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This exquisite control of the neuropeptides that govern the feeding behavior could be a focal point in the pathogenesis of obesity. We reported that inactivation of C\u2010terminal binding protein 2 (CtBP2), a transcriptional corepressor with metabolite\u2010sensing capabilities, contributes to the pathogenesis of obesity in liver tissues and pancreatic \u03b2\u2010cells. Here, we describe a transcriptional system regulated by CtBP2 in the hypothalamus. Our global mapping of CtBP2 binding sites using ChIP\u2010seq combined with functional analyses revealed that CtBP2 functions as a corepressor for orexigenic neuropeptide promoters. In response to the metabolic abnormalities associated with obesity, CtBP2 undergoes allosteric inactivation and dissociates from these promoters, thereby resulting in the derepression of orexigenic neuropeptide expression. Consistently, the loss of CtBP2 in hypothalamic neurons in mice increases the expression of orexigenic neuropeptides, thus leading to increased feeding behavior. These findings highlight how obesity disrupts homeostatic mechanisms that normally maintain body weight within a healthy range.<\/jats:p>","DOI":"10.1096\/fj.202602322r","type":"journal-article","created":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T11:10:24Z","timestamp":1785323424000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Obesity Disrupts\n                    <scp>CtBP2<\/scp>\n                    \u2010Mediated Maintenance of Transcriptional Equilibrium in Hypothalamic Feeding Circuitry"],"prefix":"10.1096","volume":"40","author":[{"given":"Wanpei","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Endocrinology and Metabolism, Institute of Medicine University of Tsukuba  Ibaraki Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenta","family":"Kainoh","sequence":"additional","affiliation":[{"name":"Department of Endocrinology and Metabolism, Institute 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