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dc.contributor.authorElibol, Emine
dc.contributor.authorAkdevelioglu, Yasemin
dc.contributor.authorYilmaz, Canan
dc.contributor.authorNarli, Belkis
dc.contributor.authorSen, Serkan
dc.contributor.authorKaplanoglu, Gulnur Take
dc.contributor.authorSeymen, Cemile Merve
dc.date.accessioned2025-12-28T16:39:58Z
dc.date.available2025-12-28T16:39:58Z
dc.date.issued2024
dc.identifier.issn1687-1979
dc.identifier.issn2090-2387
dc.identifier.urihttps://doi.org/10.1016/j.ajg.2023.12.007
dc.identifier.urihttps://hdl.handle.net/20.500.12933/2277
dc.description.abstractBackground and study aims: Ghrelin is an appetite hormone-containing 28-amino acid and has 4 different forms in the body. Ghrelin forms have different physiological functions in the body. This study aims to analyze the effect of acyl and desacyl ghrelin hormone on hepatic steatosis and biochemical findings in 36 male Wistar rats. Materials and methods: Rats were split into 6 equal groups, consisting of control, acyl ghrelin, desacyl ghrelin, acyl/desacyl 3:1, acyl/desacyl 1:1, and acyl/desacyl 1:3 groups, and administered placebo or 200 ng/kg hormone subcutaneous twice a day for 14 days. Oral Glucose Tolerance Test (OGTT) was performed on Day 15, Insulin Tolerance Test (ITT) on Day 16, and scarification procedure on Day 17. Certain biochemical data and liver diacylglycerol (DAG), glycogen, protein kinase C and PPAR-gamma levels were detected in the blood. Histological analyses were also conducted on the liver tissues. Results: The highest plasma total cholesterol and VLDL-K levels were found in the acyl/desacyl 1:3 group, and lower insulin, and HOMA-IR levels were found in groups where acyl and desacyl were administered together (p < 0.05). PPAR-gamma gene expression level increased in acyl ghrelin and acyl/desacyl 1:3 groups compared to the control group. Protein kinase C gene expression was highest in the acyl/desacyl 1:3 group. The most severe degenerative findings compliant with steatosis in the liver were observed in the acyl ghrelin group (p < 0.05). Conclusion: It was determined that administering rats acyl alone and acyl/desacyl by 1:3 caused the highest PPAR-gamma gene expression, serum total cholesterol, HDL-K, and VLDL-K levels in the body. Besides, it is shown that desacyl ghrelin effectively regulates the blood glucose level when administered alone.
dc.description.sponsorshipGazi University Scientific Research Project (SRP) [47/2019-12]
dc.description.sponsorshipResearch funding This research has been supported by Gazi University Scientific Research Project (SRP) according to the decision numbered 47/2019-12.
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofArab Journal of Gastroenterology
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAcyl ghrelin
dc.subjectDesacyl ghrelin
dc.subjectDiacylglycerol
dc.subjectHepatic steatosis
dc.subjectProtein kinase C
dc.titleAcyl ghrelin, desacyl ghrelin and their ratio affect hepatic steatosis via PPAR? signaling pathway
dc.typeArticle
dc.identifier.orcid0000-0002-6166-0825
dc.identifier.orcid0000-0002-2884-4753
dc.identifier.orcid0000-0002-6799-6522
dc.departmentAfyonkarahisar Sağlık Bilimleri Üniversitesi
dc.identifier.doi10.1016/j.ajg.2023.12.007
dc.identifier.volume25
dc.identifier.issue2
dc.identifier.startpage109
dc.identifier.endpage117
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.department-temp[Elibol, Emine] Ankara Yildirim Beyazit Univ, Dept Nutr & Dietet, TR-06760 Ankara, Turkiye; [Akdevelioglu, Yasemin] Gazi Univ, Dept Nutr & Dietet, Emek mah Biskek Cad 6 Cad 2, TR-06490 Ankara, Turkiye; [Yilmaz, Canan; Narli, Belkis] Gazi Univ, Fac Med, Dept Med Biochem, TR-06500 Ankara, Turkiye; [Sen, Serkan] Afyonkarahisar Hlth Sci Univ, Dept Med Biochem, Ali Cetinkaya Kampusu Afyon Izmir Karayolu 5 Km, Afyonkarahisar, Turkiye; [Kaplanoglu, Gulnur Take; Seymen, Cemile Merve] Gazi Univ, Fac Med, Dept Histol & Embryol, TR-06500 Ankara, Turkiye
dc.identifier.pmid38383264
dc.identifier.scopus2-s2.0-85185765230
dc.identifier.scopusqualityQ3
dc.identifier.wosWOS:001250600800002
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.snmzKA_WoS_20251227


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