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dc.creatorStanojević, A
dc.creatorMarković, V M
dc.creatorMaćešić, Stevan
dc.creatorKolar-Anić, Ljiljana
dc.creatorVukojević, V
dc.date.accessioned2019-05-31T06:40:34Z
dc.date.available2019-05-31T06:40:34Z
dc.date.issued2018
dc.identifier.issn1878-5190
dc.identifier.urihttp://cer.ihtm.bg.ac.rs/handle/123456789/2920
dc.description.abstractThe sex hormone testosterone (TTS) and the hypothalamic–pituitary–adrenal (HPA) axis mutually control one another’s activity, wherein TTS suppresses corticotrophin releasing hormone (CRH) stimulated HPA axis activity, whereas the activation of HPA axis has an inhibitory effect on TTS secretion. With an intention to explain these phenomena, a network reaction model is developed from the previously postulated stoichiometric models for HPA activity where main dynamic behaviors are controlled by two catalytic steps (one autocatalytic and one autoinhibitory) with respect to cortisol, both found experimentally. The capacity of the model to emulate TTS effects on HPA axis dynamics and its response to acute CRH-induced stress is examined using numerical simulations. Model predictions are compared with empirically obtained results reported in the literature. Thus, the reaction kinetic examinations of nonlinear biochemical transformations that constitute the HPA axis, including the negative feedback effect of TTS on HPA axis activity, recapitulates the well-established fact that TTS dampens HPA axis basal activity, decreasing both cortisol level and the amplitude of ultradian cortisol oscillations. The model also replicates TTS inhibitory action on the HPA axis response to acute environmental challenges, particularly CRH-induced stress. In addition, kinetic modelling revealed that TTS induced reduction in ultradian cortisol amplitude arises because the system moves towards a supercritical Hopf bifurcation as TTS is being increased. © 2017, The Author(s).en
dc.language.isoen
dc.publisherSpringer Netherlands
dc.relationCMST COST Action CM 1304 ‘‘Emergence and Evolution of Complex Chemical Systems’’
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/172015/RS//
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/45001/RS//
dc.rightsopenAccess
dc.sourceReaction Kinetics, Mechanisms and Catalysis
dc.subjectAutoinhibition
dc.subjectKinetics
dc.subjectCortisol
dc.subjectTestosterone
dc.subjectSupercritical Hopf bifurcation
dc.subjectStoichiometric models
dc.subjectKinetic modelling
dc.subjectStresses
dc.subjectReaction kinetics
dc.subjectMathematical transformations
dc.subjectKinetic theory
dc.titleKinetic modelling of testosterone-related differences in the hypothalamic–pituitary–adrenal axis response to stressen
dc.typearticleen
dc.rights.licenseBY
dcterms.abstractСтанојевић, A; Марковић, В М; Маћешић, С; Колар-Aнић, Л; Вукојевић, В;
dc.rights.holderThe Authors
dc.citation.volume123
dc.citation.issue1
dc.citation.spage17
dc.citation.epage30
dc.citation.rankM23
dc.identifier.doi10.1007/s11144-017-1315-7
dc.identifier.fulltexthttp://cer.ihtm.bg.ac.rs/bitstream/id/7098/bitstream_7098.pdf
dc.identifier.scopus2-s2.0-85034231216
dc.identifier.wos000419514200002
dc.type.versionpublishedVersion


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