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Insulin resistance: a new consequence of altered carotid body chemoreflex?

2017Journal article Open access
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datacite.subject.sdg03:Saúde de Qualidade
datacite.subject.sdg04:Educação de Qualidade
datacite.subject.sdg17:Parcerias para a Implementação dos Objetivos
dc.contributor.authorConde, Silvia V.
dc.contributor.authorRibeiro, Maria J.
dc.contributor.authorMelo, Bernardete F.
dc.contributor.authorGuarino, Maria P.
dc.contributor.authorSacramento, Joana F.
dc.date.accessioned2026-01-21T11:18:44Z
dc.date.available2026-01-21T11:18:44Z
dc.date.issued2017
dc.description.abstractMetabolic diseases affect millions of individuals across the world and represent a group of chronic diseases of very high prevalence and relatively low therapeutic success, making them suitable candidates for pathophysiological studies. The sympathetic nervous system (SNS) contributes to the regulation of energy balance and energy expenditure both in physiological and pathological states. For instance, drugs that stimulate sympathetic activity decrease food intake, increase resting metabolic rate and increase the thermogenic response to food, while pharmacological blockade of the SNS has opposite effects. Likewise, dysmetabolic features such as insulin resistance, dyslipidaemia and obesity are characterized by a basal overactivation of the SNS. Recently, a new line of research linking the SNS to metabolic diseases has emerged with the report that the carotid bodies (CBs) are involved in the development of insulin resistance. The CBs are arterial chemoreceptors that classically sense changes in arterial blood O2 , CO2 and pH levels and whose activity is known to be increased in rodent models of insulin resistance. We have shown that selective bilateral resection of the nerve of the CB, the carotid sinus nerve (CSN), totally prevents diet-induced insulin resistance, hyperglycaemia, dyslipidaemia, hypertension and sympathoadrenal overactivity. These results imply that the beneficial effects of CSN resection on insulin action and glucoregulation are modulated by target-related efferent sympathetic nerves through a reflex that is initiated in the CBs. It also highlights modulation of CB activity as a putative future therapeutic intervention for metabolic diseases.eng
dc.description.sponsorshipJ.F.S. and M.J.R. are supported by PhD Grants from the Portuguese Foundation for Science and Technology (FCT), PD/BD/105890/2014 and SFR/BD/88983/2012, respectively.
dc.identifier.citationConde SV, Ribeiro MJ, Melo BF, Guarino MP, Sacramento JF. Insulin resistance: a new consequence of altered carotid body chemoreflex? J Physiol. 2017 Jan 1;595(1):31-41. doi: 10.1113/JP271684. Epub 2016 Jun 27. PMID: 27027507; PMCID: PMC5199745
dc.identifier.doi10.1113/jp271684
dc.identifier.issn0022-3751
dc.identifier.issn1469-7793
dc.identifier.urihttp://hdl.handle.net/10400.8/15433
dc.language.isoeng
dc.peerreviewedyes
dc.publisherWiley
dc.relationModulation of carotid body activity as a therapeutic intervention in metabolic diseases.
dc.relationSFR/BD/88983/2012
dc.relation.hasversionhttps://physoc.onlinelibrary.wiley.com/journal/14697793
dc.relation.ispartofThe Journal of Physiology
dc.rights.uriN/A
dc.titleInsulin resistance: a new consequence of altered carotid body chemoreflex?eng
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleModulation of carotid body activity as a therapeutic intervention in metabolic diseases.
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//PD%2FBD%2F105890%2F2014/PT
oaire.citation.endPage41
oaire.citation.issue1
oaire.citation.startPage31
oaire.citation.titleThe Journal of Physiology
oaire.citation.volume595
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
person.familyNameGuarino
person.givenNameMaria Pedro
person.identifier.ciencia-idF21A-BD01-2D52
person.identifier.orcid0000-0001-6079-1105
person.identifier.ridB-5594-2015
person.identifier.scopus-author-id56348477000
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
relation.isAuthorOfPublicationf163d4df-1e45-4278-affa-5994f206becf
relation.isAuthorOfPublication.latestForDiscoveryf163d4df-1e45-4278-affa-5994f206becf
relation.isProjectOfPublication8d184299-84d1-4918-9ab6-1ae18bb57139
relation.isProjectOfPublication.latestForDiscovery8d184299-84d1-4918-9ab6-1ae18bb57139

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