Insulin Resistance in Liver Cirrhosis

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dc.contributor.authorGoral, Vedat
dc.contributor.authorAtalay, Roni
dc.contributor.authorKucukoren, Mehmet
dc.date.accessioned2024-04-24T17:37:33Z
dc.date.available2024-04-24T17:37:33Z
dc.date.issued2010
dc.departmentDicle Üniversitesien_US
dc.description.abstractBackground/Aims: Liver cirrhosis is a chronic disease by degeneration, regeneration and fibrosis in the liver parenchyma, caused by many diseases. Insulin resistance can be defined as any type of decrease in the effect that may occur at the phases following insulin's secretion from B-cells of the pancreas, where it is produced, until it has the expected effects in the target cells. The aim of the present study is to demonstrate the presence of insulin resistance in LC, which is common in our country and region, and investigate the existence of association between insulin resistance occuring in LC and cytokine levels, age, gender, CRP, Hs-CRP, Child-Pugh score and etiology of LC. Methodology: A total of 79 patients with liver cirrhosis (group 1) were included in the study, and 50 subjects as controls (group 2). Of liver cirrhosis patients, 49 (62%) were male and 30 (38%) were female, with a mean age of 54.71 +/- 14.68. Of the controls, 23 (46%) were male and 27 (54%) were female, with a mean age of 41.9 +/- 11.54. Severity of cirrhosis was assessed by Modified Child-Turcoutte-Pugh score. Seven cases (8.9%) were at the Child-Pugh stage A, 35 cases (44.3%) at the Child-Pough stage B, and 37 cases (46.8%) at the Child-Pough stage C. HOMA-IR was calculated and values >2.7 were regarded as presence of insulin resistance (HOMA-IR +). Serum glucose, albumin, bilirubin values were studied with enzymatic method (Architect C-16000); serum CRP, Hs-CRP values with nephelometric method by Beckman Coulter Image Nephelometer (immunochemistry system); insulin, C-peptide with electrochemiluminance immunological method; prothrombin time with radiation method by ACL-Advance brand device. Results: In this study, glucose (p=0.004), insulin (p=0.010), C-peptide (p<0.001), HOMA-IR (p<0.001), TNF-alpha (p<0.001), IL-2RES (p<0.001), IL-6 (p=0.002), CRP (p<0.001) and HsCRP (p=0.006) levels are elevated in LC patients, compared to control group. Consequently, high HOMA-IR in LC supports the fact that insulin resistance develops in LC, as it is reported in similar studies. When HOMA-IR positive and negative patients within LC patients are compared, it is seen that insulin resistance develops independently of age, etiology, gender, Child-Pugh classification, spleen size, TNF-alpha, IL-1 beta, IL-2RES, IL-6, IL-10, CRP, Hs-CRP (p>0.05) levels.en_US
dc.identifier.endpage315en_US
dc.identifier.issn0172-6390
dc.identifier.issue98en_US
dc.identifier.pmid20583433
dc.identifier.scopus2-s2.0-77954118624
dc.identifier.scopusqualityN/A
dc.identifier.startpage309en_US
dc.identifier.urihttps://hdl.handle.net/11468/21017
dc.identifier.volume57en_US
dc.identifier.wosWOS:000278938200024
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherH G E Update Medical Publishing S Aen_US
dc.relation.ispartofHepato-Gastroenterology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectInsulin Resistanceen_US
dc.subjectLiver Cirrhosisen_US
dc.titleInsulin Resistance in Liver Cirrhosisen_US
dc.titleInsulin Resistance in Liver Cirrhosis
dc.typeArticleen_US

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