Serum Leptin Levels Following Acute Experimental Spinal Cord Injury

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dc.authoridGunduz, Bulent/0000-0003-0497-8287
dc.contributor.authorGezici, Ali Riza
dc.contributor.authorErgun, Ruchan
dc.contributor.authorKarakas, Alper
dc.contributor.authorGunduz, Bulent
dc.date.accessioned2025-01-27T21:01:34Z
dc.date.available2025-01-27T21:01:34Z
dc.date.issued2009
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
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.
dc.identifier.doi10.1080/10790268.2009.11753205
dc.identifier.endpage421
dc.identifier.issn1079-0268
dc.identifier.issn2045-7723
dc.identifier.issue4
dc.identifier.pmid19777863
dc.identifier.startpage416
dc.identifier.urihttps://doi.org/10.1080/10790268.2009.11753205
dc.identifier.urihttps://hdl.handle.net/20.500.12428/27102
dc.identifier.volume32
dc.identifier.wosWOS:000207861800008
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofJournal of Spinal Cord Medicine
dc.relation.publicationcategoryinfo:eu-repo/semantics/openAccess
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20250125
dc.subjectSpinal cord injuries
dc.subjectNeuroprotection
dc.titleSerum Leptin Levels Following Acute Experimental Spinal Cord Injury
dc.typeArticle

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