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1 Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph N1G 2W1; and 2 Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
Leptin has been shown to acutely
stimulate fatty acid oxidation and triacylglycerol hydrolysis in
skeletal muscle. These effects are similar to those induced by muscle
contraction alone. Several studies have demonstrated that, during
aerobic exercise, plasma leptin concentrations are well maintained;
however, none has examined whether the stimulatory effects of leptin
and contraction on muscle lipid metabolism are additive. This is the
first study to examine the direct effect of leptin on lipid and
carbohydrate (CHO) metabolism in isolated oxidative muscle over a range
of contraction intensities. We examined the effect of leptin (10 µg/ml) on the synthesis and degradation of muscle lipid pools
[phospholipid (PL), diacylglycerol (DG), triacylglycerol (TG)] and
palmitate oxidation in isolated resting and contracting (2, 8, and 20 tetani/min) soleus muscles. At rest, leptin increased fatty acid
oxidation (+40%, P < 0.05) and TG hydrolysis (+47%,
P < 0.05), while blunting TG esterification (
20%,
P < 0.05). Glucose oxidation was unaffected at rest in the presence of leptin. During tetanic contraction, fatty acid oxidation (+20-114%, P < 0.05) and TG
esterification (+19-33%, P < 0.05) as well as
net TG utilization (+23%, P < 0.05) were all
significantly increased. However, leptin was without further effect on
any of these parameters during contraction. Net utilization of
intramuscular glycogen, as well as glucose oxidation, was unaffected during contraction by leptin. The findings of the present study indicate that leptin has an important influence on lipid metabolism in
resting muscle, but not during contraction.
hydrolysis; esterification; oxidation; pulse-chase; triacyglycerol; diacylglycerol; phospholipid
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