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Received August 25, 2005
Revised September 2, 2005
Accepted after revision September 6, 2005
1 University of Guelph
2 University of Copenhagen
* To whom correspondence should be addressed. E-mail: dbattram{at}uoguelph.ca.
While caffeine (CAF) impedes insulin-mediated glucose disposal in humans, its effect on endogenous glucose production (EGP) remains unknown. In addition, the mechanism involved in these effects is unclear, but may be due to the accompanying increase in adrenaline [Adr] concentration. We studied caffeine's effect on EGP and glucose infusion rates (GIR) and whether or not Adr can account for all CAF effects. Subjects completed 3 isoglycemic-hyperinsulinemic clamps (with 3-[3H ]glucose infusion) 30 min after ingesting 1) placebo capsules (PL)(n=12), 2) caffeine capsules (CAF)(5 mg · kg-1) (n=12), and either 3) PL plus an Adr infusion ([HAdr]=1.2 nM)(n=8), or 4) PL plus an Adr infusion ([LAdr] of 0.75nM)(n=6). With CAF Adr increased to 0.6 nM but no effect on EGP was observed. While CAF and HAdr decreased GIR by 13 (P < 0.05) and 34% (P < 0.05) vs PL respectively, LAdr did not result in a significant reduction (5%) in GIR vs PL. Due to the fact that both CAF and LAdr resulted in similar [Adr], but resulted in different decreases in GIR, it is concluded that Adr alone does not account for CAF effects and additional mechanisms must be involved.
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