Serum leptin levels following acute experimental spinal cord injury

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dc.contributor.authorGezici, Ali Rıza
dc.contributor.authorErgün, Rüçhan
dc.contributor.authorKarakaş, Alper
dc.contributor.authorGündüz, Bülent
dc.date.accessioned2021-06-23T19:26:10Z
dc.date.available2021-06-23T19:26:10Z
dc.date.issued2009
dc.departmentBAİBÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.description.abstractBackground/Objective: Spinal cord injury influences many hormones that are known to be involved in the modulation of neurotrophic, neurogenic, and neuroprotective events. Recent studies showed that leptin could be neuroprotective, enhancing neuronal survival in vitro and in vivo. The objective of this study was to evaluate the pattern of the serum leptin levels in rats during acute traumatic SCI. Methods: Forty male Sprague-Dawley rats were divided randomly into 4 groups. In the control group, neither laminectomy nor SCI was performed; only laminectomy was performed without SCI in the sham group. In the cervical and thoracic spinal trauma groups, laminectomies were performed following the same trauma procedure. Blood samples were drawn 2, 6, 12, and 24 hours after the procedures and assayed immediately. Results: In the first 2 hours, levels of leptin were similar in control and sham-operated groups and higher in neurotrauma groups (P < 0.05). At the sixth hour, leptin levels increased in the sham-operated group, decreased in the neurotrauma groups (P < 0.05), and did not change in the control group (P > 0.05). At the 12th hour, the levels of leptin increased in all groups (P > 0.05). At the 24th hour, they decreased in the control, sham-operated, and cervical groups (P < 0.05); levels did not change in the thoracic group (P > 0.05). The decrease was higher in the control group than in the other groups (P < 0.05). Conclusions: Activation of endogenous leptin secretion started immediately after the SCI. The level of neurologic lesion (either cervical or thoracic regions) affected the levels of serum leptin differently, but with the exception of the first 12-hour period, this difference did not reach a statistically significant level.en_US
dc.identifier.doi10.1080/10790268.2009.11753205
dc.identifier.endpage421en_US
dc.identifier.issn1079-0268
dc.identifier.issn2045-7723
dc.identifier.issue4en_US
dc.identifier.pmid19777863en_US
dc.identifier.scopus2-s2.0-70349572916en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage416en_US
dc.identifier.urihttps://doi.org/10.1080/10790268.2009.11753205
dc.identifier.urihttps://hdl.handle.net/20.500.12491/6440
dc.identifier.volume32en_US
dc.identifier.wosWOS:000207861800008en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorGezici, Ali Rıza
dc.institutionauthorErgün, Rüçhan
dc.institutionauthorKarakaş, Alper
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofJournal Of Spinal Cord Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectSpinal Cord Injuriesen_US
dc.subjectNeuroprotectionen_US
dc.titleSerum leptin levels following acute experimental spinal cord injuryen_US
dc.typeArticleen_US

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