11 Bile Formation and Bile Salts
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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 -
Classical Liver (Hepatic) Lobules It Is Formed of a Polygonal Mass of A- Capsule: Glisson’S Capsule
LIVER & SPLEEN Color index: Slides.. Important ..Notes ..Extra.. Objectives: By the end of this lecture, the student should be able to describe: 1. The histological structure of liver with special emphasis on: . Classical hepatic (liver) lobule. Hepatocytes. Portal tract (portal area). Hepatic (liver) blood sinusoids. Space of Disse (perisinusoidal space of Disse) . Bile canalculi. 2. The histological structure of spleen with special emphasis on: . White pulp. Red Pulp. LIVER 1-Stroma; 2-Parenchyma; mainly C.T, but not in humans. Classical liver (hepatic) lobules It is formed of a polygonal mass of a- Capsule: Glisson’s Capsule. liver tissue, bounded by b- Septa (absent in human) interlobular septa with portal areas & Portal areas (Portal tracts) at the periphery & central Portal area: surrounded by (centrolobular) vein in the center. other structures. Central vein: surrounded by c- Network of reticular fibers. hepatocytes LIVER Contents of the Classic Liver Lobule: Borders of the Classical Liver Lobule the rows of hepatocytes should be next to each other; 1- Septa: C.T. septa (e.g. in pigs). remember canaliculi 2- Portal areas (Portal tracts): 1- Anastomosing plates of hepatocytes. Are located in the corners of the classical hepatic 2- Liver blood sinusoids (hepatic blood lobule (usually 3 in No.). sinusoids): between the plates. Contents of portal area: 3- Spaces of Disse (perisinusoidal spaces of a- C.T. b- Bile ducts (interlobular bile ducts). Disse) between the hepatocytes and sinusoids c- Venule (Branch of portal vein). 4- Central vein. d- Arteriole (Branch of hepatic artery). 5- Bile canaliculi. Hepatic artery: surrounded by smooth muscles while the bile duct is not. -
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 -
Nomina Histologica Veterinaria, First Edition
NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria. -
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. -
Junction Between Kupffer Cells and Hepatic Sinusoidal Endothelium. a Review This Short Review Was Prepared on the Basis of Trans
Okajimas Folia Anat. Jpn., 57(2-3) : 145-158, August 1980 Junction between Kupffer Cells and Hepatic Sinusoidal Endothelium. A Review By TOSHIO ITO, YUTAKA TANUMA and SUSUMU SHIBASAKI Department of Anatomy, Teikyo University School of Medicine, Tokyo 173 and Department of Anatomy, Gunma University School of Medicine, Maebashi 371, Japan -Received for Publication, January 24, 1980- Key Words : Kupffer-endothelial junction, Human and bat liver, TEM and SEM. Summary. In this review, the junctions between Kupffer and sinusoidal endothelial cells previously revealed by the present authors under the transmission electron microscope in both normal human and bat livers has been discussed and compared with stereo- images of the connections between the two cell types reported by other authors in scanning electron microscopic studies. It is concluded that Kupffer cells lie on the gap or opening of the endothelial lining of the sinusoid, that part of the perisinusoidal surface of the cell body which is applied to the opening directly faces the perisinusoidal space, and that the margin of this part of the perisinusoidal surface of the Kupffer cell and the margin of the endothelial opening are circularly bound by means of a peculiar close junctional area identical in structure and appearance with the so-called "junctional complex" (Wisse) between endothelial cells . The two junctional areas between the Kupffer cell and the endothelial sheet which are found in a pair in trans- mission electron microscopic preparations on two diametrical parts of the perisinusoidal surface of the Kupffer cell, should be derived from the perpendicular section of such a circular margin of the endothelial opening attached to the Kupffer cell body. -
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. -
(Hepatic Stellate Cells) in Diagnosis of Liver Fibrosis
Gastroenterology & Hepatology: Open Access Research Article Open Access Ito stellate cells (hepatic stellate cells) in diagnosis of liver fibrosis Introduction Volume 10 Issue 4 - 2019 Adverse outcome of most chronic diffuse liver lesions of various etiologies including chronic hepatitis C (CHC) is liver fibrosis in the Vladimir Tsyrkunov,1 Viktor Andreev,2 Rimma development of which main participants are activated fibroblasts. Kravchuk,3 Iryna Kаndratovich1 Activated hepatic stellate cells (HSC) are the main source of activated 1 1,2 Department of Infectious Diseases, Grodno State Medical fibroblasts. University, Belarus 2 HSC, a synonym - stellate cells of liver, Ito cells, perisinusoidal Department of Histology, Grodno State Medical University, Belarus lipocytes, stellate cells. HSC were firstly described in 1876 and named 3Department of Science, Grodno State Medical University, by K. Kupffer stellate cells T. Ito, finding in them a drop of fat firstly Belarus marked them as lipophagic («shibo-sesshusaibo») but then finding that the fat elaborated by the cells from glycogen named them as Correspondence: Iryna Kаndratovich, Department of fat-storing cells or Ito sells («shibo-chozosaibo»).3 In 1971, K.Wake Infectious Diseases, Grodno State Medical University, Gorkogo str 80, Grodno 230009, Belarus, Tel +375152434286, Fax proved the identity of stellate cells of Kupffer and Ito cells and that +375152434286, Email these cells are “stored” vitamin A.4 Received: October 29, 2018 | Published: July 25, 2019 About 80% of vitamin A which is in the body accumulates in the liver and up to 80% of liver retinoids deposited in fat droplets of HSC. Ethers of retinol in formulation of chylomicrons entered to Methods hepatocytes, where they are converted to retinol and form of vitamin A complex with retinol binding protein (RBP), which is secreted in Lifetime liver biopsy obtained by performing aspiration biopsy perisinusoidal space where it deposited by cells.5 of the liver of patients with CHC (HCV ribonucleic acid+).