Molecular basis of functional gastrointestinal disorders

Abstract There are a number of abnormalities of gastrointestinal function, including sensory and motor dysfunction, which are believed to play a role in the manifestation of symptoms in patients with functional gastrointestinal disorders (FGID). In addition, there is a remarkable psychiatric comorbidity. Family and twin studies have provided strong evidence for a clustering of FGID in families and an increased concordance in monozygotic compared to dizygotic twins. This points towards the role of one or more hereditary (genetic) factors. Considering these disorders of function and the psychiatric comorbidity, polymorphisms of adrenergic, opioidergic or serotonergic receptors as well as G-protein β3 ( GNB 3) subunit gene polymorphisms (C825T) and polymorphisms of 5-HT transporter genes are suitable causes. In addition, mediators or regulators of mucosal inflammation may trigger events that ultimately result in the manifestation of FGID. Thus, relevant polymorphisms of genes with immunmodulating and/or neuromodulating features (OPRM1, IL-4, IL-4R, TNFα) may also play a role in the manifestation of FGIDs.