Increased lipid oxidation, but normal muscle glycogen response to
epinephrine in humans with iddm.
Cohen, Neil, Meyer Halberstam, Luciano Rossetti, Harry Shamoon.
Department of Medicine, Diabetes Research Center, Albert Einstein
College of Medicine, Bronx, NY
APStracts 3:0083E, 1996.
The effects of physiologic increments in epinephrine and insulin on
glucose production (GP), skeletal muscle glycogen metabolism, and
substrate oxidation were studied in eight IDDM and nine control
subjects. Epinephrine was co-infused for the final 120 min of a 240
min euglycemic, hyperinsulinemic clamp. In both groups, insulin
increased glucose uptake, glycogen synthesis, and whole-body
carbohydrate (CHO) oxidation, and inhibited GP (by 70-80%) and lipid
oxidation (by 50%), while epinephrine antagonized the effect of
insulin on glucose uptake and glycogen synthesis. In contrast, GP
increased in IDDM (p<0.02) but remained suppressed by insulin in
controls. CHO oxidation fell (1.37+/-0.25 vs 2.08+/-0.32 mg/kg.min)
and lipid oxidation increased to baseline in IDDM, with increments in
plasma FFA and glycerol. In contrast in controls, plasma FFA and
glycerol remained suppressed, and lipid oxidation decreased further
with epinephrine (p<0.005). Epinephrine completely reversed
insulin's activation of muscle glycogen synthase in both groups.
Thus, during hyperinsulinemia, the hepatic response to epinephrine in
IDDM may be dependent on activation of lipid oxidation. Skeletal
muscle glycogen metabolism is exquisitely sensitive to epinephrine
despite the presence of hyperinsulinemia.
Received 27 December 1995; accepted in final form 29 March 1996.
APS Manuscript Number E605-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 23 April 96