplification 2 Pituitary Control Space Occupying Lesions Tumors Embryonic rests Squeeze gland out of existence. Generalized failure Visual field changes Visual Fields Loss of temporal fields. Nasal retina Damage to decusating optic nerve fibers 3 Acromegaly Pituitary Adenomas Rare Growth hormone excess after closing Make nothing or of epiphyses. Prolactin Periosteal bone ACTH, GH,TSH are very rare growth. More often end up with pituitary Diabetes failure. Prognathism Squeeze the daylights out of the -
11 Hormonal Coordination Table 1 the Main Roles of Hormones Produced by the Different Endocrine Glands
B 11 Hormonal ■ B11 Hormonal coordination Table 1 The main roles of hormones produced by the different endocrine glands Endocrine gland Role of the hormones coordination Pituitary Controls growth in children Stimulates the thyroid gland to make thyroxine to control the rate of metabolism 11.1 Principles of hormonal control In women – stimulates the ovaries to produce and release eggs and make the female sex hormone oestrogen Learning objectives In Chapter B 10 you discovered how the nervous system acts to coordinate In men – stimulates the testes to make sperm and the male sex After this topic, you should know: and control your body, reacting in seconds to changes in your internal and hormone testosterone external environments. However, it is very important that your body acts as Thyroid Controls the metabolic rate of the body ● what a hormone is a coordinated whole, not just from minute to minute but from day to day Pancreas Controls the levels of glucose in the blood Figure 2 It isn’t just humans who need ● the main organs of the endocrine and year to year throughout your life. You have a second coordination and hormones – without the hormones from system Adrenal Prepares the body for stressful situations – ‘fight or flight’ response control system to help with this – the endocrine system. their thyroid glands, these tadpoles will ● the role of the pituitary gland. Ovaries Controls the development of the female secondary sexual characteristics and is involved in the menstrual cycle never become frogs The endocrine system Testes Controls the development of the male secondary sexual The endocrine system is made up of glands that secrete chemicals called characteristics and is involved in the production of sperm hormones directly into the bloodstream.