Key result
Chemogenetic activation of G12 signaling synergistically enhanced beige adipogenesis triggered by Gs-coupled β3AR stimulation, potentiating the thermogenic effect in vivo.
Activation of G12 signaling enhances adipose tissue browning, suggesting a potential novel therapeutic pathway for combating obesity.
Does not support clinical adoption; hypothesis-generating for G12-targeted obesity therapies pending human studies.
Beige adipocytes, which increase energy expenditure by dissipating energy as heat, have gained attention as a therapeutic target for combating obesity. 1 Adipocytes express many types of G-protein-coupled receptors (GPCRs), each of which has a unique preference for the G s , G i , G q , and G 12 subfamilies. While the function of G s -coupled β-adrenergic receptors in beige adipocyte induction is well established, 2 little is known about the function of G 12 -coupled GPCRs beyond its suppressive roles in white adipocyte maturation. 3 In this study, we generated transgenic mice conditionally expressing a G 12 -coupled designer GPCR using a Cre-loxP system and investigated the potential effects of G 12 signaling on adipocyte biology.
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Ono et al. (2023) conducted a letter in Adipose tissue browning. Chemogenetic activation of G12 signaling (CNO) and CL316,243 vs. Control littermates was evaluated on Thermogenic gene expression and oxygen consumption. Chemogenetic activation of G12 signaling synergistically enhanced beige adipogenesis triggered by Gs-coupled β3AR stimulation, potentiating the thermogenic effect in vivo.
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