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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Effected of insulin and insulin-like growth factor-I on glucose transport and its transporters in soleus muscle of lean and obese mice.

The mechanisms underlying insulin and insulin-like growth factor-I (IGF-I) action on glucose transport share similar processes leading to Glut 4 translocation after respective receptor activation. Among these steps are phosphorylation of insulin receptor substrate-1 (IRS-1) and activation of phosphatidylinositol-3-kinase (P13-kinase). This enzyme could be involved in stimulated glucose transport in muscle, since its inhibitor, wortmannin, blocks the hormonal effect in muscle. P13-kinase is activated by insulin and IGF-I in a rapid and transient manner in incubated soleus muscles. When P13-kinase activation was studied in muscle of obese insulin-resistant mice, there was a marked alteration in the response to insulin both in vivo and in vitro. P13-kinase activation by IGF-I was also altered in obese mice, although to a lesser degree.[1]

References

  1. Effected of insulin and insulin-like growth factor-I on glucose transport and its transporters in soleus muscle of lean and obese mice. Le Marchand-Brustel, Y., Heydrick, S.J., Jullien, D., Gautier, N., Van Obberghen, E. Metab. Clin. Exp. (1995) [Pubmed]
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