AJP - Endo Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab 288: E178-E186, 2005; doi:10.1152/ajpendo.00310.2004
0193-1849/05 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (5)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Guy, D. A.
Right arrow Articles by Davis, S. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Guy, D. A.
Right arrow Articles by Davis, S. N.

Differing physiological effects of epinephrine in type 1 diabetes and nondiabetic humans

Deanna Aftab Guy,1 Darleen Sandoval,2 M. A. Richardson,2 Donna Tate,2 Paul J. Flakoll,4 and Stephen N. Davis2,3

2Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, and 1Division of Pediatric Endocrinology, Department of Pediatrics, Vanderbilt University School of Medicine, and 3Nashville Veteran Affairs Medical Center, Nashville, Tennessee; and 4Center for Food Science and Human Nutrition, Iowa State University, Iowa City, Iowa

Submitted 14 July 2004 ; accepted in final form 2 September 2004

Acute increases of the key counterregulatory hormone epinephrine can be modified by a number of physiological and pathological conditions in type 1 diabetic patients (T1DM). However, it is undecided whether the physiological effects of epinephrine are also reduced in T1DM. Therefore, the aim of this study was to determine whether target organ (liver, muscle, adipose tissue, pancreas, cardiovascular) responses to epinephrine differ between healthy subjects and T1DM patients. Thirty-four age- and weight-matched T1DM (n = 17) and healthy subjects (n = 17) underwent two randomized, single-blind, 2-h hyperinsulinemic euglycemic clamp studies with (Epi) and without epinephrine infusion. Muscle biopsy was performed at the end of each study. Epinephrine levels during Epi were similar in all groups (4,039 ± 384 pmol/l). Glucose (5.3 ± 0.06 mmol/l) and insulin levels (462 ± 18 pmol/l) were also similar in all groups during the glucose clamps. Glucagon responses to Epi were absent in T1DM and significantly reduced compared with healthy subjects. Endogenous glucose production during the final 30 min was significantly greater during Epi in healthy subjects compared with T1DM (8.4 ± 1.3 vs. 4.4 ± 0.6 µmol·kg–1·min–1, P = 0.041). Glucose uptake showed almost a twofold greater decrease with Epi in healthy subjects vs. T1DM ({Delta}31 ± 2 vs. {Delta}17 ± 2 nmol·kg–1·min–1, respectively, P = 0.026). Glycerol, {beta}-hydroxybutyrate, and nonesterified fatty acid (NEFA) all increased significantly more in T1DM compared with healthy subjects. Increases in systolic blood pressure were greater in healthy subjects, but reductions of diastolic blood pressure were greater in T1DM patients with Epi. Reduction of glycogen synthase was significantly greater during epinephrine infusion in T1DM vs. healthy subjects. In summary, despite equivalent epinephrine, insulin, and glucose levels, changes in glucose flux, glucagon, and cardiovascular responses were greater in healthy subjects compared with T1DM. However, T1DM patients had greater lipolytic responses (glycerol and NEFA) during Epi. Thus we conclude that there is a spectrum of significant in vivo physiological differences of epinephrine action at the liver, muscle, adipose tissue, pancreas, and cardiovascular system between T1DM and healthy subjects.

epinephrine; catecholamines; metabolic target organ; glucose clamp technique



Address for reprint requests and other correspondence: S. N. Davis, 715 PRB, Division of Diabetes, Endocrinology & Metabolism, Vanderbilt Univ. School of Medicine, Nashville, TN 37232-6303




This article has been cited by other articles:


Home page
DiabetesHome page
V. J. Briscoe, A. C. Ertl, D. B. Tate, and S. N. Davis
Effects of the Selective Serotonin Reuptake Inhibitor Fluoxetine on Counterregulatory Responses to Hypoglycemia in Individuals With Type 1 Diabetes
Diabetes, December 1, 2008; 57(12): 3315 - 3322.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
V. J. Briscoe, A. C. Ertl, D. B. Tate, S. Dawling, and S. N. Davis
Effects of a Selective Serotonin Reuptake Inhibitor, Fluoxetine, on Counterregulatory Responses to Hypoglycemia in Healthy Individuals
Diabetes, September 1, 2008; 57(9): 2453 - 2460.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
P. Kishore, I. Gabriely, M.-H. Cui, J. Di Vito, S. Gajavelli, J.-H. Hwang, and H. Shamoon
Role of Hepatic Glycogen Breakdown in Defective Counterregulation of Hypoglycemia in Intensively Treated Type 1 Diabetes
Diabetes, March 1, 2006; 55(3): 659 - 666.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
P. E. Cryer
Mechanisms of Hypoglycemia-Associated Autonomic Failure and Its Component Syndromes in Diabetes
Diabetes, December 1, 2005; 54(12): 3592 - 3601.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
D. Aftab Guy, D. Sandoval, M. A. Richardson, D. Tate, and S. N. Davis
Effects of glycemic control on target organ responses to epinephrine in type 1 diabetes
Am J Physiol Endocrinol Metab, August 1, 2005; 289(2): E258 - E265.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.