Acute exercise reduces feeding by activating IL-6/Tubby axis in the mouse hypothalamus

• Autor(a) principal: de Oliveira Micheletti, Thayana
• Data de Publicação: 2022
• Outros Autores: Cassia dos Santos, Andressa, Rocha, Guilherme Zweig, Silva, Vagner Ramon Rodrigues, Quaresma, Paula Gabriele Fernandes, Assalin, Heloisa Balan, Junqueira, Felipe Silva, Ropelle, Eduardo Rochete, Oliveira, Alexandre Gabarra [UNESP], Saad, Mario Jose Abdalla, Prada, Patricia de Oliveira
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.3389/fphys.2022.956116; http://hdl.handle.net/11449/246391
• topic: exercise; food intake; hypothalamus; IL-6; JAK2; Tubby mouse

Background: Acute exercise contributes to decreased feeding through leptin and interleukin/Janus kinase 2/signal transducers and activators of transcription 3 (IL-6/JAK2/STAT3) signaling. Considering the pleiotropic use of substrates by JAK2 and that JAK2 can phosphorylate the Tubby protein (TUB) in CHO-IR cells, we speculated that acute exercise can activate the IL-6/JAK2/TUB pathway to decrease food intake. Aims: We investigated whether acute exercise induced tyrosine phosphorylation and the association of TUB and JAK2 in the hypothalamus and if IL-6 is involved in this response, whether acute exercise increases the IL-6/TUB axis to regulate feeding, and if leptin has an additive effect over this mechanism. Methods: We applied a combination of genetic, pharmacological, and molecular approaches. Key findings: The in vivo experiments showed that acute exercise increased the tyrosine phosphorylation and association of JAK2/TUB in the hypothalamus, which reduced feeding. This response was dependent on IL-6. Leptin had no additive effect on this mechanism. Significance: The results of this study suggest a novel hypothalamic pathway by which IL-6 released by exercise regulates feeding and reinforces the beneficial effects of exercise.