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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...
Tallennettuna:
| Päätekijät: | , , , , , , |
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| Aineistotyyppi: | Artigo |
| Kieli: | Inglês |
| Julkaistu: |
Elsevier
2014
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| Aiheet: | |
| Linkit: | 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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