期刊
JOURNAL OF CELL BIOLOGY
卷 207, 期 3, 页码 365-374出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201403080
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资金
- Wenner-Gren Foundations
- Australian Research Council Linkage International fellowship [LX0989791]
- National Health and Medical Research Council (NHMRC) CJ Martin Overseas Biomedical Fellowship [606763]
- NHMRC Career Development Fellowship [545952]
- Vetenskapsradet Medicin (VR-M) from the Swedish Research Council
- Novonordiskfonden
- Stiftelsen Svenska Diabetesforbundets Forskningsfond
- Magnus Bergvall foundation
- Carl Tryggers foundation
- Australian Research Council [LX0989791] Funding Source: Australian Research Council
Brown adipose tissue is the primary site for thermogenesis and can consume, in addition to free fatty acids, a very high amount of glucose from the blood, which can both acutely and chronically affect glucose homeostasis. Here, we show that mechanistic target of rapamycin (mTOR) complex 2 has a novel role in beta(3)-adrenoceptor-stimulated glucose uptake in brown adipose tissue. We show that beta(3)-adrenoceptors stimulate glucose uptake in brown adipose tissue via a signaling pathway that is comprised of two different parts: one part dependent on cAMP-mediated increases in GLUT1 transcription and de novo synthesis of GLUT1 and another part dependent on mTOR complex 2-stimulated translocation of newly synthesized GLUT1 to the plasma membrane, leading to increased glucose uptake. Both parts are essential for beta(3)-adrenoceptor-stimulated glucose uptake. Importantly, the effect of beta(3)-adrenoceptor on mTOR complex 2 is independent of the classical insulin-phosphoinositide 3-kinase-Akt pathway, highlighting a novel mechanism of mTOR complex 2 activation.
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