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1 Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, ON, Canada
* To whom correspondence should be addressed. E-mail: crbruce{at}uoguelph.ca.
Interleukin-6 (IL-6) and tumor necrosis factor-
(TNF-) 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- on skeletal muscle FA metabolism. Here we used a pulse-chase technique to determine the effect of IL-6 (50-5000 pg/mL) and TNF- (50-5000 pg/mL) on FA metabolism in isolated rat soleus muscle. IL-6 (5000 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- had no effect on FA oxidation but increased FA incorporation into diacylglycerol (DAG) by 45% (P<0.05). When both IL-6 (5000 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 (TAG) by 22% (P<0.05). When added in combination with IL-6 or leptin (10µg/mL), the TNF--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- had no effect on FA oxidation but increased FA incorporation into DAG, which may be involved in the development of TNF--induced insulin resistance in skeletal muscle.
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