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To address this question, we used a chemogenetic approach to selectively stimulate G\n            <jats:sub>12\/13<\/jats:sub>\n            signaling in POMC neurons. We found that receptor-mediated activation of G\n            <jats:sub>12\/13<\/jats:sub>\n            signaling in POMC neurons caused notable improvements in glucose homeostasis in lean and obese mice. Stimulation of G\n            <jats:sub>12\/13<\/jats:sub>\n            signaling in POMC neurons also enhanced the physiological actions of leptin. Studies with G\n            <jats:sub>12\/13<\/jats:sub>\n            knockout mice showed that G\n            <jats:sub>12\/13<\/jats:sub>\n            signaling in POMC neurons mediated the beneficial metabolic effects of lorcaserin, an appetite-suppressant drug that selectively activates serotonin 5-HT\n            <jats:sub>2C<\/jats:sub>\n            receptors. 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