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Leptin Resistance and the Neuro-Adipose Connection

dc.contributor.authorBarateiro, Andreia
dc.contributor.authorMahú, Ines
dc.contributor.authorDomingos, Ana I.
dc.date.accessioned2017-03-24T18:32:17Z
dc.date.available2017-03-24T18:32:17Z
dc.date.issued2017-03-06
dc.descriptionThis article was submitted to Cellular Endocrinology, a section of the journal Frontiers in Endocrinology.pt_PT
dc.description.abstractObesity is a public health concern affecting both genders at all ages around the world. The worldwide prevalence of obesity is rapidly increasing and has nearly doubled between 1980 and 2016. Consequently, it places a large financial burden on the economy due to the increased morbidity and mortality, as well as the reduced quality of life and development of chronic diseases. Obesity is typically characterized by excessive amounts of the hormone leptin, a cytokine-like molecule produced in white adipose tissue (WAT) that is secreted into the systemic circulation. The circulating levels of leptin are proportional to the amount of fat and function as the afferent signal in a negative feedback loop that seeks to maintain body fat in a very narrow range of variation. Leptin has a central role in body weight homeostasis due to its inhibition of food intake inhibition and stimulation of energy expenditure. The effect of leptin on body weight is attributed to its action in a specific brain region, the hypothalamus. Hence, leptin is released by adipocytes in proportion to the size of fat depots, enters the circulation, and reaches the central nervous system by crossing the blood-brain barrier (BBB) through receptor-mediated endocytosis in which it acts mainly through the arcuate nucleus of the hypothalamus to mediate most of its actions. Specifically, leptin modulates the activity of two types of neurons to inhibit appetite, through production of anorexigenic peptides by the pro-opiomelanocortin (POMC) neurons and suppression of the orexigenic agouti-related protein (AgRP) neurons. Besides acting on the hypothalamus to suppress appetite, leptin also induces lipolysis in WAT and thermogenesis in brown adipose tissue (BAT) and browning of WAT, via the activation of the sympathetic nervous system (SNS). However, in most obese subjects, despite its high serum levels, leptin fails to perform its physiological functions and consequently fails to reduce weight. This effect has been coined as leptin resistance.pt_PT
dc.description.sponsorshipFundação para Ciência e Tecnologia grants: (PD/BD/52437/2013, PTDC-BIM-MET-3750-2014); EMBO grant: (IG3077); Prémios Maratona Saúde 2015: (Diabetes); Human Frontiers Science Program grant:(RGY0070/2016).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationBarateiro A, Mahú I and Domingos AI (2017) Leptin Resistance and the Neuro-Adipose Connection. Front. Endocrinol. 8:45. doi: 10.3389/fendo.2017.00045pt_PT
dc.identifier.doi10.3389/fendo.2017.00045pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/740
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherFrontiers Mediapt_PT
dc.relationTE ROLE OF S100B IN MULTIPLE SCLEROSIS: FROM A BIOMARKER TO A THERAPEUTIC TARGET
dc.relation.publisherversionhttp://journal.frontiersin.org/article/10.3389/fendo.2017.00045/fullpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectleptin resistancept_PT
dc.subjectmetabolic syndromept_PT
dc.subjectMONA LISA hypothesispt_PT
dc.subjectobesitypt_PT
dc.subjectsympathetic neuronspt_PT
dc.titleLeptin Resistance and the Neuro-Adipose Connectionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleTE ROLE OF S100B IN MULTIPLE SCLEROSIS: FROM A BIOMARKER TO A THERAPEUTIC TARGET
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBPD%2F96794%2F2013/PT
oaire.citation.endPage4pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleFrontiers in Endocrinologypt_PT
oaire.citation.volume8pt_PT
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublicationc20cdf6d-d9d6-4eb6-8db5-473da1dd5574
relation.isProjectOfPublication.latestForDiscoveryc20cdf6d-d9d6-4eb6-8db5-473da1dd5574

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