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Articles in PresS, published online ahead of print February 1, 2002
J Appl Physiol, 10.1152/jap.01229.2001
Submitted on December 14, 2001
Accepted on January 21, 2002
1 Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada
* To whom correspondence should be addressed. E-mail: fthong{at}uoguelph.ca.
The caffeine-induced impairment of insulin action is commonly attributed to adenosine receptor (AR) antagonism in skeletal muscle. However, epinephrine, a potent inhibitor of insulin actions, is increased following caffeine ingestion. We tested the hypothesis that the insulin antagonistic effects of caffeine are mediated by epinephrine, and not by AR antagonism, in 7 healthy males. On 4 separate occasions, they received: (1) dextrose (Placebo, PL), (2) 5 mg/kg caffeine (CAF), (3) 80 mg propranolol (PR), and (4) 5 mg/kg caffeine + 80 mg propranolol (CAF+PR) prior to an oral glucose tolerance test (OGTT). Blood glucose was similar among trials before and during the OGTT. Plasma epinephrine was elevated (p<0.05) in CAF and CAF+PR. Area under the insulin and C-peptide curves were 42% and 39% greater (p<0.05) respectively in CAF compared to PL, PR and CAF+PR. In the presence of propranolol (CAF+PR), these responses were similar to PL and PR. These data suggest that the insulin antagonistic effects of caffeine in vivo are mediated by elevated epinephrine, rather than peripheral AR antagonism.
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