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Activation of mTORC1 is essential for β-adrenergic stimulation of adipose browning
Activation of mTORC1 is required for fat browning triggered by beta-adrenergic signals
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Abstract
Activation of the p70 ribosomal S6 kinase (S6K1) through mTORC1 is triggered by PKA activation in both mouse and human fat cells.
- Insulin is known to promote energy storage, while catecholamines stimulate the release of energy from fat.
- Mice with impaired mTORC1 signaling did not show the expected increase in uncoupling protein UCP1 expression or browning of white adipose tissue when stimulated by β-adrenergic receptors.
- PKA directly phosphorylated mTOR and RAPTOR, affecting S6K1 activation independently of insulin signaling.
- Disruption of the PKA site on RAPTOR hindered βAR/mTORC1 activation of S6K1, but did not interfere with insulin-induced mTORC1 activation.
- A phosphomimetic version of RAPTOR increased S6K1 activity, suggesting a regulatory role in adipose browning.
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