{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T05:06:41Z","timestamp":1789535201014,"version":"build-2803163510"},"reference-count":63,"publisher":"MDPI AG","issue":"18","license":[{"start":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T00:00:00Z","timestamp":1788998400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01HL160860"],"award-info":[{"award-number":["R01HL160860"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01HL160908"],"award-info":[{"award-number":["R01HL160908"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"award":["R01HL160860"],"award-info":[{"award-number":["R01HL160860"]}],"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R01HL160908"],"award-info":[{"award-number":["R01HL160908"]}],"id":[{"id":"https:\/\/ror.org\/045p44t13","id-type":"ROR","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002129","name":"The Heart Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100002129","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Adipose tissue dysfunction drives obesity-associated metabolic disease, yet the transcriptional regulators of pathological adipose remodeling remain undefined. Here, we identify adipocyte Gata3 as a diet-inducible regulator that is dispensable for basal adipogenesis but necessary and sufficient for diet-induced obesity and systemic metabolic dysfunction. Adipocyte-specific Gata3 deletion redirects adipose expansion from hypertrophic to hyperplastic growth and improves glucose tolerance, insulin sensitivity, and adipose inflammation, whereas human GATA3 re-expression in adipocytes restores obesity and metabolic dysfunction, suggesting cross-species conservation and establishing both necessity and sufficiency for a causal driver. Multi-omic profiling, integrating proteomics, metabolomics, and single-cell mass cytometry, reveals that Gata3 loss suppresses a STAT3-anchored inflammatory myeloid program while enhancing mitochondrial oxidative capacity. Through further tracing of this adipocyte-intrinsic program to distal metabolic organs, systemic lipidomic and chemokine profiling identifies a two-pronged mechanism through which adipocyte Gata3 drives hepatic dysfunction: selective remodeling of lipoprotein-surface lipids and a coordinated CXCL5\/CXCL2\/CXCL9 chemokine axis. Collectively, these findings reposition Gata3 from a putative anti-adipogenic brake to a diet-inducible master regulator of pathological adipose remodeling and nominate adipocyte-targeted Gata3 inhibition as a strategy to uncouple adipose expansion from systemic metabolic disease.<\/jats:p>","DOI":"10.3390\/cells15181644","type":"journal-article","created":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T14:11:22Z","timestamp":1789049482000},"page":"1644","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Adipocyte Gata3 Is a Diet-Inducible Driver of Pathological Adipose Remodeling and Systemic Metabolic Disease"],"prefix":"10.3390","volume":"15","author":[{"given":"Minghui","family":"Qin","sequence":"first","affiliation":[{"name":"The Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute Cedars-Sinai Med. Ctr., Los Angeles, CA 90048, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fuqiang","family":"Li","sequence":"additional","affiliation":[{"name":"The Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute Cedars-Sinai Med. Ctr., Los Angeles, CA 90048, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingjie","family":"Yang","sequence":"additional","affiliation":[{"name":"The Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute Cedars-Sinai Med. Ctr., Los Angeles, CA 90048, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lai","family":"Wang","sequence":"additional","affiliation":[{"name":"The Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute Cedars-Sinai Med. 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