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1 Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1; and 2 Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
We examined the
effect of insulin on the synthesis and degradation of muscle lipid
pools [phospholipid (PL), diacylglycerol (DG), triacylglycerol (TG)]
and palmitate oxidation in isolated resting and contracting (20 tetani/min) soleus muscles. Lipid metabolism was monitored using the
previously defined pulse-chase procedure. At rest, insulin
significantly increased total palmitate uptake into soleus muscle
(+49%, P < 0.05), corresponding to enhanced DG
(+60%, P < 0.05) and TG (+61%, P < 0.05) esterification, but blunted palmitate oxidation (
38%,
P < 0.05) and TG hydrolysis (34%, P < 0.05). During muscle contraction, when total palmitate uptake was
increased, insulin further enhanced uptake (+21%, P < 0.05) and esterification of fatty acids (FA) to PL (+73%,
P < 0.05), DG (+19%, P < 0.05), and
TG (+161%, P < 0.01). Despite a profound shift in the
relative partitioning of FA away from esterification and toward
oxidation during contraction, the increase in palmitate oxidation and
TG hydrolysis was significantly blunted by insulin [oxidation, 24%
(P = 0.05); hydrolysis, 83% (P < 0.01)]. The effects of insulin on FA esterification (stimulation) and
oxidation (inhibition) during contraction were reduced in the presence
of the phosphatidylinositol 3-kinase inhibitor LY-294002. In summary,
the effects of insulin and contraction on palmitate uptake and
esterification are additive, while insulin opposes the stimulatory
effect of contraction on FA oxidation and TG hydrolysis. Insulin's
modulatory effects on muscle FA metabolism during contraction are
mediated at least in part through phosphatidylinositol 3-kinase.
fatty acids; hydrolysis; oxidation; pulse-chase technique; triacylglycerol; diacylglycerol; phospholipid
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