Cited by 21Regulation of Appetite and ObesityAdipose Tissue and MetabolismAdipokines, Inflammation, and Metabolic Diseases

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

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Gaspar, Rafael Calais, Muñoz, Vitor Rosetto, Kuga, Gabriel Keine, Nakandakari, Susana Castelo Branco Ramos, Minuzzi, Luciele Guerra, Botezelli, José Diego, da Silva, Adelino S.R., Cintra, Dennys Esper +3 more·2019·Journal of Cellular Biochemistry

Abstract

Abstract 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 (VO 2) 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.

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Crossref · 10.1002/jcb.27426

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Authors
Gaspar, R. C., Muñoz, V. R., Kuga, G. K., Nakandakari, S. C. B. R., Minuzzi, L. G., Botezelli, J. D., da Silva, A. S. R., Cintra, D. E., de Moura, L. P., Ropelle, E. R., & Pauli, J. R.
Affiliations
  • Universidade Estadual de Campinas (UNICAMP) (BR)
  • Laboratory of Molecular Biology of Exercise (LaBMEx) University of Campinas (UNICAMP) Limeira São Paulo Brazil
  • Universidade Estadual Paulista (Unesp) (BR)
  • School of Physical Education and Sports of Ribeirão Preto Post‐graduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, USP Ribeirão Preto São Paulo Brazil
Corresponding author
Pauli, José Rodrigo
Venue
Journal of Cellular Biochemistry
Publisher
Wiley
Published
2018-09-11
Volume
120
Issue
1
Pages
697-704
ISSN
  • 0730-2312 (ISSN-L)
  • 1097-4644
OpenAlex
W2890910766
Cited by
21
References
27
Citations by year
2026: 1 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 6 · 2020: 3 · 2019: 3
FWCI
1.69
Type
journal article
Language
en
Open access
Locations
  • Journal of Cellular Biochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
  • UNESP Institutional Repository (São Paulo State University) (submittedVersion)
Funders
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (306535/2017‐3)
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2016/18488‐8OCRC)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
acute exercise, leptin, ERK1/2 phosphorylation, hypothalamus, thermogenesis, obesity, brown adipose tissue, UCP1, energy expenditure, oxygen consumption, fasting blood glucose
MeSH terms
Uncoupling Protein 1, Animals, Body Weight, Adipose Tissue, Brown, Energy Metabolism, Hypothalamus, Injections, Intraperitoneal, Mice, Obese, Obesity, Oxygen Consumption, Phosphorylation, Physical Conditioning, Animal, Leptin, MAP Kinase Signaling System, Thermogenesis, Mice, Diet, High-Fat

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