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2006-08-04

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cc-by (c) Cantó et al. , 2006
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/205902

Neuregulins mediate calcium-induced glucose transport during muscle contraction

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Recurs relacionat

https://doi.org/10.1074/jbc.M600475200

Resum

Neuregulin, a growth factor involved in myogenesis, has rapid effects on muscle metabolism. In a manner analogous to insulin and exercise, neuregulins stimulate glucose transport through recruitment of glucose transporters to surface membranes in skeletal muscle. Like muscle contraction, neuregulins have additive effects with insulin on glucose uptake. Therefore, we examined whether neuregulins are involved in the mechanism by which muscle contraction regulates glucose transport. We show that caffeine-induced increases in cytosolic Ca2+ mediate a metalloproteinase-dependent release of neuregulins, which stimulates tyrosine phosphorylation of ErbB4 receptors. Activation of ErbB4 is necessary for Ca2+-derived effects on glucose transport. Furthermore, blockage of ErbB4 abruptly impairs contraction-induced glucose uptake in slow twitch muscle fibers, and to a lesser extent, in fast twitch muscle fibers. In conclusion, we provide evidence that contraction-induced activation of neuregulin receptors is necessary for the stimulation of glucose transport and a key element of energetic metabolism during muscle contraction.

Matèries

Factors de creixement, Miogènesi, Contracció muscular, Glucosa

Matèries (anglès)

Growth factors, Myogenesis, Muscle contraction, Glucose

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Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

Citació

CANTÓ, Carles, CHIBALIN, Alexander v., BARNES, Brian r., GLUND, Stephan, SUÁREZ, Elisabet, RYDER, Jeffrey w., PALACÍN PRIETO, Manuel, ZIERATH, Juleen r., ZORZANO OLARTE, Antonio, GUMÀ I GARCIA, Anna maria. Neuregulins mediate calcium-induced glucose transport during muscle contraction. _Journal of Biological Chemistry_. 2006. Vol. 281, núm. 31, pàgs. 21690-21697. [consulta: 21 de gener de 2026]. ISSN: 0021-9258. [Disponible a: https://hdl.handle.net/2445/205902]

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