Up‐regulation of uncoupling proteins by β‐adrenergic stimulation in L6 myotubes

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Abstract
Catecholamine-induced and β-adrenergic receptor (β-AR)-mediated thermogenesis in skeletal muscle is a significant component of whole-body energy expenditure. Skeletal muscle expresses uncoupling protein (UCP) 2 and UCP3, which can dissipate the transmitochondrial electrochemical gradient and thereby may be involved in regulation of energy metabolism. We investigated the effects of β-AR stimulation on UCP2 and UCP3 expression in L6 myotubes. Stimulation of the cells with epinephrine increased the UCP3 mRNA level transiently at 6 h, and also the UCP2 mRNA level at 6–24 h. The stimulatory effects of epinephrine were also observed in the presence of carbacyclin and 9-cis retinoic acid, and mimicked by isoproterenol and salbutamol (β2-AR agonists), but abolished by propranolol and ICI-118,551 (β2-AR antagonists). Pharmacological and mRNA analyses revealed the existence of β2-AR, but not β1- and β3-ARs, in L6 myotubes. These results suggested that catecholamines up-regulate UCP2 and UCP3 expression through direct action on the β2-AR in skeletal muscle

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