Acute physical exercise increases leptin-induced hypothalamic extracellular signal-regulated kinase1/2 phosphorylation and thermogenesis of obese mice

Autor(es):Mostrar menos -

Gaspar, Rafael Calais ^[1] ; Munoz, Vitor Rosetto ^[1] ; Kuga, Gabriel Keine ^[2] ; Branco Ramos Nakandakari, Susana Castelo ^[3] ; Minuzzi, Luciele Guerra ^{[1, 4]} ; Botezelli, Jose Diego ^[1] ; da Silva, Adelino S. R. ^[5] ; Cintra, Dennys Esper ^{[6, 3]} ; de Moura, Leandro Pereira ^{[7, 6, 1, 3]} ; Ropelle, Eduardo Rochete ^{[7, 6, 1]} ; Pauli, Jose Rodrigo ^{[7, 6, 1]}

Afiliação do(s) autor(es)

^[1] Univ Campinas UNICAMP, Lab Mol Biol Exercise LaBMEx, Limeira, SP - Brazil

^[2] Sao Paulo State Univ UNESP, Dept Phys Educ, Postgrad Program Movement Sci, Rio Claro, SP - Brazil

^[3] Univ Campinas UNICAMP, Lab Nutr Genom LabGeN, Limeira, SP - Brazil

^[4] Univ Coimbra, Fac Sports Sci & Phys Educ, Res Ctr Sport & Phys Activ IUD DTP 04213 2016, Coimbra - Portugal

^[5] Univ Sao Paulo, Sch Phys Educ & Sports Ribeirao Preto, Ribeirao Preto Med Sch, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP - Brazil

^[6] Univ Estadual Campinas, OCRC, Lab Cell Signaling, Campinas, SP - Brazil

^[7] Univ Campinas UNICAMP, Sch Appl Sci, CEPECE Ctr Res Sport Sci, Limeira, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Cellular Biochemistry; v. 120, n. 1, p. 697-704, JAN 2019.
• Citações Web of Science: 1

Resumo

The obesity is a result of energy imbalance and the increase in thermogenesis seems an interesting alternative for the treatment of this disease. The mechanism of energy expenditure through thermogenesis is tightly articulated in the hypothalamus by leptin. The hypothalamic extracellular signal-regulated kinase-1/2 (ERK1/2) is a key mediator of the thermoregulatory effect of leptin and mediates the sympathetic signal to the brown adipose tissue (BAT). In this context, physical exercise is one of the main interventions for the treatment of obesity. Thus, this study aimed to verify the effects of acute physical exercise on leptin-induced hypothalamic ERK1/2 phosphorylation and thermogenesis in obese mice. Here we showed that acute physical exercise reduced the fasting glucose of obese mice and increased leptin-induced hypothalamic p-ERK1/2 and uncoupling protein 1 (UCP1) content in BAT (P < 0.05). These molecular changes are accompanied by an increased oxygen uptake (VO2) and heat production in obese exercised mice (P < 0.05). The increased energy expenditure in the obese exercised animals occurred independently of changes in spontaneous activity. Thus, this is the first study demonstrating that acute physical exercise can increase leptin-induced hypothalamic ERK1/2 phosphorylation and energy expenditure of obese mice. (AU)

• Processo FAPESP: 16/18488-8 - O papel do exercício físico nas vias moleculares de captação de glicose em camundongos nocautes para GLUT-4
• Beneficiário: José Rodrigo Pauli
• Modalidade de apoio: Auxílio à Pesquisa - Regular