Lipolytic responsiveness to epinephrine in nondiabetic and diabetic humans. Divertie, G. D., M. D. Jensen, P. E. Cryer, J. M. Miles. Endocrine Research Unit, Departments of Medicine and Anesthesiology, Mayo Clinic, Rochester, MN and Jacksonville, FL; and Division of Metabolism, Washington University, St. Louis, MO.
APStracts 4:0048E, 1997.
To determine whether the sensitivity of adipose tissue lipolysis to catecholamines is increased in poorly controlled insulin-dependent diabetes (IDDM), the lipolytic response to epinephrine was measured in seven nondiabetic volunteers and seven poorly controlled diabetic subjects using [1-14C] palmitate as a tracer. Subjects received sequential one-hour infusions of epinephrine at 5, 10, 20 and 40 ng x kg-1 x min-1, with a one-hour equilibration period between each dose. Corresponding epinephrine concentrations were _1000, _ 1750, _3500 and _6000 pmol/L. A pancreatic clamp (somatostatin, insulin, and growth hormone) was used to maintain constant plasma hormone levels. Concentration-response curves were constructed for each subject from the integrated lipolytic response during each epinephrine infusion. In control subjects, the lipolytic response to epinephrine was similar whether epinephrine was infused sequentially on a single day or on separate days. There was no difference in maximal lipolytic response (117 +/- 19 vs. 152 +/- 11 [mu]mol x kg-1 x h-1) nor in maximally effective (3171 +/- 267 vs. 3357 +/- 349 pmol/l) or half -maximally effective (1081 +/- 109 vs. 1015 +/- 120 pmol/l) epinephrine concentrations between non-diabetic and diabetic subjects, respectively (all P = NS). Plasma concentrations of insulin and C-peptide were constant throughout the study. In control subjects, maximum [beta]-hydroxybutyrate concentrations were achieved at lower epinephrine concentrations than those required for a maximum lipolytic effect. Thus, under pancreatic clamp conditions, the lipolytic response in nondiabetic and diabetic subjects to epinephrine was similar. Lipolytic sensitivity to epinephrine does not appear to be increased in poorly controlled IDDM. Acute normalization of glycemic control could have obscured an underlying abnormality of lipolytic sensitivity in these studies. 

Received 19 August 1996; accepted in final form 13 February 1997.
APS Manuscript Number E408-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 5 March 1997