Moderate Exercise Reduces Food Consumption in Obese Mice for Activate Jak-2/Stat-3 Pathway in the Hypothalami

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dc.contributor.authorMoura, Leandro P. [UNESP]
dc.contributor.authorMarinho, Rodolfo [UNESP]
dc.contributor.authorRopelle, Eduardo R.
dc.contributor.authorCintra, Dennys E.
dc.contributor.authorSouza, Claudio T.
dc.contributor.authorSilva, Adelino S.
dc.contributor.authorRodrigues, Barbara A.
dc.contributor.authorPauli, Luciana S.
dc.contributor.authorPauli, Jose Rodrigo
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniv Extreme South Santa Catarina
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2015-03-18T15:56:00Z
dc.date.available2015-03-18T15:56:00Z
dc.date.issued2014-05-01
dc.description.abstractIt is very known that due to inflammatory processes the obesity leads to resistance to leptin, it reduces phosphorylation via JAK-2/STAT-3, which generates lower STAT-3 activity in the cell nucleus, and it leads to decrease the number of transcription of anorexigenic neurons (POMC/CART) and allowing transcription of orexigenic (NPY/AgRP). PURPOSE: The present study aimed to evaluate the effects of moderate aerobic training on food intake of obese mice through analysis of activity of hypothalamic proteins JAK-2/STAT-3. METHODS: It were used 30 Swiss mice (30 days old) divided into 3 groups: Control Group (C): sedentary animals fed with balanced diet ; Obese (OB) sedentary animals fed with high-fat diet throughout the experiment and Trained Obese (TOB) : animals fed with high fat diet throughout the experiment , kept sedentary during the first half of the experiment (8 weeks) and submitted to physical training protocol during the second half of the experiment (8 weeks). The exercise program consisted of treadmill running 1h, 5 days/week during 8 weeks at a speed equivalent to 60 % of maximum potency determined at the beginning of training period. To assess the leptin resistance, after rats were deprived of food for 6h with free access to water, they received i.p injection with leptin (2.0µl, 10-6M), after this, the chow was returned and food intake was determined by measuring the quantity and Kcal consumed at the end of 2h. The hypothalami was removed for determination of JAK-2 and STAt-3 activity. RESULTS: Our results showed that moderate physical exercise was effective in improving the JAK/STAT signaling pathway in the hypothalamus of obese animals. This has made these obese animals had reduced food intake and consequently lower body mass gain. CONCLUSION: It can be concluded that physical exercise, for restoring leptin signaling in the hypothalamus, controls the synthesis of neurons responsible for appetite and thus is an important tool in the treatment of obesity.
dc.description.affiliationSao Paulo State Univ, UNESP, Rio Claro, Brazil
dc.description.affiliationUniv Estadual Campinas, Limeira, Brazil
dc.description.affiliationUniv Extreme South Santa Catarina, Criciuma, Brazil
dc.description.affiliationUniv Sao Paulo, BR-14049 Ribeirao Preto, Brazil
dc.description.affiliationUnespSao Paulo State Univ, UNESP, Rio Claro, Brazil
dc.format.extent631-631
dc.identifierhttp://dx.doi.org/10.1249/01.mss.0000451232.86798.fb
dc.identifier.citationMedicine And Science In Sports And Exercise. Philadelphia: Lippincott Williams & Wilkins, v. 46, n. 5, p. 631-631, 2014.
dc.identifier.doi10.1249/01.mss.0000451232.86798.fb
dc.identifier.issn0195-9131
dc.identifier.urihttp://hdl.handle.net/11449/117379
dc.identifier.wosWOS:000339115904164
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofMedicine And Science In Sports And Exercise
dc.relation.ispartofjcr4.291
dc.relation.ispartofsjr2,073
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.titleModerate Exercise Reduces Food Consumption in Obese Mice for Activate Jak-2/Stat-3 Pathway in the Hypothalamien
dc.typeResumo
dcterms.rightsHolderLippincott Williams & Wilkins
unesp.author.orcid0000-0003-1655-9557[3]
unesp.author.orcid0000-0002-9679-8357[6]
unesp.author.orcid0000-0002-1751-8485[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt

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