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Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles, California 90089-9142
To examine whether growth hormone (GH) induces
peripheral insulin resistance by altering plasma free fatty acid (FFA)
or insulin levels, the effects of GH infusion on insulin-stimulated
glucose fluxes were studied in conscious rats under two protocols. In study 1, either saline
(n = 7) or human recombinant GH (21 µg · kg
1 · h1;
n = 8) was infused for 300 min, and
insulin-stimulated glucose fluxes were estimated during the final
150-min period of hyperinsulinemic euglycemic clamps. In
study 2, hyperinsulinemic euglycemic
clamps were first conducted for 150 min (to raise plasma insulin and suppress FFA levels), and saline or GH
(n = 7 for each) was subsequently infused for the following 300-min clamp period. In
study 1, GH infusion in the basal
state did not significantly alter plasma FFA or insulin levels. In
contrast, GH infusion decreased insulin-stimulated glucose uptake,
glycolysis, and glycogen synthesis by 32, 27, and 40%, respectively
(P < 0.05). In
study 2, GH infusion during hyperinsulinemic euglycemic clamps did not alter plasma FFA or insulin
levels (P > 0.05). GH infusion had
no effect on insulin-stimulated glucose uptake during the initial 150 min but eventually decreased insulin-stimulated glucose uptake by 37%
(P < 0.05), similar to the results
in study 1. These data indicate that
GH induces peripheral insulin resistance independent of plasma FFA and
insulin levels. The induction of insulin resistance was preceded by
suppression of glycogen synthesis, consistent with the hypothesis that
metabolic impairment precedes and causes development of peripheral
insulin resistance.
glycolysis; glycogen synthesis; skeletal muscle; glucose 6-phosphate; growth hormone; free fatty acid
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