G protein-coupled receptors (GPCRs) are a major therapeutic target for the treatment of many diseases and disorders, including type 2 diabetes and potentially obesity. For example, adrenoceptor (AR) agonists have beneficial effects in brown adipose tissue via activation of β3-ARs, skeletal muscle via β2-ARs and cardiac myocytes via α1A-ARs, by increasing glucose uptake in vitro and in vivo. We show that ARs increase glucose uptake in these three tissues via a mechanism that does not involve PI3K or Akt, kinases that are integral to insulin-mediated glucose uptake. We do show that mammalian target of rapamycin (mTOR) complex 2 (but not complex 1) has a novel role in AR- stimulated glucose uptake in all three tissues. In brown adipocytes, β3-ARs increase glucose uptake via a signaling pathway that comprises two different parts: one part dependent upon cAMP- mediated increases in GLUT1 transcription and de novo synthesis of GLUT1, and another part dependent on mTOR complex 2-stimulated translocation of GLUT1 to the plasma membrane. In skeletal muscle, β2-ARs increase glucose uptake via a signaling pathway dependent upon cAMP mediated activation of mTOR complex 2, resulting in translocation of GLUT4 to the plasma membrane. In cardiac myocytes, α1A-ARs increase glucose uptake via a signaling pathway comprising two parts: one dependent upon calcium-AMPK-mediated GLUT4 translocation, and the other dependent upon mTOR complex 2-mediated GLUT4 translocation. Hence mTOR complex 2 appears to have a central role in AR-mediated increases in glucose uptake.