{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T19:22:53Z","timestamp":1774898573483,"version":"3.50.1"},"reference-count":44,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2010,3,4]],"date-time":"2010-03-04T00:00:00Z","timestamp":1267660800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p>\n                    Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in the pathogenesis of a variety of autoimmune inflammatory diseases. Here, we investigated the role of MIF in the pathogenesis of non\u2010insulin\u2010dependent diabetes mellitus (NIDDM) using MIF\u2212\/\u2212 mice and a mouse model of streptozotocin (STZ)\u2010induced NIDDM. Following single injection of STZ, MIF\n                    <jats:sup>+\/+<\/jats:sup>\n                    BALB\/c mice showed a significant increase in blood glucose levels, developed polyuria, and succumbed to disease. In contrast, no such increase in blood glucose was observed in MIF \u2212\/\u2212 BALB\/c mice treated with STZ. These mice produced significantly less inflammatory cytokines and resistin as compared with MIF\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice and failed to develop clinical disease. Finally, oral administration of a smallmolecule MIF antagonist, CPSI\u20101306, to outbred ICR mice following induction of NIDDM significantly lowered blood glucose levels in the majority of animals, which was also associated with a significant reduction in the levels of the proinflammatory cytokines IL\u20106 and TNF\u2010\u03b1 in the sera. Taken together, these results demonstrate that MIF is involved in the pathogenesis of NIDDM and is a therapeutic target to treat this disease.\u2014Sanchez\u2010Zamora, Y., Terrazas, L. I., Vilches\u2010Flores, A, Leal, E., Jua\u00b4rez, I., Whitacre, C, Kithcart, A., Pruitt, J., Sielecki, T., Satoskar, A. R, Rodriguez\u2010Sosa, M. Macrophage migration inhibitory factor is a therapeutic target in treatment of non\u2010insulin\u2010dependent diabetes mellitus.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    24, 2583\u20132590 (2010).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.09-147066","type":"journal-article","created":{"date-parts":[[2010,3,4]],"date-time":"2010-03-04T20:51:47Z","timestamp":1267735907000},"page":"2583-2590","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["Macrophage migration inhibitory factor is a therapeutic target in treatment of non\u2010insulin\u2010dependent diabetes mellitus"],"prefix":"10.1096","volume":"24","author":[{"given":"Yuriko","family":"Sanchez\u2010Zamora","sequence":"first","affiliation":[{"name":"Department of 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