Semaglutide engages distinct brainstem-to-hypothalamus circuits to suppress motivated feeding and regulate ketogenesis and energy expenditure
stimulation of semaglutide-responsive NTS projections to both hypothalamic regions recapitulates key effects of the corresponding Adcyap1NTS pathways on palatable-food intake and metabolism, while also suppressing fasting-induced AgRP neuron activation, demonstrating that these pathway-specific functions are retained w...