Xx. Han et A. Bonen, EPINEPHRINE TRANSLOCATES GLUT-4 BUT INHIBITS INSULIN-STIMULATED GLUCOSE-TRANSPORT IN RAT MUSCLE, American journal of physiology: endocrinology and metabolism, 37(4), 1998, pp. 700-707
We examined the effects of epinephrine (25, 50, and 150 nM) on 1) basa
l and insulin-stimulated S-O-methylglucose (3-MG) transport in perfuse
d rat muscles and 2) GLUT-4 in skeletal muscle plasma membranes. Insul
in increased glucose transport 330-600% in three types of skeletal mus
cle [white (WG) and red (RG) gastrocnemius and soleus (SOL)]. Glucose
transport was also increased by epinephrine (22-48%) in these muscles
(P < 0.05). In contrast, the insulin-stimulated 3-MG transport was red
uced by epinephrine in all three types of muscles; maximal reductions
were observed at 25 nM epinephrine in WG (-25%) and RG (-32.5%). A dos
e-dependent decrease occurred in SOL (-27% at 25 nM; -55% at 150 nM, P
< 0.05). Insulin (20 mU/ml) and epinephrine (150 nM) each translocate
d GLUT-4 to the plasma membrane, and no differences in translocation w
ere observed between insulin and epinephrine (P > 0.05). In addition,
epinephrine did not inhibit insulin-stimulated GLUT-4 translocation, a
nd the combined epinephrine and insulin effects on GLUT-4 translocatio
n were not additive. The increase in surface GLUT-4 was associated wit
h increases in muscle cAMP concentrations, but only when epinephrine a
lone was present. No relationship was evident between muscle cAMP conc
entrations and surface GLUT-4 in the combined epinephrine and insulin-
stimulated muscles. These studies indicate that epinephrine can transl
ocate GLUT-4 while at the same time increasing glucose transport when
insulin is absent, or can inhibit glucose transport when insulin is pr
esent.