Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca(2+) release

Understanding how muscle contraction orchestrates insulin-independent muscle glucose transport may enable development of hyperglycemia-treating drugs. The prevailing concept implicates Ca(2+) as a key feed forward regulator of glucose transport with secondary fine-tuning by metabolic feedback signal...

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Detalles Bibliográficos
Autores principales: Jensen, Thomas E., Sylow, Lykke, Rose, Adam J., Madsen, Agnete B., Angin, Yeliz, Maarbjerg, Stine J., Richter, Erik A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2014
Materias:
Original Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209358/
https://www.ncbi.nlm.nih.gov/pubmed/25353002
http://dx.doi.org/10.1016/j.molmet.2014.07.005

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209358/
https://www.ncbi.nlm.nih.gov/pubmed/25353002
http://dx.doi.org/10.1016/j.molmet.2014.07.005

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