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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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Main Authors: | , , , , , , |
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Formáid: | Artigo |
Teanga: | Inglês |
Foilsithe: |
Elsevier
2014
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Ábhair: | |
Rochtain Ar Líne: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4209358/ https://ncbi.nlm.nih.gov/pubmed/25353002 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.molmet.2014.07.005 |
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