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We thus performed OGTTs on Glp1r OB-hM3Dq WD mice after chemogenetic activation of OB Glp1r -expressing neurons with concurrent blockade of GABA A R in the PVN, using a local injection of the GABA A R antagonist bicuculline (Fig

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Therefore, it can not be excluded that the existence of the disulfide bridge may contribute to the formation of tetramer, while no such disulfide bridge is present in rhGPx3 mutant