Central leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weight

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dc.contributor.authorBassi, Mirian [UNESP]
dc.contributor.authorGiusti, Humberto
dc.contributor.authorLeite, Cristiane Mota
dc.contributor.authorAnselmo-Franci, Janete A.
dc.contributor.authordo Carmo, Jussara M.
dc.contributor.authorda Silva, Alexandre A.
dc.contributor.authorHall, John E.
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.authorGlass, Mogens L.
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversity of Mississippi
dc.date.accessioned2014-05-20T13:46:10Z
dc.date.available2014-05-20T13:46:10Z
dc.date.issued2012-08-01
dc.description.abstractPrevious studies showed that leptin-deficient (ob/ob) mice develop obesity and impaired ventilatory responses to CO2 . In this study, we examined if leptin replacement improves chemorespiratory responses to hypercapnia (7 % CO2) in ob/ob mice and if these effects were due to changes in body weight or to the direct effects of leptin in the central nervous system (CNS). was measured via plethysmography in obese leptin-deficient- (ob/ob) and wild-type- (WT) mice before and after leptin (10 mu g/2 mu l day) or vehicle (phosphate buffer solution) were microinjected into the fourth ventricle for four consecutive days. Although baseline was similar between groups, obese ob/ob mice exhibited attenuated compared to WT mice (134 +/- 9 versus 196 +/- 10 ml min(-1)). Fourth ventricle leptin treatment in obese ob/ob mice significantly improved (from 131 +/- 15 to 197 +/- 10 ml min(-1)) by increasing tidal volume (from 0.38 +/- 0.03 to 0.55 +/- 0.02 ml, vehicle and leptin, respectively). Subcutaneous leptin administration at the same dose administered centrally did not change in ob/ob mice. Central leptin treatment in WT had no effect on . Since the fourth ventricle leptin treatment decreased body weight in ob/ob mice, we also examined in lean pair-weighted ob/ob mice and found it to be impaired compared to WT mice. Thus, leptin deficiency, rather than obesity, is the main cause of impaired in ob/ob mice and leptin appears to play an important role in regulating chemorespiratory response by its direct actions on the CNS.en
dc.description.affiliationSão Paulo State Univ, Sch Dent, Dept Physiol & Pathol, UNESP, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Sch Med Ribeiro Preto, Dept Physiol, BR-14801903 São Paulo, Brazil
dc.description.affiliationUniv Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA
dc.description.affiliationUnespSão Paulo State Univ, Sch Dent, Dept Physiol & Pathol, UNESP, São Paulo, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipNIH
dc.description.sponsorshipIdFAPESP: 04/01934-8
dc.description.sponsorshipIdCNPq: 141227/04-4
dc.description.sponsorshipIdNIH: PO1HL51971
dc.format.extent145-153
dc.identifierhttp://dx.doi.org/10.1007/s00424-012-1111-1
dc.identifier.citationPflugers Archiv-european Journal of Physiology. New York: Springer, v. 464, n. 2, p. 145-153, 2012.
dc.identifier.doi10.1007/s00424-012-1111-1
dc.identifier.issn0031-6768
dc.identifier.lattes4544450092427426
dc.identifier.urihttp://hdl.handle.net/11449/16319
dc.identifier.wosWOS:000306337900002
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofPflugers Archiv: European Journal of Physiology
dc.relation.ispartofjcr2.765
dc.relation.ispartofsjr1,479
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectRespiratory chemoreceptionen
dc.subjectObesityen
dc.subjectHypercapniaen
dc.subjectLeptinen
dc.subjectVentilationen
dc.titleCentral leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weighten
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dcterms.rightsHolderSpringer
unesp.author.lattes4544450092427426[8]
unesp.author.orcid0000-0002-1395-4036[8]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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