DOCSLIB.ORG

The Gastrointestinal System (消化系統)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Gastrointestinal System (消化系統) The Gastrointestinal System (消化系統) 台北醫學大學醫學系生理學科 蔡麗雪教授 (Li-Hsueh Tsai, PhD) E-mail: [email protected] 27361661-3181 1 References: ¾ Guyton : Human Physiology and Mechanisms of Disease (16th edition) ¾ Ganong : Review of medical Physiology (22 edition) ¾ William J. German and Cindy L. Stanfield: Principles of Human Physiology (Third edition) ¾ Sherwood L: Human Physiology-From Cells to Systems (Seventh edition). 2 Chapter Outline I. Overview of the gastrointestinal (GI) system II. General Principles of GI Regulation Neural regulation Hormonal regulation III. Functional Anatomy of the Gastrointestinal System (secretion, disgestion, absorption) 1. Mouth, pharynx, and esophagus 2. Stomach 3. Pancreas 4. Liver 5. Small intestine 6. Large intestine 3 Overview of Gastrointestinal System 4 Gastrointestinal System 5 Accessory Glands Secrete products into lumen of digestive tract – Salivary glands • Saliva – Pancreas • Pancreatic juice – Liver • Bile 6 Sphincter Locations 7 Sphincters of GI Tract • Consider as traffic control devices • Total of seven – Upper and lower esophageal sphincters – Pyloric sphincter – Sphincter of Oddi - common bile duct entry into duodenum – Ileocecal – Internal and external anal sphincters - think how much you appreciate these! • Resting tone is > in segments above & below 8 9 Digestive System • Primary function – Transfer nutrients, water, and electrolytes from ingested food into body’s internal environment • Four functions – Motility – Secretion – Digestion – Absorption 10 General Principles of GI Regulation 11 General Principles of GI Regulation – Neural and endocrine pathways of gastrointestinal control – Regulation of food intake 12 Wall of GI Tract 13 General Principles of GI Regulation •Neural Control (神經的控制) •Gastrointestinal peptides 14 What is the enteric nervous system? 15 Neural Control A. Enteric Neurons Myenteric plexus (腸間肌神經叢) Submucosal plexus (黏膜下神經叢) B. Autonomic Nervous System (自主神經之控制) 16 The Enteric Nervous System 17 Parasympathetic n.s Sympathetic n.s. Vagal nuclei CNS Preganglionic fibres Preganglionic fibres Sacral spinal cord Sympathetic ganglia Postganglionic fibres Enteric nervous system Myenteric Submucosal plexus plexus Smooth Secretory Endocrine Blood muscle cells cells vessels 18 Gastrointestinal Peptides 19 20 Neurocrines NO ACh Norepinephrine GRP (bombesin) Gastrin Releasing Peptide 21 Paracrines 22 23 Hormone 24 Gastrointestinal peptides 25 26 Gastrin family 27 Gastrin 胃泌素 (G cell) 90% in antral tissue 10% in duodenum G34, G17, G14 28 Cholecystokinin-Pancreozymin (CCK) 膽囊收縮素 (I cell) 29 Digestion - fat in duodenum stimulates CCK release from I cells FAT CCK Gall bladder contraction BILE Sphincter of Oddi relaxes30 Cholecystokinin stomach duodenum CCK I cells Peptides Amino acids,H+ Fat pancreas Enzymes 31 32 Secretin family 33 Secretin (S cell) ;腸泌素 In 1902, Bayliss and Starling 34 35 Secretin Fat H+ S cells - HCO3 Secretin 36 In fasting state Liver Bile stored in gall bladder& concentrated Aqueous secretion - from duct epithelium HCO3 - rich in HCO3 and stim. by secretin - HCO3 Cl- Na+ H O 2 Sphincter of Oddi Fluid & electrolytes (closed) absorbed by active 37 transport of Na+ GIP (Glucose-dependent insulinotropic polypeptide) K cell 38 Gastric Inhibitory Peptide 葡萄糖倚賴型胰島素控制胜肽 • Inhibits emptying of the stomach when fats and large amounts of sugar are present • K cells in duodenum and jejunum • Potentiates insulin release and increases anabolic activity in fat cells 39 40 41 Functional Anatomy of the Gastrointestinal System 42 Gastrointestinal motility and its regulation 43 Slow wave 0 Membrane potential (mV) -60 Tension Acetylcholine 0 Membrane potential (mV) -60 Tension 44 The contraction of smooth muscle : Syncytium Spikes potentials 45 46 Receptive Relaxation of Stomach Swallowing center also initiates relaxation of stomach smooth muscle as it prepares for receipt of bolus 47 Law of the Gut smooth muscle relaxation downstream (anally) = receptive relaxation 48 MOUTH & ESOPHAGUS 49 Salivary Glands – Saliva • Bicarbonate • Mucus • Salivary amylase • Lysozyme 50 唾液的分泌 Sublingual gland (舌下腺) 51 • Saliva – Produced largely by three major pairs of salivary glands – Composition • 99.5% H2O • 0.5% electrolytes and protein (amylase, mucus, lysozyme) – Functions • Salivary amylase begins digestion of carbohydrates • Facilitates swallowing by moistening food • Mucus provides lubrication • Antibacterial action – Lysozyme destroys bacteria – Saliva rinses away material that could serve as food source for bacteria • Solvent for molecules that stimulate taste buds • Aids speech by facilitating movements of lips and tongue • Helps keep mouth and teeth clean 52 • Rich in bicarbonate buffers Control of Salivary Secretion 53 食道 54 Pharynx and Esophagus • Swallowing – Motility associated with pharynx and esophagus – Sequentially programmed all-or-none reflex – Initiated when bolus is voluntarily forced by tongue to rear of mouth into pharynx – Most complex reflex in body – Can be initiated voluntarily but cannot be stopped once it has begun – Process divided into two stages • Oropharyngeal stage • Esophageal stage (moves bolus from mouth through pharynx and into esophagus) 55 Stomach (胃) 56 Stomach 57 Gastric Motility • Four aspects – Filling • Involves receptive relaxation – Enhances stomach’s ability to accommodate the extra volume of food with little rise in stomach pressure – Triggered by act of eating – Mediated by vagus nerve –Storage • Takes place in body of stomach –Mixing • Takes place in antrum of stomach –Emptying • Largely controlled by factors in duodenum 58 Gastric Emptying • Factors in stomach – Amount of chyme in stomach is main factor that influences strength of contraction • Factors in duodenum –Fat • Fat digestion and absorption takes place only within lumen of small intestine • When fat is already in duodenum, further gastric emptying of additional fatty stomach contents is prevented –Acid • Unneutralized acid in duodenum inhibits further emptying of acidic gastric contents until neutralization can be accomplished – Hypertonicity • Gastric emptying is reflexly inhibited when osmolarity of duodenal contents starts to rise – Distension • Too much chyme in duodenum inhibits emptying of even more gastric contents 59 Gastric Emptying • Factors trigger either – Neural response • Mediated through both intrinsic nerve plexuses (short reflex) and autonomic nerves (long reflex) • Collectively called enterogastric reflex – Hormonal response • Involves release of hormones from duodenal mucosa collectively known as enterogastrones – Secretin – Cholecystokinin (CCK) • Additional factors that that influence gastric motility – Emotions • Sadness and fear – tend to decrease motility • Anger and aggression – tend to increase motility – Intense pain – tends to inhibit motility 60 Gastric Motility – Functions • Mix chyme • Regulate gastric emptying – Mechanism • Segmentation • Peristalsis Coordinated by enteric nervous system 61 Migrating Motility Complex – Wave of intense contractions – Travel short distances – Occur between meals to clear stomach 62 胃酸之成分 (Pepsinogen) 63 Oxyntic Gastric mucosa pit Mucosa Stomach lumen Pyloric gland area Submucosa 64 In oxyntic mucosa In pyloric gland area Surface epithelial cells Gastric pit Mucosa cells Gastric G cells gland Chief cells D cells Parietal cells Enterochomaffin- like (ECL) cells 65 Autocatalysis PepsinogenPage 16.11 Pepsin Digestion Page 611Protein Peptide fragments Gastric HCI lumen 66 Stomach acid 67 Parietal cell F O O D Acid production by the parietal cells in the stomach depends on the generation of carbonic acid; subsequent movement of hydrogen ions into the gastric lumen results from primary active transport. 68 1988 Nobel Prize Cimetidine and propranolol 69 ECL Cells • Enterochomaffin-like cells 70 One inhibitory and three stimulatory signals that alter acid secretion by parietal cells in the stomach. 71 72 73 74 Regulation of Gastric Secretion 1. Cephalic Phase 2. Gastric Phase 3. Intestinal Phase 75 1. Cephalic Phase 1883 –Beaumont Martin Ivan Paulov (1904 Nobel Prize) 2. Gastric Phase Heindenhain pouch Ivy 3. Intestinal Phase Ivy 76 What Is Helicobacter pylori? 1983, Western Australia Robin Warren and Barry Marshall UBT (urea breath test) C13 or C14 CO2 NH3 77 The Nobel Prize in Physiology or Medicine 2005 Barry J. Marshall J. Robin Warren 78 Peptic ulcer (消化性潰瘍） Risk Factors and Contributing Factors 1. Genetic Factors 2. Psychological Stress 3. NSAIDs (nonsteroidal anti-inflammatory drugs) such as aspirin and ibuprofen. 4. Cigarette smoking 5. Breverages Foods such as caffeine 6. Ethanol 79 Drug treatment a. antacid drug: Al(OH)3 , Mg(OH)2 , NaHCO3. b. anticholinergic drug : atropine; H2 blocker: cimetidine, ranitidine c. H+-K+-ATPase inhibitor: omeprazole d. antibiotics 80 Pancreas (胰臟) 81 82 Normal Human Pancreatic Juice • Cations: Na+, K+, Ca2+, Mg2+ (pH approximately 8.0) - - 2- 2- • Anions: HCO3 , Cl , SO4 , HPO4 • Digestive enzymes (95% proteins in juice) • Other proteins 83 Pancreas – Exocrine and endocrine gland – Pancreatic juice • Bicarbonate • Pancreatic amylase • Pancreatic lipases • Proteases • Nucleases 84 What are zymogens, and why are they present in the pancreas? 85 Zymogens Inactive forms of digestive enzymes – Stored in zymogen granules of acinar cells – Activated, usually by proteolytic enzymes, in lumen of intestinal tract 86 Pancreatic secretion - secretion in 3 phases Cephalic phase - only 10-15% of total secretion activation of vagal efferents stimulates enzyme release Gastric phase - only present
Load more

Recommended publications
  • Cells Using Gene Expression Profiling and Insulin Gene Methylation
    RESEARCH ARTICLE Comparison of enteroendocrine cells and pancreatic β-cells using gene expression profiling and insulin gene methylation ☯ ☯ Gyeong Ryul Ryu , Esder Lee , Jong Jin Kim, Sung-Dae MoonID, Seung-Hyun Ko, Yu- Bae Ahn, Ki-Ho SongID* Division of Endocrinology & Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea ☯ These authors contributed equally to this work. a1111111111 * [email protected] a1111111111 a1111111111 a1111111111 a1111111111 Abstract Various subtypes of enteroendocrine cells (EECs) are present in the gut epithelium. EECs and pancreatic β-cells share similar pathways of differentiation during embryonic develop- ment and after birth. In this study, similarities between EECs and β-cells were evaluated in OPEN ACCESS detail. To obtain specific subtypes of EECs, cell sorting by flow cytometry was conducted Citation: Ryu GR, Lee E, Kim JJ, Moon S-D, Ko S- from STC-1 cells (a heterogenous EEC line), and each single cell was cultured and pas- H, Ahn Y-B, et al. (2018) Comparison of saged. Five EEC subtypes were established according to hormone expression, measured enteroendocrine cells and pancreatic β-cells using by quantitative RT-PCR and immunostaining: L, K, I, G and S cells expressing glucagon-like gene expression profiling and insulin gene methylation. PLoS ONE 13(10): e0206401. https:// peptide-1, glucose-dependent insulinotropic polypeptide, cholecystokinin, gastrin and doi.org/10.1371/journal.pone.0206401 secretin, respectively. Each EEC subtype was found to express not only the corresponding Editor: Wataru Nishimura, International University gut hormone but also other gut hormones. Global microarray gene expression profiles of Health and Welfare School of Medicine, JAPAN revealed a higher similarity between each EEC subtype and MIN6 cells (a β-cell line) than Received: March 29, 2018 between C2C12 cells (a myoblast cell line) and MIN6 cells, and all EEC subtypes were highly similar to each other.
    [Show full text]
  • Enteric Nervous System (ENS): 1) Myenteric (Auerbach) Plexus & 2
    Enteric Nervous System (ENS): 1) Myenteric (Auerbach) plexus & 2) Submucosal (Meissner’s) plexus à both triggered by sensory neurons with chemo- and mechanoreceptors in the mucosal epithelium; effector motors neurons of the myenteric plexus control contraction/motility of the GI tract, and effector motor neurons of the submucosal plexus control secretion of GI mucosa & organs. Although ENS neurons can function independently, they are subject to regulation by ANS. Autonomic Nervous System (ANS): 1) parasympathetic (rest & digest) – can innervate the GI tract and form connections with ENS neurons that promote motility and secretion, enhancing/speeding up the process of digestion 2) sympathetic (fight or flight) – can innervate the GI tract and inhibit motility & secretion by inhibiting neurons of the ENS Sections and dimensions of the GI tract (alimentary canal): Esophagus à ~ 10 inches Stomach à ~ 12 inches and holds ~ 1-2 L (full) up to ~ 3-4 L (distended) Duodenum à first 10 inches of the small intestine Jejunum à next 3 feet of small intestine (when smooth muscle tone is lost upon death, extends to 8 feet) Ileum à final 6 feet of small intestine (when smooth muscle tone is lost upon death, extends to 12 feet) Large intestine à 5 feet General Histology of the GI Tract: 4 layers – Mucosa, Submucosa, Muscularis Externa, and Serosa Mucosa à epithelium, lamina propria (areolar connective tissue), & muscularis mucosae Submucosa à areolar connective tissue Muscularis externa à skeletal muscle (in select parts of the tract); smooth muscle (at least 2 layers – inner layer of circular muscle and outer layer of longitudinal muscle; stomach has a third layer of oblique muscle under the circular layer) Serosa à superficial layer made of areolar connective tissue and simple squamous epithelium (a.k.a.
    [Show full text]
  • S41467-019-14258-Z.Pdf
    ARTICLE https://doi.org/10.1038/s41467-019-14258-z OPEN Erythroid differentiation regulator-1 induced by microbiota in early life drives intestinal stem cell proliferation and regeneration Hirohito Abo1, Benoit Chassaing 1,2,3,4, Akihito Harusato 1, Miguel Quiros5, Jennifer C. Brazil5, Vu L. Ngo1, Emilie Viennois6, Didier Merlin6,7, Andrew T. Gewirtz1, Asma Nusrat5 & Timothy L. Denning1* 1234567890():,; Gut microbiota and their metabolites are instrumental in regulating intestinal homeostasis. However, early-life microbiota associated influences on intestinal development remain incompletely understood. Here we demonstrate that co-housing of germ-free (GF) mice with specific-pathogen free (SPF) mice at weaning (exGF) results in altered intestinal gene expression. Our results reveal that one highly differentially expressed gene, erythroid dif- ferentiation regulator-1 (Erdr1), is induced during development in SPF but not GF or exGF mice and localizes to Lgr5+ stem cells and transit amplifying (TA) cells. Erdr1 functions to induce Wnt signaling in epithelial cells, increase Lgr5+ stem cell expansion, and promote intestinal organoid growth. Additionally, Erdr1 accelerates scratch-wound closure in vitro, increases Lgr5+ intestinal stem cell regeneration following radiation-induced injury in vivo, and enhances recovery from dextran sodium sulfate (DSS)-induced colonic damage. Col- lectively, our findings indicate that early-life microbiota controls Erdr1-mediated intestinal epithelial proliferation and regeneration in response to mucosal damage. 1 Center for Inflammation, Immunity & Infection, Institute for Biomedical Sciences, Georgia State University, 100 Piedmont Ave, Atlanta, GA 30303, USA. 2 Neuroscience Institute and Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, USA. 3 INSERM, U1016, Paris, France. 4 Université de Paris, Paris, France.
    [Show full text]
  • Neural and Neuroendocrine Control of Digestion: Regulation of Gastrointestinal Hormone Secretion
    Neural and Neuroendocrine Control of Digestion: Regulation of Gastrointestinal Hormone Secretion (Chapter 15 in “Eckert Animal Physiology) (Chapter 4 in Hill, Wise & Anderson: “Animal Physiology”) (Chapter 10 in Hadley: “Endocrinology”) General Concepts Covered: — neural and neuroendocrine integration of a complex physiological process — co-ordination of endocrine and exocrine secretion — exocrine secretion affecting endocrine status — endocrine influences on neural, muscle and secretory functions — paracrine and autocrine effects — local influences — positive and negative “feed-back” actions — enzymatic cascades — integration of carbohydrate, fat and protein digestion and appetite control General Introduction — digestion requires co-ordination of movement of food particles, mechanical and chemical digestion of food — opening and closing of sphincter muscles to contain food particles in certain gut compartments for appropriate processing, also control passage through compartments — proper sequential enzymatic processing General Introduction (cont.) — peristaltic action to move food through gut — kneading movement to mix food particles with enzymes and to expose new surfaces for digestion, as well as for absorption From Eckert Secretin - first proposed hormone — 1902, WM Baylist and EH Starling (observations in dogs) — addition of food or acid in stomach is usually followed by pancreatic enzyme secretion into intestine — dennervate and tie off duodenum from stomach, then 1) add acid to stomach - no pancreatic enzyme secretion 2) add acid to
    [Show full text]
  • Pancreatic Amylase
    1. Functional Anatomy • The pancreas which lies parallel to and beneath the stomach is composed of: 1. The endocrine islets of Langerhans which secrete: Hormone Type of cell % of secretion Insulin Beta cells 60% crucial for normal regulation of glucose, Glucagon Alpha cells ~25% lipid & protein metabolism Somatostatin delta cells ~10% 1. Acinar gland tissues which produce pancreatic juice (the main source of digestive enzymes). • The pancreatic digestive enzymes are secreted by pancreatic acini. • Large volumes of sodium Bicarbonate solution are secreted by the small ductules and larger ducts leading from the acini. • Pancreatic juice is secreted in Response to the presence of Chyme in the upper portions of the small intestine. 2. Major Components of Pancreatic Secretion and Their Physiologic Roles & 5. Activation of Pancreatic Enzymes • The major functions of pancreatic secretion: 1. To neutralize the acids in the duodenal chyme to optimum range (pH= 7.0-8.0) for activity of pancreatic enzymes. 2. To prevent damage to duodenal mucosa by acid & pepsin. 3. To produce enzymes involved in the digestion of dietary carbohydrate, fat, and protein. Pancreatic Enzymes: The pancreas secrests enzymes that act on all major types of food stuffs. 1. Pancreatic Proteolytic Enzymes (Trypsin, Chymotrypsin, Carboxypolypeptidase, Elastase) • Trypsin & Chymotrypsin split whole and partially digested proteins into peptides of various sizes but do not cause release of individual amino acids. • Carboxypolypeptidase splits some peptides into individual amino acids, thus completing digestion of some proteins to amino acids. • When first synthesized in the pancreatic cells, digestive enzymes are in the inactive forms; these enzymes become activated only after they are secreted into the intestinal tract.
    [Show full text]
  • Secretin Stimulates the Secretion of Bile from the Liver. It Also Increases Watery Bicarbonate Solution from Pancreatic Duct Epithelium
    Name Secretin acetate Cat # PP-1670 Size 1 g, 10 g, 100, g and bulk custom packages CAS# 17034-35-4 Mol. Mass 3055.47 Formula C130H220N44O41 Sequence H-His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Glu-Leu-Ser-Arg-Leu-Arg-Asp-Ser- Ala-Arg-Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH2 Purity >95% Secretin is a peptide hormone produced in the S cells of the duodenum in the crypts of Lieberkühn. Its primary effect is to regulate the pH of the duodenal contents via the control of gastric acid secretion and buffering with bicarbonate. Secretin stimulates the secretion of bile from the liver. It also increases watery bicarbonate solution from pancreatic duct epithelium. Pancreatic acinar cells have secretin receptors in their plasma membrane. As secretin binds to these receptors, it stimulates adenylate cyclase activity and converts ATP to cyclic AMP.[12] Cyclic AMP acts as second messenger in intracellular signal transduction and leads to increase in release of watery carbonate.It is known to promote the normal growth and maintenance of the pancreas. Secretin increases water and bicarbonate secretion from duodenal Brunner's glands in order to buffer the incoming protons of the acidic chyme.[13] It also enhances the effects of cholecystokinin to induce the secretion of digestive enzymes and bile from pancreas and gallbladder, respectively. It counteracts blood glucose concentration spikes by triggering increased insulin release from pancreas, following oral glucose intake.<[14] It also reduces acid secretion from the stomach by inhibiting gastrin release from G cells.[citation needed] This helps neutralize the pH of the digestive products entering the duodenum from the stomach, as digestive enzymes from the pancreas (eg, pancreatic amylase and pancreatic lipase) function optimally at neutral pH.[citation needed] In addition, secretin simulates pepsin secretion which can help break down proteins in food digestion.
    [Show full text]
  • Cellular Localization of Gastric Inhibitory Polypeptide in the Duodenum and Jejunum
    Gut: first published as 10.1136/gut.14.4.284 on 1 April 1973. Downloaded from Gut, 1973, 14, 284-288 Cellular localization of gastric inhibitory polypeptide in the duodenum and jejunum JULIA M. POLAK, S. R. BLOOM', MARION KUZIO, J. C. BROWN, AND A. G. E. PEARSE From the Department ofHistochemistry, Royal Postgraduate Medical School, Hammersmith Hospital, London, and the Department ofPhysiology, University ofBritish Columbia, Vancouver, Canada SUMMARY Indirect immunofluorescence studies using an antiserum to purified porcine gastric inhibitory polypeptide indicate, in the gastrointestinal tract of dog and man, that this polypeptide is present in cells situated predominantly in the mid-zone of the glands in the duodenum and, to a lesser extent, in the jejunum. Absolute correlation of the gastric inhibitory polypeptide cell with one or other of the known endocrine-like cells identified by electron microscopy awaits confirmation by electron immunocytochemistry. It is here identified as an endocrine polypeptide cell of the APUD series and, provisionally, as the D, cell. While the hormonal status of a given polypeptide depends ultimately on physiological experiments the present results strengthen the view that gastric inhibitory polypeptide is indeed a hormone. In 1969 Brown, Pederson, Jorpes, and Mutt described We report here the results of immunofluorescence an enterogastrone, extractable from porcine intestine, studies on the localization of GIP in human and http://gut.bmj.com/ which strongly inhibited gastric acid secretion. The canine intestine. purification of an apparently similar enterogastrone was reported in the same year by Lucien, Itoh, Sun, Material and Methods Meyer, Carlton, and Schally. The first of these poly- peptides, named gastric inhibitory polypeptide Operative samples of duodenal and jejunal mucosa (GIP) by Brown, Mutt, and Pederson (1970), was from seven human subjects were studied.
    [Show full text]
  • Stomach, Duodenum, and Jejunum
    Gut, 1970, 11, 649-658 The endocrine polypeptide cells of the human Gut: first published as 10.1136/gut.11.8.649 on 1 August 1970. Downloaded from stomach, duodenum, and jejunum A. G. E. PEARSE, I. COULLING, B. WEAVERS, AND S. FRIESEN' From the Department of Histochemistry, Royal Postgraduate Medical School, London SUMMARY Thirty specimens of stomach, duodenum, and jejunum, removed at operation, were examined by optical microscopical, cytochemical, and electron microscopical techniques. The overall distribution of four types of endocrine polypeptide cell in the stomach, and three in the intestine, was determined. The seven cell types are described by names and letters belonging to a scheme for nomenclature agreed upon at the 1969 Wiesbaden conference o* gastrointestinal hormones. The gastrin-secreting G cell was the only cell for which firm identification with a known hormone was possible. Although there was wide variation in the distribution of the various cells, from one case to another, striking differences were never- theless observable, with respect to the G cell, between antra from carcinoma and from ulcer cases. http://gut.bmj.com/ This study was undertaken with a view to estab- tive shorthand terminology. Correlation with the lishing the overall topographical distribution of terminology used by Solcia, Vassallo, and Capella the various types of endocrine polypeptide cells (1969b) and by Vassallo, Solcia, and Capella in the human stomach and upper intestine. (1969) had to be equated, if possible, with the Adequate sampling was regarded as a pre- scheme used by Forssmann, Orci, Pictet, Renold, on September 28, 2021 by guest. Protected copyright.
    [Show full text]
  • 19780525 Gr Im.Pdf
    0 0 0 2 TABLE OF CONTENTS I INTRODUCTION II HISTORICAL BACKGROUND III ORIGIN AND NATURE OF GI HORMONES: NEUROENDOCRINE SECRETION AND RELEASE OF PEPTIDES IV ANATOMIC AND CELLULAR DISTRIBUTION OF GI HORMONES V CHEMICAL AND BIOLOGICAL FEATURES OF GI HORMONES: STRUCTURE AS A GUIDE TO BIOLOGICAL ACTION VI GI HORMONES IN PHYSIOLOGY 1. Secretin 7. Pancreatic Polypeptide 2 .. Gastrin 8. Vasoactive Intestinal Polypeptide 3. Cholecystokinin-Pancreozymin 9. Somatostatin 4. Gastric Inhibitory Polypeptide 1o. Substance P 5. Motilin 11. Bombesin 6. Glucagon, Enteroglucagon 12. Other Peptides VII GI HORMONES IN DISEASE A. GI Hormone-Secreting Tumors: Gastrinoma (Zollinger-Ellison Syndrome), and other causes of Hypergastrinemia; MEA Syndromes; VIP-oma (Watery­ Diarrhea, WDHH or Werner-Morrison Syndrome); Glucagonoma; Somatostatinoma; Pancreatic Polypeptide in Tumors; Substance P (Carcinoid). B. GI Hormones in Other Pathologic States. C. Diagnostic & Therapeutic Uses. VIII CONCLUSION 3 GLOSSARY ACTH - Corticotropin (adrenocorticotropic hormone) AMP - Adenosine monophosphate APUD - Amine precursor uptake and decarboxylation CCK, CCK- PZ - Cholecystokinin-pancreozymin EC - Enterochromaffin EG - Enteroglucagon GI - Gastrointestinal GIP - Gastric-inhibitory polypeptide LES - Lower esophageal sphincter MEA - Multiple endocrine adenomatosis MSH - Melanocyte-stimulating hormone (melanotropin) PP - Pancreatic polypeptide PZ - Pancreozymin RIA - Radioimmunoassay SP - Substance P STM - Standard test meal VIP - Vasoactive intestinal polypeptide WDHH (or WDHA) - Watery
    [Show full text]
  • Pancreas and Fat/Lipid Digestion
    Exocrine Pancreas Physiology Pancreatic Anatomy Pancreatic secretion Pancreatic enzymes Daniel S. Kamin MD Boston Children’s Hospital [email protected] Content Reviewers: Sohail Z. Husain, MD Veronique Morinville MD, FRCP(C) NASPGHAN Physiology Education Series Series Editors: Christine Waasdorp Hurtado, MD, MSCS, FAAP [email protected] Daniel Kamin, MD [email protected] Learning Objectives • Understand the normal development and anatomy of the pancreas • Understand the stimuli and cellular factors giving rise to pancreatic secretion • Know the mechanisms by which pancreatic enzymes are activated and remain functional • Be aware of age-related deficiency in exocrine pancreatic function Night blindness • A young man with morbid obesity undergoes roux-en-y gastric bypass. • 1 year later he notices that in the evening he falls down his stairs. • Vitamin A deficiency is diagnosed. Understanding the physiology of pancreatic and bile secretion, Used with permission intraluminal lipolysis, and micellar function explains why this happens! http://www.citelighter.com/science/surgery/knowledgecards/gastric-bypass Pancreas Physiology Overview • Bulk of bicarbonate secretion (more than what secreted in bile and from duodenum) • Enzymes for intra- luminal digestion • Secretin and CCK regulate • Maturational pancreatic insufficiency Used with permission Image from http://www.aboutcancer.com/pancreas1.htm Pancreatic Development • See Embryology and Anatomy of the Gastrointestinal Tract Pancreatic Microanatomy Pancreatic Acinar Secretory Products A • Proteases • Trypsinogen* • Chymotrypsinogen* A • Proelastase* • Procarboxypeptidase* • Procarboxypeptidase B* • Amylolytic enzyme • Amylase A • Lipases • Lipase • B Nonspecific esterase • Prophospholipase A2* • Nucleases • Deoxyribonuclease • Ribonuclease • Others • Pro-colipase* • Trypsin inhibitors A. Exocrine pancreas-- ascinar cells filled • Monitor peptid with secretory granules, cuboidal duct Stored and secreted in inactive form cells secrete bicarbonate-rich fluid B.
    [Show full text]
  • Secretin: Structure of the Precursor and Tissue Distribution of the Mrna (Intestine/Preprohormone/Cdna/Polymerase Chain Reaction) ALAN S
    Proc. Nati. Acad. Sci. USA Vol. 87, pp. 2299-2303, March 1990 Biochemistry Secretin: Structure of the precursor and tissue distribution of the mRNA (intestine/preprohormone/cDNA/polymerase chain reaction) ALAN S. KoPIN*, MICHAEL B. WHEELER, AND ANDREW B. LEITER Division of Gastroenterology, Department of Medicine, New England Medical Center, Boston, MA 02111 Communicated by Donald F. Steiner, January 5, 1990 (receivedfor review, November 17, 1989) ABSTRACT Secretin is a 27-amino acid gastrointestinal denum, while the levels reported for hypothalamus, thala- hormone that stimulates the secretion of bicarbonate-rich mus, and olfactory lobe were comparable to those in small pancreatic fluid. The unusually high number ofserine, leucine, intestine (9). Others report that brain contains either small and arginine residues in secretin has precluded the use of amounts (10, 11) or no secretin-like immunoreactivity (12). oligonucleotides to screen cDNA libraries to isolate a secretin In the present study, we have isolated cDNAs encoding the cDNA. In the present study, a short cDNA encoding porcine rat and porcine secretin precursors.t The deduced amino acid secretin was amplified from duodenal mucosal first-strand sequence includes a signal peptide, an N-terminal peptide, cDNA template by using 16,384- and 4096-fold degenerate secretin, and a 72-amino acid C-terminal peptide. We have primers in the DNA polymerase chain reaction. From the used the secretin cDNA as a probe in Northern blot hybrid- sequence of the amplified cDNA, an unambiguous oligonucle- izations to address unresolved questions regarding the tissue otide probe was designed to screen a cDNA library. Here we localization of secretin biosynthesis in the rat CNS and report the sequences of cDNAs encoding the porcine and rat gastrointestinal tract.
    [Show full text]
  • Secretin Cells in Coeliac Disease
    Gut: first published as 10.1136/gut.14.11.870 on 1 November 1973. Downloaded from Gut, 1973, 14, 870-874 Secretin cells in coeliac disease JULIA M. POLAK, A. G. E. PEARSE, SUSAN VAN NOORDEN, S. R. BLOOM, AND MARY A. ROSSITER From the Department of Histochemistry, Royal Postgraduate Medical School, London, the Department of Clinical Research, Middlesex Hospital, London, and the Department of Gastroenterology, Queen Elizabeth Hospital, London SUMMARY Immunofluorescence (anti-secretin), cytochemical, and ultrastructural studies were carried out on jejunal biopsies from 16 children with coeliac disease and from 17 controls with suspected malabsorption but normal jejunal morphology. In 11 of the 16 coeliacs there was generalized hyperplasia of endocrine cells and, specifically, of the secretin (S) cells. Further studies, on adult coeliacs as well as on children, combined with serum secretin assays, may establish whether the S cells are abnormally storing hormone because of inability to release it or because of excess production. Present observations suggest that abnormal secretion children with coeliac disease only minimal changes in of certain gut hormones may be involved in the serum insulin were observed during a glucose toler- malfunction of the intestine in coeliac disease. ance test (Grant, 1973). In this disorder the secretory response of the The evidence summarized above points to the http://gut.bmj.com/ exocrine pancreas to a standard meal is reduced conclusion that the pancreas itself is capable of (Worming, Mullertz, Thaysen, and Bang, 1967), as normal function in coeliac disease but that normal it also is after perfusion of the intestine with amino stimulation by secretin and/or CCK/PZ is not acids (which stimulate cholecystokinin secretion).
    [Show full text]