Artigo Acesso aberto Revisado por pares

Nesfatin-1 in Human and Murine Cardiomyocytes: Synthesis, Secretion, and Mobilization of GLUT-4

2013; Oxford University Press; Volume: 154; Issue: 12 Linguagem: Inglês

10.1210/en.2013-1497

ISSN

1945-7170

Autores

Sandra Feijóo‐Bandín, Diego Rodríguez‐Penas, Vanessa García‐Rúa, Ana Mosquera‐Leal, Manuel Otero, Eva Campos Pereira, José Antonio Rubio, Isabel Martínez‐Alcalá, Luísa M. Seoane, Oreste Gualillo, Manuel Calaza, Tomás García‐Caballero, Manuel Portolés, Esther Roselló‐Lletí, Carlos Diéguez, Miguel Rivera, José Ramón González–Juanatey, Francisca Lago,

Tópico(s)

Metabolism, Diabetes, and Cancer

Resumo

Nesfatin-1, a satiety-inducing peptide identified in hypothalamic regions that regulate energy balance, is an integral regulator of energy homeostasis and a putative glucose-dependent insulin coadjuvant. We investigated its production by human cardiomyocytes and its effects on glucose uptake, in the main cardiac glucose transporter GLUT-4 and in intracellular signaling. Quantitative RT-PCR, Western blots, confocal immunofluorescence microscopy, and ELISA of human and murine cardiomyocytes and/or cardiac tissue showed that cardiomyocytes can synthesize and secrete nesfatin-1. Confocal microscopy of cultured cardiomyocytes after GLUT-4 labeling showed that nesfatin-1 mobilizes this glucose transporter to cell peripherals. The rate of 2-deoxy-d-[3H]glucose incorporation demonstrated that nesfatin-1 induces glucose uptake by HL-1 cells and cultured cardiomyocytes. Nesfatin-1 induced dose- and time-dependent increases in the phosphorylation of ERK1/2, AKT, and AS160. In murine and human cardiac tissue, nesfatin-1 levels varied with diet and coronary health. In conclusion, human and murine cardiomyocytes can synthesize and secrete nesfatin-1, which is able to induce glucose uptake and the mobilization of the glucose transporter GLUT-4 in these cells. Nesfatin-1 cardiac levels are regulated by diet and coronary health.

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