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Role of brain c-Jun N-terminal kinase 2 in the control of the insulin receptor and its relationship with cognitive performance in a high-fat diet pre-clinical model

dc.contributor.authorBusquets O.
dc.contributor.authorEritja À.
dc.contributor.authorLópez B.M.
dc.contributor.authorEttcheto M.
dc.contributor.authorManzine P.R.
dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorVerdaguer E.
dc.contributor.authorOlloquequi J.
dc.contributor.authorVázquez-Carrera M.
dc.contributor.authorAuladell C.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:13:36Z
dc.date.available2020-09-02T22:13:36Z
dc.date.issued2019
dc.identifier10.1111/jnc.14682
dc.identifier.citation149, 2, 255-268
dc.identifier.issn00223042
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3807
dc.descriptionInsulin resistance has negative consequences on the physiological functioning of the nervous system. The appearance of type 3 diabetes in the brain leads to the development of the sporadic form of Alzheimer's disease. The c-Jun N-terminal kinases (JNK), a subfamily of the Mitogen Activated Protein Kinases, are enzymes composed by three different isoforms with differential modulatory activity against the insulin receptor (IR) and its substrate. This research focused on understanding the regulatory role of JNK2 on the IR, as well as study the effect of a high-fat diet (HFD) in the brain. Our observations determined how JNK2 ablation did not induce compensatory responses in the expression of the other isoforms but led to an increase in JNKs total activity. HFD-fed animals also showed an increased activity profile of the JNKs. These animals also displayed endoplasmic reticulum stress and up-regulation of the protein tyrosine phosphatase 1B (PTP1B) and the suppressor of cytokine signalling 3 protein. Consequently, a reduction in insulin sensitivity was detected and it is correlated with a decrease on the signalling of the IR. Moreover, cognitive impairment was observed in all groups but only wild-type genotype animals fed with HFD showed neuroinflammatory responses. In conclusion, HFD and JNK2 absence cause alterations in normal cognitive activity by altering the signalling of the IR. These affectations are related to the appearance of endoplasmic reticulum stress and an increase in the levels of inhibitory proteins like PTP1B and suppressor of cytokine signalling 3 protein. (Figure presented.). Cover Image for this issue: doi: 10.1111/jnc.14502. © 2019 International Society for Neurochemistry
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.subjectER stress
dc.subjecthigh-fat diet
dc.subjectJNK
dc.subjectmetabolism
dc.subjectneuroinflammation
dc.subjectPTP1B
dc.subjectbiological marker
dc.subjectinsulin receptor
dc.subjectisoprotein
dc.subjectmitogen activated protein kinase 9
dc.subjectprotein tyrosine phosphatase 1B
dc.subjectsuppressor of cytokine signaling 3
dc.subjectX box binding protein 1
dc.subjectinsulin receptor
dc.subjectmitogen activated protein kinase 9
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectcognition
dc.subjectcognitive defect
dc.subjectcontrolled study
dc.subjectdendritic spine
dc.subjectendoplasmic reticulum stress
dc.subjectenzyme activity
dc.subjectgenotype
dc.subjecthippocampus
dc.subjectinsulin sensitivity
dc.subjectlipid diet
dc.subjectmacroglia
dc.subjectmale
dc.subjectmetabolic parameters
dc.subjectmicroglia
dc.subjectmouse
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectnovel object recognition test
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectregulatory mechanism
dc.subjectsignal transduction
dc.subjectupregulation
dc.subjectwild type
dc.subjectadverse event
dc.subjectanimal
dc.subjectbrain
dc.subjectC57BL mouse
dc.subjectcognition
dc.subjectdisease model
dc.subjectinsulin resistance
dc.subjectknockout mouse
dc.subjectlipid diet
dc.subjectmetabolism
dc.subjectphysiology
dc.subjectAnimals
dc.subjectBrain
dc.subjectCognition
dc.subjectDiet, High-Fat
dc.subjectDisease Models, Animal
dc.subjectEndoplasmic Reticulum Stress
dc.subjectInsulin Resistance
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMitogen-Activated Protein Kinase 9
dc.subjectReceptor, Insulin
dc.titleRole of brain c-Jun N-terminal kinase 2 in the control of the insulin receptor and its relationship with cognitive performance in a high-fat diet pre-clinical model
dc.typeArticle


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