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Mifepristone is not only an antagonist of the glucocorticoid receptor but also an agonist of PPAR\u03b3. Therefore, the present study investigated the effect of mifepristone on adipocyte differentiation.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Mouse 3T3-L1 cells were used as a model for adipocyte differentiation. The lipid droplet formation was evaluated with Bodipy493\/503 staining and the expression of adipocyte markers [adiponectin and adipocyte fatty acid binding protein-4 (Fabp4)] was evaluated with quantitative PCR and immunoblot analyses for indication of adipocyte differentiation. siRNA and neutralizing antibodies were used to elucidate the molecular mechanism of mifepristone-induced adipocyte differentiation. Luciferase reporter assay was used to examine the effect of mifepristone on the promoter activity of PPAR-response element (PPRE). The DNA microarray analysis was used to characterize the transcriptome of the mifepristone-induced adipocytes. In vivo adipogenic effect of mifepristone was examined in mice.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Mifepristone not only enhanced adipocyte differentiation induced by the conventional protocol consisting of insulin, dexamethasone and 3-isobutyl-1-methylxanthine but also induced adipocyte differentiation alone, as evidenced by lipid droplets formation and induction of the expression of adiponectin and Fabp4. These effects were inhibited by an adiponectin-neutralizing antibody and a PPAR\u03b3 antagonist. Mifepristone activated the promoter activity of PPRE in a manner sensitive to PPAR\u03b3 antagonist. A principal component analysis (PCA) of DNA microarray data revealed that the mifepristone-induced adipocytes represent some characteristics of the in situ adipocytes in normal adipose tissues to a greater extent than those induced by the conventional protocol. Mifepristone administration induced an increase in the weight of epididymal, perirenal and gluteofemoral adipose tissues.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Mifepristone alone is capable of inducing adipocyte differentiation in 3T3-L1 cells and adipogenesis in vivo. PPAR\u03b3 plays a critical role in the mifepristone-induced adipocyte differentiation. Mifepristone-induced adipocytes are closer to the in situ adipocytes than those induced by the conventional protocol. The present study proposes a single treatment with mifepristone as a novel protocol to induce more physiologically relevant adipocytes in 3T3-L1 cells than the conventional protocol.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s11658-024-00559-9","type":"journal-article","created":{"date-parts":[[2024,3,29]],"date-time":"2024-03-29T15:01:46Z","timestamp":1711724506000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Effects of mifepristone on adipocyte differentiation in mouse 3T3-L1 cells"],"prefix":"10.1186","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-8232-9656","authenticated-orcid":false,"given":"Takeshi","family":"Hashimoto","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katsuya","family":"Hirano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,3,29]]},"reference":[{"issue":"4","key":"559_CR1","doi-asserted-by":"publisher","first-page":"242","DOI":"10.1038\/s41580-018-0093-z","volume":"20","author":"AL Ghaben","year":"2019","unstructured":"Ghaben AL, Scherer PE. 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All animal experiments were approved by the Animal Care and Use Committee for Kagawa University (approval no. 19609 and 22606), which follows the Basel Declaration, and were carried out according to the guidelines of established by Ministry of the Environment of Japan, Ministry of Education, Culture, Sports, Science and Technology of Japan, Science Council of Japan.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"The authors declare no competing interests in association with the present study.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"45"}}