The Interdigestive Motor Complex of Normal Subjects and Patients with Bacterial Overgrowth of the Small Intestine
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Common Bile-Duct Mucosa in Choledochoduodenostomy Patients--- Histological and Histochemical Study
HPB Surgery 1988, Vol. 1, pp. 15-20 (C) 1988 Harwood Academic Publishers GmbH Reprints available directly from the publisher Printed in Great Britain Photocopying permitted by license only COMMON BILE-DUCT MUCOSA IN CHOLEDOCHODUODENOSTOMY PATIENTS--- HISTOLOGICAL AND HISTOCHEMICAL STUDY E. ELEFTHERIADIS*, V. TZIOUFA 1, K. KOTZAMPASSI and H. ALETRAS Departments of Surgery and Pathology1, University of Thessaloniki, Greece We describe the histological and histochemical changes of the common bile-duct mucosa in specimens obtained by means of peroral cholangioscopy, 1-12 years after choledochoduodenal anastomosis. Our findings- hyperplasia of the superficial epithelium, metaplastic goblet cells containing predominantly acid sialomucins, and pyloric-like gland formation containing neutral mucins- express a morphological and functional differentiation of the common bile-duct mucosa that probably facilitates its survival in a different environment. We consider that these adaptive changes may explain the uneventful long-term postoperative period of choledochoduodenostomized patients. KEY WORDS" Common bile duct, choledochoduodenal anastomosis, adaptation, peroral cholangio- scopy. INTRODUCTION After choledochoduodenal anastomosis (CDA), the common bile-duct mucosa (CBDM) is exposed to a different environment, no longer being protected by the sphincter of Oddi. Although, theoretically, this new environment i.e. gastric acid and food flowing through the anastomosis- should affect it, both clinical practice and experimental data have shown no evidence -
Ost , Is Essential for Intestinal Bile Acid Transport and Homeostasis
The organic solute transporter ␣-, Ost␣-Ost, is essential for intestinal bile acid transport and homeostasis Anuradha Rao*, Jamie Haywood*, Ann L. Craddock*, Martin G. Belinsky†, Gary D. Kruh‡, and Paul A. Dawson*§ *Department of Internal Medicine, Section on Gastroenterology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston–Salem, NC 27157; †Medical Science Division, Fox Chase Cancer Center, Philadelphia, PA 19111; and ‡Department of Medicine, Section of Hematology/Oncology, University of Illinois, Chicago, IL 60612 Communicated by David W. Russell, University of Texas Southwestern Medical Center, Dallas, TX, December 28, 2007 (received for review November 28, 2007) The apical sodium-dependent bile acid transporter (Asbt) is respon- Ost␣-Ost efficiently transports the major species of bile acids sible for transport across the intestinal brush border membrane; when expressed in transfected cells (3, 4); and (iv) expression of however, the carrier(s) responsible for basolateral bile acid export Ost␣ and Ost mRNA is positively regulated via the bile into the portal circulation remains to be determined. Although the acid-activated nuclear receptor farnesoid X receptor (FXR) heteromeric organic solute transporter Ost␣-Ost exhibits many (6–9), thereby providing a mechanism to ensure efficient export properties predicted for a candidate intestinal basolateral bile acid of bile acids and protection against their cytotoxic accumulation. transporter, the in vivo functions of Ost␣-Ost have not been Although these data are consistent with a role in bile acid investigated. To determine the role of Ost␣-Ost in intestinal bile transport, the in vivo functions of Ost␣-Ost have not been acid absorption, the Ost␣ gene was disrupted by homologous investigated. -
Does Your Patient Have Bile Acid Malabsorption?
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 Carol Rees Parrish, MS, RDN, Series Editor Does Your Patient Have Bile Acid Malabsorption? John K. DiBaise Bile acid malabsorption is a common but underrecognized cause of chronic watery diarrhea, resulting in an incorrect diagnosis in many patients and interfering and delaying proper treatment. In this review, the synthesis, enterohepatic circulation, and function of bile acids are briefly reviewed followed by a discussion of bile acid malabsorption. Diagnostic and treatment options are also provided. INTRODUCTION n 1967, diarrhea caused by bile acids was We will first describe bile acid synthesis and first recognized and described as cholerhetic enterohepatic circulation, followed by a discussion (‘promoting bile secretion by the liver’) of disorders causing bile acid malabsorption I 1 enteropathy. Despite more than 50 years since (BAM) including their diagnosis and treatment. the initial report, bile acid diarrhea remains an underrecognized and underappreciated cause of Bile Acid Synthesis chronic diarrhea. One report found that only 6% Bile acids are produced in the liver as end products of of British gastroenterologists investigate for bile cholesterol metabolism. Bile acid synthesis occurs acid malabsorption (BAM) as part of the first-line by two pathways: the classical (neutral) pathway testing in patients with chronic diarrhea, while 61% via microsomal cholesterol 7α-hydroxylase consider the diagnosis only in selected patients (CYP7A1), or the alternative (acidic) pathway via or not at all.2 As a consequence, many patients mitochondrial sterol 27-hydroxylase (CYP27A1). are diagnosed with other causes of diarrhea or The classical pathway, which is responsible for are considered to have irritable bowel syndrome 90-95% of bile acid synthesis in humans, begins (IBS) or functional diarrhea by exclusion, thereby with 7α-hydroxylation of cholesterol catalyzed interfering with and delaying proper treatment. -
Bile Physiology
BILE PHYSIOLOGY DIPENDRA PARAJULI University of Louisville BILE COMPLEX LIPID-RICH MICELLAR SOLUTION ISO-OSMOTIC WITH PLASMA VOLUME OF HEPATIC BILE = 500 – 600 CC/DAY University of Louisville COMPOSITION University of Louisville FUNCTION OF BILE INDUCE BILE FLOW AND PHOSPHOLIPID AND CHOLESTEROL SECRETION ESSENTIAL FOR INTESTINAL ABSORPTION OF DIETARY CHOLESTEROL , FATS AND VITAMINS BIND CALCIUM AND HELP TO PREVENT Ca GALLSTONES AND OXALATE KIDNEY STONE FORMATION EXCRETION OF LIPID SOLUBLE XENOBIOTICS, DRUGS AND HEAVY UniversityMETALS of Louisville BILE FORMATION AND CIRCULATION University of Louisville University of Louisville BILE ACID SYNTHESIS TWO PATHWAYS 1) CLASSICAL / NEUTRAL - RESULTS IN THE SYNTHESIS OF APPROXIMATELY 1:1 RATIO OF CHOLIC AND CHENODEOXYCHOLIC ACIDS 2)ALTERNATE / ACIDIC - YIELDS PREDOMINANTLY UniversityCHENODEOXYCHOLIC of LouisvilleACID BILE ACID SYNTHESIS CLASSICAL / NEUTRAL PATHWAY - PREDOMINANT PATHWAY IN HEALTH - POSTCHOLECYSTECTOMY PATIENTS WITH BILE FISTULA - INFUSED WITH RADIOLABELLED PRECURSORS * [3H]7αOH CHOLESTEROL University* [3H]27-OH CHOLESTEROL of Louisville [3H]7αOH CHOLESTEROL 70-95% CONVERTED TO BILE ACIDS [3H]27-OH CHOLESTEROL <20% CONVERTED TO BIL ACIDS University of Louisville BILE ACID SYNTHESIS ALTERNATE / ACIDIC PATHWAY - MORE IMPORTANT IN CHRONIC LIVER DISEASE -CIRRHOTICS - LOW RATE OF BILE ACID SYNTHESIS - ALMOST EXCLUSIVELY UniversityCHENODEOXYCHOLIC of Louisville BILE ACID SYNTHESIS FINAL STEP = - CONJUGATION OF CHOLIC AND CHENODEOXYCHOLIC ACIDS WITH GLYCINE AND TAURINE - CONJUGATION -
Gastrointestinal Motility
Gastrointestinal Motility H. J. Ehrlein and M.Schemann 1. Motility of the stomach Anatomic regions of the stomach are the fundus, corpus (body), antrum and pylorus. The functional regions of the stomach do not correspond to the anatomic regions. Functionally, the stomach can be divided into the gastric reservoir and the gastric pump (Fig. 1). The gastric reservoir consists of the fundus and corpus. The gastric pump is represented by the area at which peristaltic waves occur: it includes the distal part of the corpus and the antrum. Due to different properties of the smooth muscle cells the gastric reservoir is characterised by tonic activity and the gastric pump by phasic activity. AB Gastric reservoir Fundus tonic contractions Pylorus Corpus Antrum Gastric pump phasic contractions Figure 1 . The stomach can be divided into three anatomic (A) and two functional regions (B) 1.1 Function of the gastric reservoir At the beginning of the 20 th century it was already observed that with increasing volume of the stomach the internal pressure of the stomach increases only slightly. In dogs, for instance, the increase in pressure is only 1.2 cm of water/100 ml volume. The small increase in gastric pressure indicates that the stomach does not behave like an elastic balloon but that it relaxes as it fills. Three kinds of gastric relaxation can be differentiated: a receptive, an adaptive and a feedback-relaxation of the gastric reservoir. The receptive relaxation consists of a brief relaxation during chewing and swallowing. The stimulation of mechano-receptors in the mouth and pharynx induces vago-vagal reflexes which cause a relaxation of the gastric reservoir (Fig. -
Glucose-Dependent Insulinotropic Polypeptide (GIP): from Prohormone to Actions in Endocrine Pancreas and Adipose Tissue
PHD THESIS DANISH MEDICAL BULLETIN Glucose-dependent Insulinotropic Polypeptide (GIP): From prohormone to actions in endocrine pancreas and adipose tissue Randi Ugleholdt The two incretins, glucagon-like peptide 1 (GLP-1) and glu- This review has been accepted as a thesis with two original papers by University of cose dependent insulinotropic polypeptide (gastric inhibitory Copenhagen 14th of December 2009 and defended on 28th of January 2010 peptide, GIP) have long been recognized as important gut hor- mones, essential for normal glucose homeostasis. Plasma levels Tutor: Jens Juul Holst of GLP-1 and GIP rise within minutes of food intake and stimulate Official opponents: Jens Frederik Rehfeld, Baptist Gallwitz & Thure Krarup pancreatic β-cells to release insulin in a glucose-dependent man- ner. This entero-insular interaction is called the incretin effect and Correspondence: Department of Biomedical Sciences, Cellular and Metabolic Re- search Section, University of Copenhagen, Faculty of Health Sciences, Blegdamsvej accounts for up to 70% of the meal induced insulin release in man 3B build. 12.2, 2200 Copenhagen N, Denmark and via this incretin effect, the gut hormones facilitate the uptake of glucose in muscle, liver and adipose tissue (2). Although the E-mail: [email protected] pancreatic effects of these two gut hormones have been the target of extensive investigation both hormones also have nu- merous extrapancreatic effects. Thus, GLP-1 decreases gastric Dan Med Bull 2011;58:(12)B4368 emptying and acid secretion and affects appetite by increasing fullness and satiety thereby decreasing food intake and, if main- THE TWO ORIGINAL PAPERS ARE tained at supraphysiologic levels, eventually body weight (3). -
(CCK); B. When Small Intestine Fills with Fatty Chyme
5. Regulation of bile release: a. Hormone = CHOLECYSTOKININ (CCK); b. When small intestine fills with fatty chyme, -cholecystokinin is released; -sphincter in common bile duct opens; -bile is released into duodenum to emulsify fat. Digestive dissection of F. domesticus Esophagus: -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers Stomach -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers Small intestine -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers Large Intestine -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers III. Digestive Organs (continued) G. Small Intestine 1. Parts of Small Intestine: a. duodenum - nearest stomach, b. jejunum - mid-region, c. ileum - near large intestine. The distal end of the ilium narrows to form the ileocecal valve (sphincter muscle between small & large intestine). 2. Mucosal Structure a. intestinal villi project into lu men (increasing SA); b. each villus is composed of simple columnar epithelium (with microvilli) and connective tissue with many blood & lymph vessel s (lacteals ); c. absorbed nutrients are carried away by blood & lacteals; d. intestinal glands are located between villi. 3. Secretions of Small Intestine a. mucus, b. digestive enzymes: peptidases * peptides-----> amino acids; sucrase, maltase, lactase * disaccharides-->monosaccharides; lipases * TG-----> 2 fatty acids + monoglyceride. G. Small Intestine 4. Absorption in Small Intestine (90% of total) a. Intestinal villi (and microvilli) increas e absorptive surface area; b. -
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. -
Bile Salts Up-Regulate MUC5AC, Not MUC5B, Mucin Expression in Cultured Airway Goblet Cell Model HT29-MTX Cell Line
Global Journal of Otolaryngology ISSN 2474-7556 Research Article Glob J Otolaryngol - Volume 7 Issue 3 May 2017 Copyright © All rights are reserved by Mahmoud El-Sayed Ali DOI: 10.19080/GJO.2017.07.555712 Bile Salts Up-Regulate MUC5AC, Not MUC5B, Mucin Expression in Cultured Airway Goblet Cell Model HT29-MTX Cell Line Mahmoud El-Sayed Ali1, 2*, Shruti Parikh2 and Jeffrey P Pearson2 1Department of Otolaryngology, Mansoura University Hospital, Egypt 2Institute for Cell and Molecular Biosciences, Faculty of Medical Sciences, Newcastle University, UK Submission: April 25, 2017; Published: May 04, 2017 *Corresponding author: Mahmoud El-Sayed Ali, Institute for Cell and Molecular Biosciences, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK, Email: Abstract Introduction: The production of MUC5AC and MUC5B, the major mucins expressed by airway mucosa, could be altered by various contents of laryngopharyngeal reflux. This study used the cell line HT29-MTX as an airway goblet cell model, to analyse the possible effect of bile salts on MUC5ACMethods: and MUC5B mucin production. Goblet cell line derived from the human colon carcinoma cells HT29-MTX was cultured and challenged by exposure to various concentrations of a physiologic combination of bile salts. Modified ELISA was employed to measure of MUC5AC and MUC5B contents before and afterResults: challenge. Cultured HT29-MTX cell line maintained full viability when challenged with bile salts up to 20 µmol/L. This stimulated MUC5AC productionDiscussion: in a dose dependant manner and occurred within the first 24 hours after challenge. MUC5B production stayed at the base line. Increased MUC5AC production by the bile salt challenged HT29-MTX cell line could be due to mucin upregulation or merely due to stimulated mucin release from mucin stores in the cells. -
Octreotide in Gastrointestinal Motility Disorders Gut: First Published As 10.1136/Gut.35.3 Suppl.S11 on 1 January 1994
Gut 1994; supplement 3: S11 -S 14 Sll Octreotide in gastrointestinal motility disorders Gut: first published as 10.1136/gut.35.3_Suppl.S11 on 1 January 1994. Downloaded from C Owyang Abstract Intestinal effects of octreotide in The effects of octreotide on six normal scleroderma subjects and five patients with sclero- About 50% of patients with scleroderma have derma were investigated. Changes in small bowel dysfunction.5 In such patients, intestinal motility and in plasma motilin manometry shows patterns (known as the were examined after a single injection of migrating motor complex) in the small bowel octreotide. Octreotide stimulated intense during fasting6 and this may be clinically intestinal motor activity in normal sub- manifested as intestinal pseudo-obstruction jects. Motility patterns in the scleroderma and bacterial overgrowth. These problems are patients were chaotic and non-pro- difficult to treat because standard stimulatory pagative, but, after octreotide was given, prokinetic agents are not effective in sclero- became well coordinated, aborally derma.6 We therefore recently undertook a directed, and nearly as intense as in study to determine the effects of octreotide in normal volunteers. Clinical responses and six normal subjects and in five patients with changes in breath hydrogen were also scleroderma who had abdominal pain, nausea, evaluated in the five scleroderma patients bloating, and a change in intestinal contrac- who had further treatment with octreotide tility.7 We examined the changes in intestinal at a dose of 50 pugtday subcutaneously for motility and in plasma motilin, a gastrointesti- three weeks. A reduction in symptoms of nal hormone that stimulates intestinal motor abdominal pain, nausea, vomiting, and activity, after single injections of octreotide bloating was seen. -
5-Hydroxytryptamine Andhuman Small Intestinal Motility
496 Gut 1994; 35:496-500 5-Hydroxytryptamine and human small intestinal motility: effect ofinhibiting 5-hydroxytryptamine reuptake D A Gorard, G W Libby, M J G Farthing Abstract nature is poorly understood.'0 In animals, Parenteral 5-hydroxytryptamine stimulates migrating motor complex cycling can be small intestinal motility, but the effect of con- modified by administration of 5-HT, its pre- tinuous stimulation with 5-hydroxytryptamine cursor 5-hydroxytryptophan, and its antago- on the human migrating motor complex is nists." '4 The effect of 5-HT on the migrating unknown. Using a selective 5-hydroxytrypta- motor complex in humans has not been studied. mine reuptake inhibitor, paroxetine, this study Tachyphylaxis to 5-HT given intravenously,45 investigated the effect of indirect 5-hydroxy- and associated cardiovascular and pulmonary tryptamine agonism on fasting small responses limit prolonged infusion of 5-HT in intestinal motility and transit. Eight healthy humans. The effect, however, of 5-HT agonism subjects were studied while receiving paroxe- on human small intestinal motor function might tine 30 mg daily for five days and while receiv- be alternatively investigated using a selective ing no treatment, in random order. Ambulant 5-HT reuptake inhibitor. Paroxetine selectively small intestinal motility was recorded from five inhibits the neuronal reuptake of 5-HT, increas- sensors positioned from the duodenojejunal ing the availability of synaptic 5-HT. Its ability flexure to the ileum for 16-18 hours. Paroxe- to inhibit 5-HT reuptake exceeds its ability to tine reduced the migrating motor complex inhibit noradrenaline reuptake by a factor of periodicity mean (SEM) from 81 (6) min to 67 320," making it four to five hundred times (4) min (p<005), and increased the propaga- as selective as the standard tricycic anti- tion velocity of phase III from 3-1 to 4-7 cm/ depressants imipramine and amitriptyline. -
Aandp2ch25lecture.Pdf
Chapter 25 Lecture Outline See separate PowerPoint slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright © McGraw-Hill Education. Permission required for reproduction or display. 1 Introduction • Most nutrients we eat cannot be used in existing form – Must be broken down into smaller components before body can make use of them • Digestive system—acts as a disassembly line – To break down nutrients into forms that can be used by the body – To absorb them so they can be distributed to the tissues • Gastroenterology—the study of the digestive tract and the diagnosis and treatment of its disorders 25-2 General Anatomy and Digestive Processes • Expected Learning Outcomes – List the functions and major physiological processes of the digestive system. – Distinguish between mechanical and chemical digestion. – Describe the basic chemical process underlying all chemical digestion, and name the major substrates and products of this process. 25-3 General Anatomy and Digestive Processes (Continued) – List the regions of the digestive tract and the accessory organs of the digestive system. – Identify the layers of the digestive tract and describe its relationship to the peritoneum. – Describe the general neural and chemical controls over digestive function. 25-4 Digestive Function • Digestive system—organ system that processes food, extracts nutrients, and eliminates residue • Five stages of digestion – Ingestion: selective intake of food – Digestion: mechanical and chemical breakdown of food into a form usable by