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Interleukin-1\u03b2 (IL-1\u03b2) is one of the most potently anorexigenic inflammatory cytokines, yet how it engages neural circuits that suppress feeding remains incompletely understood. Specifically, the role of peripheral sensory neurons in mediating IL-1\u03b2-induced anorexia is unresolved. Here, using DREADD-mediated inhibition of discrete peripheral sensory neuron populations and fiber photometry, we show that IL-1\u03b2-induced anorexia occurs in at least two temporally and mechanistically distinct phases. Shortly after IL-1\u03b2 administration, prostaglandin signaling through non-vagal sensory afferents rapidly inhibits hypothalamic AgRP neurons to suppress food intake. At later time points, anorexia becomes partially prostaglandin-independent and vagal afferent neuron-dependent. Our findings demonstrate that multiple molecular signals mediate IL-1\u03b2-induced anorexia, and that diverse peripheral sensory pathways, including a previously unappreciated contribution from non-vagal afferents, are critical links between systemic inflammation and neural control of appetite.<\/jats:p>","DOI":"10.64898\/2026.02.23.707454","type":"posted-content","created":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T00:25:19Z","timestamp":1771979119000},"source":"Crossref","is-referenced-by-count":0,"title":["IL-1\u03b2 engages distinct peripheral sensory circuits to suppress feeding across time"],"prefix":"10.64898","author":[{"given":"Nikolas W.","family":"Hayes","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Endocrinology, Metabolism and Molecular Medicine, Northwestern University, Chicago, IL 60611, USA"},{"name":"Northwestern Interdepartmental Neuroscience Graduate Program, Northwestern University, Chicago, IL 60611, 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