The effect of caffeine on glucose kinetics in humans - influence of adrenaline

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The effect of caffeine on glucose kinetics in humans - influence of adrenaline. / Battram, Danielle S.; Graham, Terry E.; Richter, Erik A.; Dela, Flemming.

I: Journal of Physiology, Bind 569, Nr. 1, 2005, s. 347-355.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Battram, DS, Graham, TE, Richter, EA & Dela, F 2005, 'The effect of caffeine on glucose kinetics in humans - influence of adrenaline', Journal of Physiology, bind 569, nr. 1, s. 347-355. https://doi.org/10.1113/jphysiol.2005.097444

APA

Battram, D. S., Graham, T. E., Richter, E. A., & Dela, F. (2005). The effect of caffeine on glucose kinetics in humans - influence of adrenaline. Journal of Physiology, 569(1), 347-355. https://doi.org/10.1113/jphysiol.2005.097444

Vancouver

Battram DS, Graham TE, Richter EA, Dela F. The effect of caffeine on glucose kinetics in humans - influence of adrenaline. Journal of Physiology. 2005;569(1):347-355. https://doi.org/10.1113/jphysiol.2005.097444

Author

Battram, Danielle S. ; Graham, Terry E. ; Richter, Erik A. ; Dela, Flemming. / The effect of caffeine on glucose kinetics in humans - influence of adrenaline. I: Journal of Physiology. 2005 ; Bind 569, Nr. 1. s. 347-355.

Bibtex

@article{21abc3f0a56011dbbee902004c4f4f50,
title = "The effect of caffeine on glucose kinetics in humans - influence of adrenaline",
abstract = "While caffeine impedes insulin-mediated glucose disposal in humans, its effect on endo-genous 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 concentration. We studied the effect of caffeine on EGP and glucose infusion rates (GIR), and whether or not adrenaline can account for all of caffeine's effects. Subjects completed three isoglycaemic-hyperinsulinaemic clamps (with 3-[3H]glucose infusion) 30 min after ingesting: (1) placebo capsules (n= 12); (2) caffeine capsules (5 mg kg-1) (n= 12); and either (3) placebo plus a high-dose adrenaline infusion (HAdr; adrenaline concentration, 1.2 nM; n= 8) or (4) placebo plus a low-dose adrenaline infusion (LAdr; adrenaline concentration, 0.75 nM; n= 6). With caffeine, adrenaline increased to 0.6 nM but no effect on EGP was observed. While caffeine and HAdr decreased GIR by 13 (P < 0.05) and 34{\%} (P < 0.05) versus the placebo, respectively, LAdr did not result in a significant reduction (5{\%}) in GIR versus the placebo. Due to the fact that both caffeine and LAdr resulted in similar adrenaline concentrations, but resulted in different decreases in GIR, it is concluded that adrenaline alone does not account for the effects of caffeine and additional mechanisms must be involved.",
author = "Battram, {Danielle S.} and Graham, {Terry E.} and Richter, {Erik A.} and Flemming Dela",
note = "PUF 2005 5200 032",
year = "2005",
doi = "10.1113/jphysiol.2005.097444",
language = "English",
volume = "569",
pages = "347--355",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "1",

}

RIS

TY - JOUR

T1 - The effect of caffeine on glucose kinetics in humans - influence of adrenaline

AU - Battram, Danielle S.

AU - Graham, Terry E.

AU - Richter, Erik A.

AU - Dela, Flemming

N1 - PUF 2005 5200 032

PY - 2005

Y1 - 2005

N2 - While caffeine impedes insulin-mediated glucose disposal in humans, its effect on endo-genous 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 concentration. We studied the effect of caffeine on EGP and glucose infusion rates (GIR), and whether or not adrenaline can account for all of caffeine's effects. Subjects completed three isoglycaemic-hyperinsulinaemic clamps (with 3-[3H]glucose infusion) 30 min after ingesting: (1) placebo capsules (n= 12); (2) caffeine capsules (5 mg kg-1) (n= 12); and either (3) placebo plus a high-dose adrenaline infusion (HAdr; adrenaline concentration, 1.2 nM; n= 8) or (4) placebo plus a low-dose adrenaline infusion (LAdr; adrenaline concentration, 0.75 nM; n= 6). With caffeine, adrenaline increased to 0.6 nM but no effect on EGP was observed. While caffeine and HAdr decreased GIR by 13 (P < 0.05) and 34% (P < 0.05) versus the placebo, respectively, LAdr did not result in a significant reduction (5%) in GIR versus the placebo. Due to the fact that both caffeine and LAdr resulted in similar adrenaline concentrations, but resulted in different decreases in GIR, it is concluded that adrenaline alone does not account for the effects of caffeine and additional mechanisms must be involved.

AB - While caffeine impedes insulin-mediated glucose disposal in humans, its effect on endo-genous 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 concentration. We studied the effect of caffeine on EGP and glucose infusion rates (GIR), and whether or not adrenaline can account for all of caffeine's effects. Subjects completed three isoglycaemic-hyperinsulinaemic clamps (with 3-[3H]glucose infusion) 30 min after ingesting: (1) placebo capsules (n= 12); (2) caffeine capsules (5 mg kg-1) (n= 12); and either (3) placebo plus a high-dose adrenaline infusion (HAdr; adrenaline concentration, 1.2 nM; n= 8) or (4) placebo plus a low-dose adrenaline infusion (LAdr; adrenaline concentration, 0.75 nM; n= 6). With caffeine, adrenaline increased to 0.6 nM but no effect on EGP was observed. While caffeine and HAdr decreased GIR by 13 (P < 0.05) and 34% (P < 0.05) versus the placebo, respectively, LAdr did not result in a significant reduction (5%) in GIR versus the placebo. Due to the fact that both caffeine and LAdr resulted in similar adrenaline concentrations, but resulted in different decreases in GIR, it is concluded that adrenaline alone does not account for the effects of caffeine and additional mechanisms must be involved.

U2 - 10.1113/jphysiol.2005.097444

DO - 10.1113/jphysiol.2005.097444

M3 - Journal article

C2 - 16150793

VL - 569

SP - 347

EP - 355

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 1

ER -

ID: 89792