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However, the roles of WNTs in human obesity remain unclear. Here, the\u00a0authors screen\u00a0all Wnt\u2010related paracrine factors in 1994 obese cases and 2161 controls using whole\u2010exome sequencing (WES) and identify that 12 obese patients harbor the same mutations in RSPO1 (p.R219W\/Q) predisposing to human obesity. RSPO1 is predominantly expressed in visceral fat, primarily in the fibroblast cluster, and is increased with adiposity. Mice overexpressing human <jats:italic>RSPO1<\/jats:italic> in adipose tissues develop obesity under a high\u2010fat diet (HFD) due to reduced brown\/beige fat thermogenesis. In contrast, <jats:italic>Rspo1<\/jats:italic>\u00a0ablation resists HFD\u2010induced adiposity by increasing thermogenesis. Mechanistically, RSPO1 overexpression or administration significantly inhibits adipocyte mitochondrial respiration and thermogenesis via LGR4\u2013Wnt\/<jats:italic>\u03b2<\/jats:italic>\u2010catenin signaling pathway. Importantly, humanized knockin mice carrying the hotspot mutation (p.R219W) display suppressed thermogenesis and recapitulate the adiposity feature of obese carriers. The mutation disrupts RSPO1's electrostatic interaction with the extracellular matrix, leading to excessive RSPO1 release that activates LGR4\u2013Wnt\/<jats:italic>\u03b2<\/jats:italic>\u2010catenin signaling and attenuates thermogenic capacity in differentiated beige adipocytes. Therefore, these findings identify that gain\u2010of\u2010function mutations and excessive expression of RSPO1, acting as a paracrine Wnt activator,\u00a0suppress fat thermogenesis and contribute to obesity in humans.<\/jats:p>","DOI":"10.1002\/advs.202207152","type":"journal-article","created":{"date-parts":[[2023,2,8]],"date-time":"2023-02-08T23:37:13Z","timestamp":1675899433000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Human RSPO1 Mutation Represses Beige Adipocyte Thermogenesis and Contributes to Diet\u2010Induced Adiposity"],"prefix":"10.1002","volume":"10","author":[{"given":"Yingkai","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Endocrine and Metabolic Diseases Shanghai Institute of Endocrine and Metabolic Diseases Ruijin Hospital Shanghai Jiao Tong University School of Medicine  197 Ruijin 2nd Road Shanghai 200025 P. R. 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