BACKGROUND: Although familial clustering of functional dyspepsia (FD) has been reported, the role of genetics in the susceptibility to FD is still not well established. Several reports indicate the associations between FD and gene polymorphisms, however the data are inconsistent. This review summarized the evidence of genetics in FD based on genetic epidemiology. RESULTS: Genetic association studies with FD symptom phenotype have limited for several candidate genes investigated. There have been no genome wide association studies in FD. G-protein beta3 (GNB3) subunit C825T was first reported as a candidate gene for FD susceptibility. However, the data are inconsistent in countries. Significant link between homozygous 825C allele of GNB3 protein and dyspepsia was reported from Germany and the USA. On the other hand, the association between T allele of GNB3 C825T polymorphism and dyspepsia was reported from Japan and Netherlands. Association of serotonin transporter promoter (SERT-P) gene polymorphism and FD was reported negatively from a USA community and Netherlands. However we found that SERT SL genotype was significantly associated with PDS. Involvement of IL-17F, migration inhibitory factor (MIF), catechol-o-methyltransferase (COMT) gene val158met, 779 TC of CCK-1 intron 1, cyclooxygenase-1 (COX-1), transient receptor potential cation channel, subfamily V, member 1 (TRPV1) 315C and regulated upon activation normal T cell expressed and secreted (RANTES) polymorphisms was reported in Japanese studies. CONCLUSIONS: Genetic factors are associated with the development of dyspeptic symptoms. Further studies are needed to confirm these data and to determine how genetic factors influence the clinical manifestation of FD patients.
BACKGROUND: Although familial clustering of functional dyspepsia (FD) has been reported, the role of genetics in the susceptibility to FD is still not well established. Several reports indicate the associations between FD and gene polymorphisms, however the data are inconsistent. This review summarized the evidence of genetics in FD based on genetic epidemiology. RESULTS: Genetic association studies with FD symptom phenotype have limited for several candidate genes investigated. There have been no genome wide association studies in FD. G-protein beta3 (GNB3) subunit C825T was first reported as a candidate gene for FD susceptibility. However, the data are inconsistent in countries. Significant link between homozygous 825C allele of GNB3 protein and dyspepsia was reported from Germany and the USA. On the other hand, the association between T allele of GNB3C825T polymorphism and dyspepsia was reported from Japan and Netherlands. Association of serotonin transporter promoter (SERT-P) gene polymorphism and FD was reported negatively from a USA community and Netherlands. However we found that SERT SL genotype was significantly associated with PDS. Involvement of IL-17F, migration inhibitory factor (MIF), catechol-o-methyltransferase (COMT) gene val158met, 779 TC of CCK-1 intron 1, cyclooxygenase-1 (COX-1), transient receptor potential cation channel, subfamily V, member 1 (TRPV1) 315C and regulated upon activation normal T cell expressed and secreted (RANTES) polymorphisms was reported in Japanese studies. CONCLUSIONS: Genetic factors are associated with the development of dyspeptic symptoms. Further studies are needed to confirm these data and to determine how genetic factors influence the clinical manifestation of FDpatients.
Authors: Yuri A Saito; G Richard Locke; Ann E Almazar; Ernest P Bouras; Colin W Howden; Brian E Lacy; John K DiBaise; Charlene M Prather; Bincy P Abraham; Hashem B El-Serag; Paul Moayyedi; Linda M Herrick; Lawrence A Szarka; Michael Camilleri; Frank A Hamilton; Cathy D Schleck; Katherine E Tilkes; Alan R Zinsmeister; Nicholas J Talley Journal: Am J Gastroenterol Date: 2017-03-14 Impact factor: 10.864