IGF-I and insulin induce different intracellular calcium signals in skeletal muscle cells

Espinosa, A.; Estrada, M; Jaimovich E.

Abstract

We studied the effect of IGF-I and insulin on intracellular Ca2+ in primary cultured myotubes. IGF-I induced a fast and transient Ca2+ increase, measured as fluo-3 fluorescence. This response was blocked by both genistein and AG538. IGF-I induced a fast inositol-1,4,5-trisphosphate (IP3) increase, kinetically similar to the Ca2+ rise. The Ca2+ signal was blocked by inhibitors of the IP3 pathway. On the other hand, insulin produced a fast (<1 s) and transient Ca2+ increase. Insulin-induced Ca2+ increase was blocked in Ca2+-free medium and by either nifedipine or ryanodine. In the normal muscle NLT cell line, the Ca2+ signals induced by both hormones resemble those of primary myotubes. GLT cells, lacking the ?1-subunit of dihydropyridine receptor (DHPR), responded to IGF-I but not to insulin, while GLT cells transfected with the ? 1-subunit of DHPR reacted to both hormones. Moreover, dyspedic muscle cells, lacking ryanodine receptors, responded to IGF-I as NLT cells, however they show no insulin-induced calcium increase. Moreover, G-protein inhibitors, pertussis toxin (PTX) and GDP?S, blocked the insulin-induced Ca2+ increase without major modification of the response to IGF-I. The different intracellular Ca2+ patterns produced by IGF-I and insulin may improve our understanding of the early action mechanisms for these hormones in skeletal muscle cells. © 2004 Society for Endocrinology.

Más información

Título según WOS: IGF-I and insulin induce different intracellular calcium signals in skeletal muscle cells
Título según SCOPUS: IGF-I and insulin induce different intracellular calcium signals in skeletal muscle cells
Título de la Revista: JOURNAL OF ENDOCRINOLOGY
Volumen: 182
Número: 2
Editorial: BioScientifica Ltd.
Fecha de publicación: 2004
Página de inicio: 339
Página final: 352
Idioma: English
URL: http://joe.endocrinology-journals.org/cgi/doi/10.1677/joe.0.1820339
DOI:

10.1677/joe.0.1820339

Notas: ISI, SCOPUS