{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T18:03:03Z","timestamp":1771956183275,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiological Genomics"],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:p> The pharmacological action of peroxisome proliferator-activated receptor (PPAR)\u03b3 in promoting sodium and water retention is well documented as highlighted by the major side-effect of body weight gain and edema associated with thiazolidinedione use. However, a possible physiological role of PPAR\u03b3 in regulation of fluid metabolism has not been reported by previous studies. Here we analyzed fluid metabolism in inducible whole-body PPAR\u03b3 knockout mice. The null mice developed severe polydipsia and polyuria, reduced urine osmolality, and modest hyperphagia. The phenomenon persisted during 3 days of pair feeding and pair drinking, accompanied by progressive weight loss. After 24 h water deprivation, the null mice had a lower urine osmolality, a higher urine volume, a greater weight loss, and a greater rise in hematocrit than the floxed control. Urinary vasopressin (AVP) excretion was not different between the genotypes under basal condition or after WD. The response of urine osmolality to acute and chronic 1-desamino-8-d-arginine vasopressin treatment was attenuated in the null mice, but the total abundance or phosphorylation of aquaporin 2 (AQP2) in the kidney or AVP-induced cAMP production in inner medullary collecting duct suspensions was unaffected. Overall, PPAR\u03b3 participates in physiological control of fluid homeostasis through an unknown mechanism involving cAMP\/AQP2-independent enhancement of AVP response. <\/jats:p>","DOI":"10.1152\/physiolgenomics.00066.2015","type":"journal-article","created":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T22:28:43Z","timestamp":1441146523000},"page":"541-547","source":"Crossref","is-referenced-by-count":10,"title":["Systemic PPAR\u03b3 deletion causes severe disturbance in fluid homeostasis in mice"],"prefix":"10.1152","volume":"47","author":[{"given":"Li","family":"Zhou","sequence":"first","affiliation":[{"name":"Institute of Hypertension, Sun Yat-sen University School of Medicine, Guangzhou, China;"},{"name":"Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexandra","family":"Panasiuk","sequence":"additional","affiliation":[{"name":"Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah; 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