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1 The Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark; The Department of Infectious Diseases, University of Copenhagen, Copenhagen, Denmark
2 The Skeletal Muscle Research Laboratory, Center for Nutrition Metabolism and Endocrinology, RMIT University, Bundoora, Australia
3 The Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark
4 St. Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Australia
5 CSIRO Health Sciences and Nutrition, Parkville, Australia
* To whom correspondence should be addressed. E-mail: bkp{at}rh.dk.
To determine whether IL-6 increases lipolysis and fat oxidation in patients Type 2 diabetes and/or whether it exerts this affect independently of changes to the hormonal milieu. Patients with type 2 diabetes (D) and healthy control subjects (CON) underwent recombinant human (rh) IL-6 infusion for 3 h. Rates of appearance (Ra) and disappearance (Rd) of [U-13C] palmitate and [6,6-2H2] glucose were determined. RhIL-6 infusion increased (P<0.05) palmitate Ra and Rd in a similar fashion in both groups. Neither plasma glucose concentration nor glucose Ra/Rd were affected by rhIL-6 infusion in either group while rhIL-6 infusion resulted in a reduction (P<0.05) in circulating insulin in D. Plasma growth hormone was increased (P<0.05) by IL-6 in CON, and cortisol increased (P<0.05) in response to IL-6 in both groups. To determine whether IL-6 was exerting its effect directly or through activation of these hormones, we performed cell culture experiments. Fully differentiated 3T3-L1 adipocytes were treated with PBS (control) IL-6 or IL-6 + dexamethasone and growth hormone. IL-6 treatment alone increased (P<0.05) lipolysis, but this affect was reduced by the addition of dexamethasone and growth hormone such that IL-6 + dexamethasone and growth hormone had blunted (P<0.05) lipolysis compared with IL-6 alone. To assess whether IL-6 increases fat oxidation, L6 myotubes were treated with PBS (Control), IL-6 or AICAR, a compound known to increase lipid oxidation. Both IL-6 and AICAR markedly increased (P<0.05) oxidation of 14C palmitate compared with Control. Acute IL-6 treatment increases fatty acid turnover in patients with type 2 diabetes as well as healthy control subjects. Moreover, IL-6 appears to be activating lipolysis independent of elevations in growth hormone and/or cortisol and appears to be a potent catalyst for fat oxidation in muscle cells.
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