Insulin resistance is an evolutionarily conserved physiological mechanism at the cellular level for protection against increased oxidative stress

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dc.contributor.authorErol A.
dc.date.accessioned2024-07-22T08:22:47Z
dc.date.available2024-07-22T08:22:47Z
dc.date.issued2007
dc.description.abstractSeveral protective cellular mechanisms protect against the accumulation of reactive oxygen species (ROS) and the concomitant oxidative stress. Therefore, any reduction in glucose or fatty acid flux into cells leading to a decrease in the production of reducing equivalents would also lead to a decreased ROS production and protect cells against oxidative stress. In the presence of insulin, FOXO proteins are localized from the nucleus to the cytoplasm and degraded. An increase in cellular glucose uptake will lead to increased production of ROS. This in turn activates the stress-responsive Jun-N-terminal kinase (JNK), which promotes nuclear translocation of FOXO proteins, upregulating some important target genes including stress resistance. Consequently, insulin resistance should result in decreased cellular ROS production. For this reason, insulin resistance could be a physiological mechanism activated at the cellular level in response to conditions stimulating ROS production and leading to the prevention of oxidative stress, and extension of life. Concerning the whole organism, however, IR is a maladaptive process in the long term causing a diabetic state. © 2007 Wiley Periodicals, Inc.
dc.identifier.DOI-ID10.1002/bies.20618
dc.identifier.issn02659247
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/19238
dc.language.isoEnglish
dc.subjectAnimals
dc.subjectCytoprotection
dc.subjectEvolution
dc.subjectGlucose
dc.subjectHumans
dc.subjectInsulin
dc.subjectInsulin Resistance
dc.subjectMitochondria
dc.subjectModels, Biological
dc.subjectOxidative Stress
dc.subjectReactive Oxygen Species
dc.subjectadenosine triphosphate
dc.subjectcatalase
dc.subjectfatty acid
dc.subjectglucose
dc.subjectinsulin
dc.subjectinsulin receptor
dc.subjectreactive oxygen metabolite
dc.subjectreduced nicotinamide adenine dinucleotide
dc.subjectstress activated protein kinase
dc.subjectsuperoxide
dc.subjecttranscription factor DAF 16
dc.subjecttranscription factor FOXO
dc.subjecttranscription factor PDX 1
dc.subjectcell proliferation
dc.subjectcell protection
dc.subjectdiabetes mellitus
dc.subjectelectron transport
dc.subjectenergy metabolism
dc.subjectglucose metabolism
dc.subjectglucose transport
dc.subjecthuman
dc.subjecthyperglycemia
dc.subjecthyperinsulinemia
dc.subjectinsulin release
dc.subjectinsulin resistance
dc.subjectinsulin response
dc.subjectinsulin sensitivity
dc.subjectinsulin synthesis
dc.subjectlifestyle modification
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpancreas islet beta cell
dc.subjectprotein function
dc.subjectprotein localization
dc.subjectprotein phosphorylation
dc.subjectprotein protein interaction
dc.subjectreview
dc.titleInsulin resistance is an evolutionarily conserved physiological mechanism at the cellular level for protection against increased oxidative stress
dc.typeReview

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