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Human Performance Laboratory and Department of Biochemistry, School of Medicine, East Carolina University, Greenville, North Carolina 27858-4353
Received 4 November 1996; accepted in final form 22 April 1997.
Hickey, Matthew S., Charles J. Tanner, D. Sean O'Neill,
Lydia J. Morgan, G. Lynis Dohm, and Joseph A. Houmard. Insulin activation of phosphatidylinositol 3-kinase in human skeletal muscle in
vivo. J. Appl. Physiol. 83(3):
718-722, 1997.
The purpose of this investigation was to determine
whether insulin-stimulated phosphatidylinositol 3-kinase (PI3-kinase)
activity is detectable in needle biopsies of human skeletal muscle.
Sixteen healthy nonobese males matched for age, percent fat, fasting
insulin, and fasting glucose participated in one of two experimental
protocols. During an intravenous glucose tolerance test (IVGTT)
protocol, insulin-stimulated PI3-kinase activity was determined from
percutaneous needle biopsies at 2, 5, and 15 min post-insulin
administration (0.025 U/kg). In the second group, a 2-h, 100 mU · m
2 · min1
euglycemic hyperinsulinemic clamp was performed, and biopsies were
obtained at 15, 60, and 120 min after insulin infusion was begun.
Insulin stimulated PI3-kinase activity by 1.6 ± 0.2-, 2.2 ± 0.3-, and 2.2 ± 0.4-fold at 2, 5, and 15 min, respectively, during
the IVGTT. During the clamp protocol, PI3-kinase was elevated by 5.3 ± 1.3-, 8.0 ± 2.6-, and 2.7 ± 1.4-fold above
basal at 15, 60, and 120 min, respectively. Insulin-stimulated
PI3-kinase activity at 15 min post-insulin administration was
significantly greater during the clamp protocol vs. the IVGTT
(P < 0.05). These observations suggest that insulin-stimulated PI3-kinase activity is detectable in
needle biopsies of human skeletal muscle, and furthermore, that the
euglycemic, hyperinsulinemic clamp protocol may be a useful tool to
assess insulin signaling in vivo.
insulin signaling; glucose; muscle biopsy
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