{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:19:39Z","timestamp":1784557179423,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,3]]},"abstract":"<jats:p>Telmisartan and irbesartan are angiotensin II receptor blockers (ARBs) and reportedly stimulate adiponectin secretion from adipocytes via partial peroxisome proliferator-activated receptor \u03b3 (PPAR\u03b3) activation. However, quantitative evaluation among different ARBs hasn\u2019t been performed. Adiponectin exerts strong protection against a number of pathological events by suppressing cell death, inhibiting inflammation and enhancing cell survival, while leptin promotes inflammation, oxidative stress, atherogenesis and thrombosis. The aim of this study was to identify the most effective ARB enhancing adiponectin secretion without raising leptin secretion from human white adipocytes (HWAs). Among seven ARBs (azilsartan, candesartan, irbesartan, losartan, olmesartan, telmisartan, valsartan), telmisartan was the most effective ARB for the increase of adiponectin secretion, and irbesartan was the second, whereas the other ARBs at 1 \u00b5M had no effect on adiponectin secretion. GW9662, a PPAR\u03b3 antagonist, completely blocked pioglitazone (PPAR\u03b3 agonist)-induced adiponectin secretion and mRNA expression, whereas it unexpectedly blocked neither telmisartan- nor irbesartan-induced adiponectin secretion and mRNA expression, but rather increased them. GW6471, PPAR\u03b1 antagonist, and siRNA for PPAR\u03b1 suppressed telmisartan- and irbesartan-induced adiponectin secretion, suggesting that PPAR\u03b1 is the main target of these ARBs to increase adiponectin secretion in HWAs. Leptin secretion was not affected by any ARBs at 1 \u00b5M and GW9662 significantly decreased the basal secretion of leptin, suggesting that basal leptin secretion is regulated in a PPAR\u03b3 dependent manner. We conclude that telmisartan is the most effective ARB to increase adiponectin secretion via PPAR\u03b1 without raising leptin secretion from HWAs.<\/jats:p>","DOI":"10.1530\/jme-21-0239","type":"journal-article","created":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T04:28:03Z","timestamp":1648700883000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":2,"title":["Telmisartan is the most effective ARB to increase adiponectin via PPAR\u03b1 in adipocyte"],"prefix":"10.1530","author":[{"given":"Naoki","family":"Hattori","sequence":"first","affiliation":[{"name":"N Hattori, Pharmaceutical Sciences, Ritsumeikan University - Biwako Kusatsu Campus, Kusatsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayato","family":"Yamada","sequence":"additional","affiliation":[{"name":"A Yamada, Pharmaceutical Sciences, Ritsumeikan University - Biwako Kusatsu Campus, Kusatsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shunya","family":"Nakatsuji","sequence":"additional","affiliation":[{"name":"S Nakatsuji, Pharmaceutical Sciences, Ritsumeikan University - Biwako Kusatsu Campus, Kusatsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeshi","family":"Matsuda","sequence":"additional","affiliation":[{"name":"T Matsuda, Pharmaceutical Sciences, Ritsumeikan University - Biwako Kusatsu Campus, Kusatsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norito","family":"Nishiyama","sequence":"additional","affiliation":[{"name":"N Nishiyama, Pharmaceutical Sciences, Ritsumeikan University - Biwako Kusatsu Campus, Kusatsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Shimatsu","sequence":"additional","affiliation":[{"name":"A Shimatsu, Advanced Medical Care Center, Omi Medical Center, Kusatsu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Molecular Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/jme.bioscientifica.com\/view\/journals\/jme\/aop\/jme-21-0239\/jme-21-0239.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/jme.bioscientifica.com\/downloadpdf\/journals\/jme\/aop\/jme-21-0239\/jme-21-0239.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:54:09Z","timestamp":1784555649000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/jme\/article\/69\/1\/259-268\/14533"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022,3]]},"references-count":0,"URL":"https:\/\/doi.org\/10.1530\/jme-21-0239","relation":{},"ISSN":["0952-5041","1479-6813"],"issn-type":[{"value":"0952-5041","type":"print"},{"value":"1479-6813","type":"electronic"}],"subject":[],"published":{"date-parts":[[2022,3]]}}}