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Using a\n                    <jats:italic>Drosophila<\/jats:italic>\n                    model for chronic kidney disease, we show that a high-fat diet (HFD) disrupts the slit diaphragm filtration structure in nephrocytes, the fly functional equivalent of mammalian podocytes. The structural disruption resulted in reduced filtration function in the affected nephrocytes. We demonstrate that HFD activates the JAK-STAT pathway in nephrocytes, which has previously been linked to diabetic kidney disease. JAK-STAT activation was initiated by increased expression and release of the adipokine, Upd2, from the fat body. This leptin-like hormone is a known ligand of JAK-STAT. Both genetic and pharmacological inhibition of JAK-STAT restored nephrocyte HFD-associated dysfunction. Altogether, our study reveals the importance of the JAK-STAT signaling pathway in the adipose tissue\u2212nephrocyte axis and its contribution to HFD-associated nephropathy. These findings open new avenues for intervention in treating diabetic nephropathy and chronic kidney disease.\n                  <\/jats:p>","DOI":"10.7554\/elife.96987","type":"journal-article","created":{"date-parts":[[2024,5,1]],"date-time":"2024-05-01T07:26:16Z","timestamp":1714548376000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.96987","source":"Crossref","is-referenced-by-count":5,"title":["JAK-STAT pathway activation compromises nephrocyte function in a Drosophila high-fat diet model of chronic kidney disease"],"prefix":"10.7554","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7942-3406","authenticated-orcid":true,"given":"Yunpo","family":"Zhao","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/055yg0521","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Precision Disease Modeling, Department of Medicine, University of Maryland School of Medicine","place":["Baltimore, United 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