Desensitization of [beta]-adrenergic receptors in adipocytes causes
increased insulin sensitivity of glucose transport.
Green, Allan, Richard M. Carroll, and Susan B. Dobias.
Division of Endocrinology, Department of Internal Medicine, The
University of Texas Medical Branch, Galveston, TX 77555
APStracts 3:0069E, 1996.
To determine the effect of desensitization of adipocyte [beta]
-adrenergic receptors on insulin sensitivity, rats were continuously
infused with isoproterenol (50 or 100 [mu]g/Kg/h) for three days, by
osmotic minipumps. Epididymal adipocytes were isolated. The cells
from treated animals were desensitized to isoproterenol, as
determined by response of lipolysis (glycerol release). Binding of
[125I]iodocyanopindolol was decreased by about 80% in adipocyte
plasma membranes isolated from treated rats, indicating that [beta]
-adrenergic receptors were down-regulated. Cellular concentrations of
Gs[alpha] and Gi[alpha] were not altered. Insulin sensitivity was
determined by measuring the effect of insulin on glucose transport
(2-deoxy [3H]glucose uptake). Cells from the isoproterenol-infused
rats were markedly more sensitivity to insulin than those from
control rats. This was evidenced by an approximate 50% increase in
maximal glucose transport rate in cells from the high-dose
isoproterenol-treated rats, and by about a 40% decrease in the half
-maximally effective concentration of insulin in both groups. 125I
-insulin binding to adipocytes was not altered by the isoproterenol
infusions, indicating that desensitization of [beta]-adrenergic
receptors results in tighter coupling between insulin receptors and
stimulation of glucose transport.
Received 18 December 1995; accepted in final form 18 March 1996.
APS Manuscript Number E588-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 April 96