{
  "id": 6378966,
  "title": "Semaglutide engages distinct brainstem-to-hypothalamus circuits to suppress motivated feeding and regulate ketogenesis and energy expenditure",
  "url": "https://urgent.news/2026/09/08/semaglutide-engages-distinct-brainstem-to-hypothalamus-circuits-to",
  "topic": "science",
  "section": "Science",
  "published": "2026-09-08T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.09.04.749561v1?rss=1"
  },
  "original_language": "en",
  "account": "Semaglutide's ability to induce weight loss appears to be linked to specific circuits within the brainstem and hypothalamus. Researchers identified neurons in the dorsal vagal complex (DVC) that play a key role in this process. Further investigation revealed that DVC-derived brain circuits coordinate semaglutide's effects on feeding and metabolism.\n\nOptogenetic stimulation demonstrated that Adcyap1+ neurons in the nucleus of the solitary tract (Adcyap1NTS) of the DVC suppress fasting-induced AgRP neuron activation. Importantly, stimulating Adcyap1NTS inputs to the arcuate nucleus and dorsomedial hypothalamus led to non-aversive suppression of feeding during heightened motivational drive, while still allowing active-phase chow intake. Conversely, stimulating the Adcyap1NTS[- ]arcuate pathway promoted ketogenesis and weight loss independent of food intake, while stimulation of the Adcyap1NTS[- ]DMH pathway decreased energy expenditure.\n\nInterestingly, stimulating semaglutide-responsive NTS projections to both hypothalamic regions replicated the effects of their respective Adcyap1NTS pathways on palatable-food intake and metabolism. Crucially, these pathway-specific functions were retained within neuronal circuits that were recruited by semaglutide's action. In summary, the findings highlight brainstem-to-hypothalamus circuit substrates through which semaglutide regulates motivated feeding and metabolic state downstream of the DVC.",
  "summary": "Semaglutide-induced weight loss requires neurons in the dorsal vagal complex (DVC), but how DVC-derived downstream brain circuits coordinate the drug's effects on feeding and metabolism is unknown. We show that semaglutide suppresses fasting-induced AgRP neuron activation through DVC neurons, including Adcyap1+ neurons of the nucleus of the solitary tract (Adcyap1NTS). Projection-specific…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}