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dc.contributor.authorLopez-Vilaret, Karel M
dc.contributor.authorCantero, Jose L
dc.contributor.authorFernandez-Alvarez, Marina
dc.contributor.authorCalero, Miguel 
dc.contributor.authorCalero, Olga 
dc.contributor.authorLindín, Mónica
dc.contributor.authorZurrón, Montserrat
dc.contributor.authorDíaz, Fernando
dc.contributor.authorAtienza, Mercedes
dc.contributor.authorLopez-Vilaret, Karel M.
dc.contributor.authorCantero, Jose L.
dc.date.accessioned2021-11-22T15:25:15Z
dc.date.available2021-11-22T15:25:15Z
dc.date.issued2021-11-03
dc.identifier.citationAging (Albany NY). 2021 Nov 3;13(21):23936-23952.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13459
dc.description.abstractEvidence suggests that aging-related dysfunctions of adipose tissue and metabolic disturbances increase the risk of diabetes and metabolic syndrome (MtbS), eventually leading to cognitive impairment and dementia. However, the neuroprotective role of adipocytokines in this process has not been specifically investigated. The present study aims to identify metabolic alterations that may prevent adipocytokines from exerting their neuroprotective action in normal ageing. We hypothesize that neuroprotection may occur under insulin resistance (IR) conditions as long as there are no other metabolic alterations that indirectly impair the action of adipocytokines, such as hyperglycemia. This hypothesis was tested in 239 cognitively normal older adults (149 females) aged 52 to 87 years (67.4 ± 5.9 yr). We assessed whether the homeostasis model assessment-estimated insulin resistance (HOMA-IR) and the presence of different components of MtbS moderated the association of plasma adipocytokines (i.e., adiponectin, leptin and the adiponectin to leptin [Ad/L] ratio) with cognitive functioning and cortical thickness. The results showed that HOMA-IR, circulating triglyceride and glucose levels moderated the neuroprotective effect of adipocytokines. In particular, elevated triglyceride levels reduced the beneficial effect of Ad/L ratio on cognitive functioning in insulin-sensitive individuals; whereas under high IR conditions, it was elevated glucose levels that weakened the association of the Ad/L ratio with cognitive functioning and with cortical thickness of prefrontal regions. Taken together, these findings suggest that the neuroprotective action of adipocytokines is conditioned not only by whether cognitively normal older adults are insulin-sensitive or not, but also by the circulating levels of triglycerides and glucose, respectively.es_ES
dc.description.sponsorshipThis work was supported by the Spanish Ministry of Economy and Competitiveness (PSI2017-85311-P to M.A., PSI2017-89389-C2-2-R to F.D., PID2020-118825GB-I00 to M.A., PID2020-119978RB-I00 to J.L.C.), CIBERNED (CB06/05/1111 to J.L.C.), the International Center on Aging CENIE-POCTEP (0348_CIE_6_E to M.A.), the Research Program for a Long-Life Society (0551_PSL_6_E to J.L.C.), the Junta de Andalucía (PY20_00858 to J.L.C.), the Andalucía-FEDER Program (UPO-1380913 to J.L.C.), and the Galician Government (ED431-2017/27 to F.D.) with ERDF/FEDER funds.es_ES
dc.language.isoenges_ES
dc.publisherImpact Journals es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectAdiponectines_ES
dc.subjectCognitive functiones_ES
dc.subjectCortical thicknesses_ES
dc.subjectLeptines_ES
dc.subjectMetabolismes_ES
dc.titleImpaired glucose metabolism reduces the neuroprotective action of adipocytokines in cognitively normal older adults with insulin resistancees_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID34731089es_ES
dc.format.volume13es_ES
dc.format.number21es_ES
dc.identifier.doi10.18632/aging.203668es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBER
dc.contributor.funderInternational Council on Active Aging 
dc.contributor.funderRegional Government of Andalusia (España) 
dc.contributor.funderXunta de Galicia (España) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1945-4589es_ES
dc.relation.publisherversionhttps://doi.org/10.18632/aging.203668es_ES
dc.identifier.journalAginges_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PSI2017-85311-Pes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PSI2017-89389-C2-2-Res_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PID2020-118825GB-I00es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PID2020-119978RB-I00es_ES


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