Hypertension, Vol 21, 618-623, Copyright © 1993 by American Heart Association
KA Jamerson, S Julius, T Gudbrandsson, O Andersson and DO Brant
Inferences about the association between sympathetic overactivity and
insulin resistance have been drawn from the infusion of sympathomimetic
amines in supraphysiological doses. We used the isolated perfused human
forearm to investigate the effect of reflex-induced sympathetic nervous
system activation on the peripheral utilization of glucose in the skeletal
muscles of 14 healthy men. Local hyperinsulinemia in the forearm (132 +/-
25 microunits/mL for 90 minutes) induced a significant increase in the
utilization of glucose from baseline (16.4 +/- 3.1 mg.dL-1.min-1 per 100 mL
forearm volume) to a plateau (85.7 +/- 15.1 mg.dL-1.min-1 per 100 mL
forearm volume) between 40 and 60 minutes of insulin infusion but did not
alter the utilization of oxygen. Reflex sympathetic nervous system
activation was elicited by unloading of cardiopulmonary receptors with
bilateral thigh cuff inflation to 40 mm Hg between 60 and 90 minutes of
insulin infusion. Blood flow in the forearm was significantly decreased
with inflation of thigh cuffs (average decrease of 19%, p < 0.0001). As
a result of thigh cuff inflation, there was a reduction in the utilization
of glucose (a decrease of 23%, p < 0.02), whereas oxygen utilization was
unchanged. We find that an increase in sympathetic nervous system
activation (within the normal range of physiological responses) can cause
acute insulin resistance in the forearm of healthy volunteers. The reflex
caused no change in oxygen utilization, but the same stimulus elicited a
decrease in the utilization of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Reflex sympathetic activation induces acute insulin resistance in the human forearm
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0356.
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