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Am J Physiol Endocrinol Metab (March 1, 2005). doi:10.1152/ajpendo.00274.2004
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Submitted on June 23, 2004
Accepted on December 6, 2004

Recombinant human interleukin-6 infusion during low intensity exercise does not enhance whole body lipolysis or fat oxidation in humans

N. Hiscock1*, C. P. Fischer2, M. Sacchetti3, G. van Hall3, M. A. Febbraio3, and B. K. Pedersen2

1 Copenhagen Muscle Research Centre, Copenhagen, Denmark; Rigshospitalet, Department of Infectious Diseases, Copenhagen, Denmark; Skeletal Muscle Research Laboratory, RMIT University, Bundoora, Australia
2 Copenhagen Muscle Research Centre, Copenhagen, Denmark; Rigshospitalet, Department of Infectious Diseases, Copenhagen, Denmark
3 Copenhagen Muscle Research Centre, Copenhagen, Denmark

* To whom correspondence should be addressed. E-mail: natalie.hiscock{at}rmit.edu.au.

The present study examined the role of the cytokine interleukin (IL)-6 in the regulation of fatty acid metabolism during exercise in humans. Six well-trained males completed three trials of 120 min of cycle ergometry at 70% VO2 peak (MOD) and 40% VO2 peak with (LOW+IL-6) and without (LOW) infusion of recombinant human (rh) IL-6. The dose of rhIL-6 during LOW+IL-6 elicited IL-6 concentration similar to those during MOD, but without altering the circulating hormonal milieu seen in MOD. Palmitate rate of appearance (Ra), rate of disappearance (Rd) and oxidation were measured by means of a constant infusion of [U-13C]palmitate (0.015 µmol.kg-1.min, prime NaHCO3, 1 µmol.kg-1). Palmitate Ra, Rd and oxidation were not affected by rhIL-6 infusion, remaining similar to LOW at all times. Palmitate Ra and oxidation were significantly greater in the MOD trial (p<0.05) compared with the LOW+IL-6 and LOW trials. Our data show that a low dose of rhIL-6, administered during low intensity exercise without altering the hormonal milieu, does not alter fatty acid metabolism. These data suggest that the increase in fatty acid utilization seen during exercise at moderate compared with low intensity is not mediated via alterations in plasma IL-6.




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