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Am J Physiol Endocrinol Metab 287: E616-E621, 2004. First published May 18, 2004; doi:10.1152/ajpendo.00150.2004
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Cytokine regulation of skeletal muscle fatty acid metabolism: effect of interleukin-6 and tumor necrosis factor-{alpha}

Clinton R. Bruce and David J. Dyck

Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1

Submitted 1 April 2004 ; accepted in final form 14 May 2004

IL-6 and TNF-{alpha} have been associated with insulin resistance and type 2 diabetes. Furthermore, abnormalities in muscle fatty acid (FA) metabolism are strongly associated with the development of insulin resistance. However, few studies have directly examined the effects of either IL-6 or TNF-{alpha} on skeletal muscle FA metabolism. Here, we used a pulse-chase technique to determine the effect of IL-6 (50–5,000 pg/ml) and TNF-{alpha} (50–5,000 pg/ml) on FA metabolism in isolated rat soleus muscle. IL-6 (5,000 pg/ml) increased exogenous and endogenous FA oxidation by ~50% (P < 0.05) but had no effect on FA uptake or incorporation of FA into endogenous lipid pools. In contrast, TNF-{alpha} had no effect on FA oxidation but increased FA incorporation into diacylglycerol (DAG) by 45% (P < 0.05). When both IL-6 (5,000 pg/ml) and insulin (10 mU/ml) were present, IL-6 attenuated insulin's suppressive effect on FA oxidation, increasing exogenous FA oxidation (+37%, P < 0.05). Furthermore, in the presence of insulin, IL-6 reduced the esterification of FA to triacylglycerol by 22% (P < 0.05). When added in combination with IL-6 or leptin (10 µg/ml), the TNF-{alpha}-induced increase in DAG synthesis was inhibited. In conclusion, the results demonstrate that IL-6 plays an important role in regulating fat metabolism in muscle, increasing rates of FA oxidation, and attenuating insulin's lipogenic effects. In contrast, TNF-{alpha} had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF-{alpha}-induced insulin resistance in skeletal muscle.

triacylglycerol; diacylglycerol; fatty acid oxidation; insulin resistance


Address for reprint requests and other correspondence: Clinton R. Bruce, Dept. of Human Biology and Nutritional Sciences, Univ. of Guelph, Guelph, ON, Canada N1G 2W1 (E-mail: crbruce{at}uoguelph.ca)




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