CORE
🇺🇦
make metadata, not war
Services
Services overview
Explore all CORE services
Access to raw data
API
Dataset
FastSync
Content discovery
Recommender
Discovery
OAI identifiers
OAI Resolver
Managing content
Dashboard
Bespoke contracts
Consultancy services
Support us
Support us
Membership
Sponsorship
Community governance
Advisory Board
Board of supporters
Research network
About
About us
Our mission
Team
Blog
FAQs
Contact us
Mechanisms of Disease: genetics of functional gastrointestinal disorders - searching the genes that matter
Authors
A Heils
A Meenagh
+65 more
A Morris-Yates
A Yeo
AE Bharucha
B Adam
B Walters
BE Viramontes
Birgit Adam
BK Kobilka
D Baumgart
D Fourmy
DA Drossman
DA Drossman
DA Drossman
DA Drossman
DM Turner
Emeran A. Mayer
F Cremonini
F Mearin
G Holtmann
G Holtmann
G Pettersson
G Varga
Gerald Holtmann
GF Longstreth
GF Longstreth
GR Locke III
H Mertz
HJ Kim
HK Tabor
I Mohammed
J Gibbs
J Tack
JP Thornley
JR Shannon
JW Lomasney
JW Regan
KR Neal
LA Houghton
LR Cardon
M Camilleri
M Camilleri
M D'Amato
M Hirafuji
M Simren
MJ Zuckerman
MO Moraes
MR der Ohe
NJ Talley
NJ Talley
PJ Whorwell
PP van der Veek
PP van der Veek
R Lazarus
RC Spiller
RC Spiller
RL Levy
RL Levy
SA Wank
SP Dunlop
T Liebregts
Tobias Liebregts
W Hall
WE Whitehead
WG Thompson
WM Gonsalkorale
Publication date
1 January 2007
Publisher
'Springer Science and Business Media LLC'
Doi
Cite
Abstract
Copyright © 2007 Nature Publishing GroupThere is evidence to suggest that genetic factors contribute to the manifestation of functional gastrointestinal disorders (FGID). As such, it is important to note that FGID are heterogeneous; they have quite different clinical features and (probably) different underlying pathophysiologic mechanisms. Evidence from family and twin studies indicates that there is clustering of FGID in families and increased concordance in monozygotic compared with dizygotic twins. The clinical features of FGID implicate polymorphisms in the genes that encode adrenergic, opioidergic or serotonergic receptors, as well as in the G-protein 3 subunit (GNB3) gene and serotonin-transporter genes, in their manifestations. As mediators or regulators of mucosal inflammation can trigger events that ultimately result in manifestations of FGID, polymorphisms in genes that encode proteins with immunomodulatory and/or neuromodulatory features (e.g. OPRM1, IL4, IL4R, TNF) might also have a role in the manifestation of FGID. A two-step model for the role of genetic factors in the manifestation of functional gastrointestinal pain can, therefore, be proposed. In the presence of specific hereditary factors, environmental factors that do not usually cause long-term functional alterations are linked to the manifestation of symptoms.Birgit Adam, Tobias Liebregts and Gerald Holtman
Similar works
Full text
Available Versions
Adelaide Research & Scholarship
See this paper in CORE
Go to the repository landing page
Download from data provider
oai:digital.library.adelaide.e...
Last time updated on 05/08/2013
Crossref
See this paper in CORE
Go to the repository landing page
Download from data provider
Last time updated on 11/12/2019