Regulation of exercise-induced lipid metabolism in skeletal muscle
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Regulation of exercise-induced lipid metabolism in skeletal muscle. / Jordy, Andreas Børsting; Kiens, Bente.
In: Experimental Physiology, Vol. 99, No. 12, 2014, p. 1586-1592.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Regulation of exercise-induced lipid metabolism in skeletal muscle
AU - Jordy, Andreas Børsting
AU - Kiens, Bente
N1 - CURIS 2014 NEXS 355
PY - 2014
Y1 - 2014
N2 - Exercise increases the utilization of lipids in muscle. The sources of lipids are long-chain fatty acids taken up from the plasma and fatty acids released from stores of intramuscular triacylglycerol by the action of intramuscular lipases. In the present review, we focus on the role of fatty acid binding proteins, particularly fatty acid translocase/cluster of differentiation 36 (FAT/CD36), in the exercise- and contraction-induced increase in uptake of long-chain fatty acids in muscle. The FAT/CD36 translocates from intracellular depots to the surface membrane upon initiation of exercise/muscle contractions. This occurs independently of AMP-activated protein kinase, and data suggest that Ca(2+)-related signalling is responsible. The FAT/CD36 has an important role; long-chain fatty acid uptake is markedly decreased in FAT/CD36 knockout mice during contractions/exercise compared with wild-type control mice. In skeletal muscle, 98% of the lipase activity is accounted for by adipose triglyceride lipase and hormone-sensitive lipase. Give that inhibition or knockout of hormone-sensitive lipase does not impair lipolysis in muscle during contraction, the data point to an important role of adipose triglyceride lipase in regulation of muscle lipolysis. Although the molecular regulation of the lipases in muscle is not understood, it is speculated that intramuscular lipolysis may be regulated in part by the availability of the plasma concentration of long-chain fatty acids.
AB - Exercise increases the utilization of lipids in muscle. The sources of lipids are long-chain fatty acids taken up from the plasma and fatty acids released from stores of intramuscular triacylglycerol by the action of intramuscular lipases. In the present review, we focus on the role of fatty acid binding proteins, particularly fatty acid translocase/cluster of differentiation 36 (FAT/CD36), in the exercise- and contraction-induced increase in uptake of long-chain fatty acids in muscle. The FAT/CD36 translocates from intracellular depots to the surface membrane upon initiation of exercise/muscle contractions. This occurs independently of AMP-activated protein kinase, and data suggest that Ca(2+)-related signalling is responsible. The FAT/CD36 has an important role; long-chain fatty acid uptake is markedly decreased in FAT/CD36 knockout mice during contractions/exercise compared with wild-type control mice. In skeletal muscle, 98% of the lipase activity is accounted for by adipose triglyceride lipase and hormone-sensitive lipase. Give that inhibition or knockout of hormone-sensitive lipase does not impair lipolysis in muscle during contraction, the data point to an important role of adipose triglyceride lipase in regulation of muscle lipolysis. Although the molecular regulation of the lipases in muscle is not understood, it is speculated that intramuscular lipolysis may be regulated in part by the availability of the plasma concentration of long-chain fatty acids.
U2 - 10.1113/expphysiol.2014.082404
DO - 10.1113/expphysiol.2014.082404
M3 - Journal article
C2 - 25398709
VL - 99
SP - 1586
EP - 1592
JO - Experimental Physiology
JF - Experimental Physiology
SN - 0958-0670
IS - 12
ER -
ID: 128341928