Serum adipokine and ghrelin levels in nonalcoholic steatohepatitis

dc.contributor.authorYalniz, Mehmet
dc.contributor.authorBahcecioglu, Ibrahim Halil
dc.contributor.authorAtaseven, Huseyin
dc.contributor.authorUstundag, Bilal
dc.contributor.authorIlhan, Fulya
dc.contributor.authorPoyrazoglu, Orhan K.
dc.contributor.authorErensoy, Ahmet
dc.date.accessioned2026-08-12T17:29:40Z
dc.date.issued2006
dc.departmentFırat Üniversitesi
dc.description.abstractAdipokines and ghrelin play role in insulin resistance, the key pathophysiological abnormality in patients with nonalcoholic fatty liver diseases. In the present study, relationship between nonalcoholic steatohepatitis (NASH) and serum adipokine and ghrelin levels was investigated. Thirty seven patients with biopsy-proven NASH and 25 age- and sex-matched controls were enrolled. Ten of NASH patients (27%) had diabetes mellitus (n=5) or impaired glucose tolerance (n=5). Body mass index (BMI) was less than 30 kg/m(2) in 67.6% of patients, while in the remaining 32.4% it was more than 30kg/m(2). Serum adiponectin, leptin, TNF alpha, and ghrelin were determined. Serum leptin (15.49 +/- 4.84 vs 10.31 +/- 2.53) and TNF-alpha (12.1 +/- 2.7 vs 10.31 +/- 2.56) levels were significantly higher in the NASH group compared to in the control group (P <.001 for each). Nevertheless, adiponectin (11.1 +/- 2.1 vs 17.3 +/- 2.8) and ghrelin (6.46 +/- 1.1 vs 7.8 +/- 1.1) levels were lower in the NASH group than in the control group (P <.001 for each). Serum levels of the adipokines and ghrelin, however, were comparable in the subgroups of patients regardless of whether BMI was < 30 or > 30 or glucose tolerance was impaired or not (P >.05). Additionally, neither adipokines nor ghrelin was correlated with histopathological grade and stage (P >.05). In conclusion; there is a significant relationship between NASH and adipokines and ghrelin independent from BMI and status of the glucose metabolism. These cytokines that appear to have role in the pathogenesis of NASH, however, do not have any effect upon the severity of the histopathology.
dc.identifier.doi10.1155/MI/2006/34295
dc.identifier.issn0962-9351
dc.identifier.issn1466-1861
dc.identifier.orcid0000-0003-4841-8644
dc.identifier.orcid0000-0001-6621-2450
dc.identifier.orcid0000-0001-7776-4154
dc.identifier.orcid0000-0001-7790-1358
dc.identifier.pmid17392582
dc.identifier.scopus2-s2.0-34248194831
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1155/MI/2006/34295
dc.identifier.urihttps://hdl.handle.net/11508/55792
dc.identifier.volume2006
dc.identifier.wosWOS:000242587600001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherHindawi Ltd
dc.relation.ispartofMediators of Inflammation
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260511
dc.subjectInsulin-Resistance
dc.subjectFatty Liver
dc.subjectTnf-Alpha
dc.subjectAdiponectin
dc.subjectAdipocyte
dc.subjectObesity
dc.subjectNash
dc.subjectAssociation
dc.subjectMetabolism
dc.subjectReceptors
dc.titleSerum adipokine and ghrelin levels in nonalcoholic steatohepatitis
dc.typeArticle

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