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Tumor Necrosis Factor- Modulates Human in Vivo Lipolysis

The Centre of Inflammation and Metabolism at Department of Infectious Diseases Rigshospitalet (P.P., C.P.F., T.I., B.K.P, G.v.H.), Faculty of Health Sciences, and Department of Biomedical Sciences (G.v.H.), University of Copenhagen, 2100 Copenhagen, Denmark; and Copenhagen Muscle Research Centre (P.P., C.P.F., T.I., G.v.H.), Rigshospitalet, 2400 Copenhagen, Denmark

Address all correspondence and requests for reprints to: Peter Plomgaard, Centre of Inflammation and Metabolism, Department of Infectious Diseases, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark. E-mail: plomgaard{at}dadlnet.dk.

Context: Low-grade systemic inflammation is a feature of most lifestyle-related chronic diseases. Enhanced TNF- concentrations have been implicated in the development of hyperlipidemia.

Objective: We hypothesized that an acute elevation of TNF- in plasma would cause an increase in lipolysis, increasing circulatory free fatty acid (FFA) levels.

Subjects and Methods: Using a randomized controlled, crossover design, healthy young male individuals (n = 10) received recombinant human (rh) TNF- (700 ng/m^–2·h^–1) for 4 h, and energy metabolism was evaluated using a combination of tracer dilution methodology and arterial-venous differences over the leg.

Results: Plasma TNF- levels increased from 0.7 ± 0.04 to 16.7 ± 1.8 pg/ml, and plasma IL-6 increased from 1.0 ± 0.2 to 9.2 ± 1.0 pg/ml (P < 0.05) after 4-h rhTNF- infusion. Here, we demonstrate that 4-h rhTNF- infusion increases whole body lipolysis by 40% (P < 0.05) with a concomitant increase in FFA clearance, with no changes in skeletal muscle FFA uptake, release, or oxidation. Of note, systemic glucose turnover and lactate and catecholamine levels were unaffected by rhTNF- infusion.

Conclusion: This study demonstrates that a relatively low dose of rhTNF- induces systemic lipolysis and that the skeletal muscle fat metabolism is unaffected.