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dc.contributorVall d'Hebron Barcelona Hospital Campus
dc.contributor.authorGabriel Medina, Pablo
dc.contributor.authorFerrer Costa, Roser
dc.contributor.authorRodríguez Frias, Francisco
dc.contributor.authorCiudin Mihai, Andreea
dc.contributor.authorAugustin Recio, Salvador
dc.contributor.authorRivera Esteban, Jesus Manuel
dc.contributor.authorPericàs Pulido, Juan Manuel
dc.contributor.authorMartinez Selva, David
dc.date.accessioned2022-09-08T08:35:55Z
dc.date.available2022-09-08T08:35:55Z
dc.date.issued2022-05
dc.identifier.citationGabriel-Medina P, Ferrer-Costa R, Rodriguez-Frias F, Ciudin A, Augustin S, Rivera-Esteban J, et al. Influence of Type 2 Diabetes in the Association of PNPLA3 rs738409 and TM6SF2 rs58542926 Polymorphisms in NASH Advanced Liver Fibrosis. Biomedicines. 2022 May;10(5):1015.
dc.identifier.issn2227-9059
dc.identifier.urihttp://hdl.handle.net/11351/8066
dc.descriptionAdvanced fibrosis; Nonalcoholic steatohepatitis; Type 2 diabetes
dc.description.abstractNonalcoholic steatohepatitis (NASH) is a leading cause of cirrhosis in western countries. Insulin resistance (IR), type 2 diabetes (T2D), and the polymorphisms patatin-like phospholipase domain-containing 3 (PNPLA3) rs738409 and transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 are independent risk factors of NASH. Nevertheless, little is known about the interaction between IR and T2D with these polymorphisms in the pathogenesis of NASH and the development of advanced fibrosis. Thus, our study aimed to investigate this relationship. This is a cross-sectional study including NASH patients diagnosed by liver biopsy, at the Vall d’Hebron University Hospital. A total of 140 patients were included (93 T2D, 47 non-T2D). T2D (OR = 4.67; 95%CI 2.13–10.20; p < 0.001), PNPLA3 rs738409 and TM6SF2 rs58542926 polymorphisms (OR = 3.94; 95%CI 1.63–9.54; p = 0.002) were independently related with advanced liver fibrosis. T2D increased the risk of advance fibrosis on top of the two polymorphisms (OR = 14.69; 95%CI 3.03–77.35; p = 0.001 for PNPLA3 rs738409 and OR = 11.45; 95%CI 3.16–41.55; p < 0.001 for TM6SF2 rs58542926). In non-T2D patients, the IR (HOMA-IR ≥ 5.2, OR = 14.33; 95%CI 2.14–18.66; p = 0.014) increased the risk of advanced fibrosis when the polymorphisms were present (OR = 19.04; 95%CI 1.71–650.84; p = 0.042). The T2D and IR status increase the risk of advanced fibrosis in patients with NASH carrying the PNPLA3 rs738409 and/or TM6SF2 rs58542926 polymorphisms, respectively.
dc.language.isoeng
dc.publisherMDPI
dc.relation.ispartofseriesBiomedicines;10(5)
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceScientia
dc.subjectDiabetis no-insulinodependent
dc.subjectPolimorfisme genètic
dc.subjectEsteatosi hepàtica - Aspectes genètics
dc.subject.meshPolymorphism, Single Nucleotide
dc.subject.meshDiabetes Mellitus, Type 2
dc.subject.meshNon-alcoholic Fatty Liver Disease
dc.titleInfluence of Type 2 Diabetes in the Association of PNPLA3 rs738409 and TM6SF2 rs58542926 Polymorphisms in NASH Advanced Liver Fibrosis
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.3390/biomedicines10051015
dc.subject.decspolimorfismo de nucleótido único
dc.subject.decsdiabetes mellitus tipo II
dc.subject.decsesteatosis hepática no alcohólica
dc.relation.publishversionhttps://doi.org/10.3390/biomedicines10051015
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.audienceProfessionals
dc.contributor.organismesInstitut Català de la Salut
dc.contributor.authoraffiliation[Gabriel-Medina P] Servei de Bioquímica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Bellaterra, Spain. Grup de Recerca en Bioquímica Clínica, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. [Ferrer-Costa R] Servei de Bioquímica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Grup de Recerca en Bioquímica Clínica, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. [Rodriguez-Frias F] Servei de Bioquímica, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Bellaterra, Spain. Grup de Recerca en Bioquímica Clínica, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), 28029 Madrid, Spain. [Ciudin A] Servei d’Endocrinologia i Nutrició, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Grup de Recerca en Diabetis i Metabolisme, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain. [Augustin S, Pericàs JM] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), 28029 Madrid, Spain. Unitat Hepàtica, Servei de Medicina Interna, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. [Rivera-Esteban J] Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Bellaterra, Spain. Unitat Hepàtica, Servei de Medicina Interna, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. [Martinez Selva D] Grup de Recerca en Diabetis i Metabolisme, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain. Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain
dc.identifier.pmid35625751
dc.identifier.wos000802501100001
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess


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