I. Yokota et al., EFFECT OF GROWTH-HORMONE ON THE TRANSLOCATION OF GLUT4 AND ITS RELATION TO INSULIN-LIKE AND ANTIINSULIN ACTION, Biochimica et biophysica acta. Molecular cell research, 1404(3), 1998, pp. 451-456
To elucidate the effect of growth hormone (GH) on the insulin signal t
ransduction pathway leading to the translocation of glucose transporte
r-4 (GLUT4), we constructed Chinese hamster ovary cells that overexpre
ssed GH receptor and GLUT4. Treatment with GH triggered GLUT4 transloc
ation, and this translocation was completely inhibited by wortmannin.
GH-induced GLUT4 translocation reached a maximum level after 30 min, a
nd then gradually decreased and returned to the basal level after 2 h.
Tyrosine phosphorylation of JAK2 also became maximal after 30 min and
then gradually decreased. In contrast, GLUT4 translocation remained u
nchanged for 2 h after insulin treatment, and tyrosine phosphorylation
of insulin receptor substrate-1 (IRS-1) also remained constant for up
to 2 h. Chronic GH treatment had almost no effect on insulin-stimulat
ed Akt kinase activation and GLUT4 translocation. These results sugges
t that GH and insulin translocate GLUT4 in a similar manner, at least
in part, and the difference in translocation depends on the difference
in the tyrosine phosphorylation of JAK2 and IRS-1. The anti-insulin a
ction of GH after chronic GH treatment does not appear to be mainly du
e to the inhibition of GLUT4 translocation. 0167-4889/98/$ - see front
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