Author(s):
Gaspar, Rafael Calais, 1992- ; Muñoz, Vitor Rosetto, 1993- ; Nakandakari, Susana Castelo Branco Ramos ; Minuzzi, Luciele Guerra ; Botezelli, José Diego ; Cintra, Dennys Esper, 1976- ; Moura, Leandro Pereira de, 1985- ; Chiarreotto-Ropelle, Eloize Cristina, 1978- ; Pauli, José Rodrigo, 1979-
Date: 2019
Persistent ID: https://hdl.handle.net/20.500.12733/1643070
Origin: Oasisbr
Subject(s): Termogênese; Obesidade - Tratamento; Tecido adiposo marrom; Hipotálamo; Adipose tissue, brown; Hypothalamus; Obesity - Treatment; Thermogenesis; Extracellular signal-regulated kinase-1/2 (ERK1/2); Physical exercise; UCP1; Artigo de pesquisa
Description
Agradecimentos: The authors thank Obesity and Comorbidities Research Center – OCRC and FAPESP (2016/18488-8) and CNPq (306535/2017-3) for all support during the experiment
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?
Resumo:
CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQ
FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP
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