Common SPINK-1 mutations do not predispose to the development of non-alcoholic fatty liver disease

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dc.contributor.authorOruc, Nevin
dc.contributor.authorOzutemiz, Omer
dc.contributor.authorAkarca, Ulus Salih
dc.contributor.authorBerdeli, Afig
dc.contributor.authorErsoz, Galip
dc.contributor.authorGunsar, Fulya
dc.contributor.authorKarasu, Zeki
dc.contributor.authorIlter, Tankut
dc.contributor.authorBatur, Yucel
dc.date.accessioned2019-10-27T20:52:30Z
dc.date.available2019-10-27T20:52:30Z
dc.date.issued2009
dc.departmentEge Üniversitesien_US
dc.description.abstractBackground: Non-alcoholic fatty liver disease (NAFLD) is common in obese and diabetics. Serine protease inhibitor Kazal-1 (SPINK-1) protein is highly expressed in the liver and adipose tissue of diabetic and obese suggesting its role in NAFLD. SPINK-1 also behaves as an acute phase reactant protein. Some genetic factors including the genetic variations in SPINK-1 protein have been linked to chronic pancreatitis and diabetes. We therefore hypothesized that SPINK-1 mutations might be a risk factor for the development of NAFLD. Methods: Liver biopsy proven fifty NAFLD cases (20 steatohepatitis, 30 diffuse fatty liver disease and 44 healthy controls were included to the study. Liver function tests were measured. Body mass index was calculated. Insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Common genetic mutations in the third exon of SPINK-1 gene were analyzed by direct sequencing method. Results: We found two cases with a SNP at N34S location in NAFLD group (allele frequency %4). One subject with diffuse fatty liver disease and other with liver cirrhosis due to NAFLD had N34S mutation. No SNPs were detected in healthy controls. In conclusions, in limited number of patients SPINK-1 mutations were not considered as a risk factor alone for NAFLD development.en_US
dc.identifier.endpage119en_US
dc.identifier.issn1665-2681
dc.identifier.issue2en_US
dc.identifier.pmid19502653en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage116en_US
dc.identifier.urihttps://hdl.handle.net/11454/43237
dc.identifier.volume8en_US
dc.identifier.wosWOS:000266929400006en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherMexican Assoc Hepatologyen_US
dc.relation.ispartofAnnals of Hepatologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSPINK1en_US
dc.subjectNAFLDen_US
dc.subjectmutationen_US
dc.subjectinsulin resistanceen_US
dc.titleCommon SPINK-1 mutations do not predispose to the development of non-alcoholic fatty liver diseaseen_US
dc.typeArticleen_US

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