Anti-inflammatory and antithrombotic effects of nicotine exposure in oral contraceptive-induced insulin resistance is glucocorticoid-independent

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dc.contributor.authorOlatunji Lawrence Aderemi
dc.contributor.authorMichael Olugbenga Samuel
dc.contributor.authorAdeyanju Oluwaseun Aremu
dc.contributor.authorAreola Emmanuel Damilare
dc.contributor.authorSoladoye Ayodele Olufemi
dc.date.accessioned2025-05-07T11:29:55Z
dc.date.available2025-05-07T11:29:55Z
dc.date.issued2016-12-16
dc.description.abstractBackground: Reports showed that estrogen-progestin oral contraceptive (COC) or tobacco smoking causes increased risk of cardiovascular diseases (CVD) in premenopausal women. Studies also suggest that nicotine; a major tobacco alkaloid may worsen or improve atherothrombotic CVD. Altered hemorheology, prothrombotic and pro-inflammatory biomarkers, have been implicated in the development of atherothrombotic CVD events. However, the effect of non-smoking nicotine exposure on these biomarkers during COC treatment is not yet established. We therefore sought to determine the effects of nicotine exposure during COC treatment on these biomarkers, and also tested the hypothesis that the nicotine effects would be glucocorticoid-dependent. Methods: Female Sprague-Dawley rats aged 10 weeks were given (po) vehicle, low-dose nicotine (0.1 mg/kg) or high-dose nicotine (1.0 mg/kg) with or without COC steroids (5.0 µg/kg ethinylestradiol and 25.0 µg/kg levonorgestrel) daily for 6 weeks. Results: COC treatment or nicotine exposure led to increased insulin resistance (IR), hemorheological (blood viscosity, hematocrit and plasma viscosity), prothrombotic (plasminogen activator inhibitor-1), pro-inflammatory (uric acid, C-reactive protein, neutrophil/lymphocyte and platelet/lymphocyte ratios) biomarkers and corticosterone. However, these effects except that on corticosterone were abrogated by nicotine exposure during COC treatment. Conclusions: Our study indicates that nicotine- or COC-induced IR may be mediated via inflammatory/thrombotic pathway. The results imply that nicotine exposure could impact negatively on atherothrombotic biomarkers in COC non-users, whereas the impact in COC users could be positive. The results also suggest that the anti-inflammatory, antithrombotic and blood viscosity-lowering effects of nicotine exposure during COC use is circulating glucocorticoid-independent.
dc.description.sponsorshipThe authors have no funding information to declare
dc.identifier.citationOlatunji, L.A., Michael, O.S., Adeyanju, O.A., Areola, E.D. & Soladoye, A.O. (2017). Anti-inflammatory and antithrombotic effects of nicotine exposure in oral contraceptive-induced insulin resistance is glucocorticoid-independent. Pharmacological Reports, 69 (3), 512-519, Published by Elsevier. Available online at: Pharmacological Reports | Vol 69, Issue 3, Pages 377-594 (June 2017) | ScienceDirect.com by Elsevier
dc.identifier.other10.1016/j.pharep.2016.12.010
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/16315
dc.language.isoen
dc.publisherPharmacological Reports
dc.relation.ispartofseries69(3); 512-519
dc.subjectAtherothrombotic CVD
dc.subjectestrogen-progestin oral contraceptive
dc.subjectproinflammatory biomarker
dc.subjectcorticosterone
dc.titleAnti-inflammatory and antithrombotic effects of nicotine exposure in oral contraceptive-induced insulin resistance is glucocorticoid-independent
dc.title.alternativeAnti-inflammatory and antithrombotic effects of nicotine during COC use
dc.typeArticle

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