Abstract:
:Insulin stimulated protein kinase B alpha (PKB alpha) more than 10-fold and decreased glycogen synthase kinase-3 (GSK3) activity by 50 +/- 10% in skeletal muscle and adipocytes. Rapamycin did not prevent the activation of PKB, inhibition of GSK3 or stimulation of glycogen synthase up to 5 min. Thus rapamycin-insensitive pathways mediate the acute effect of insulin on glycogen synthase in the major insulin-responsive tissues. The small and very transient effects of EGF on phosphatidylinositol (3,4,5)P3 PKB alpha and GSK3 in adipocytes, compared to the strong and sustained effects of insulin, explains why EGF does not stimulate glucose uptake or glycogen synthesis in adipocytes.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Cross DA,Watt PW,Shaw M,van der Kaay J,Downes CP,Holder JC,Cohen Pdoi
10.1016/s0014-5793(97)00240-8subject
Has Abstractpub_date
1997-04-07 00:00:00pages
211-5issue
1-2eissn
0014-5793issn
1873-3468pii
S0014579397002408journal_volume
406pub_type
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