{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T02:48:38Z","timestamp":1791341318634,"version":"4.3.1"},"reference-count":41,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5661","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2004,2,20]]},"abstract":"<jats:p>The association between obesity and diabetes supports an endocrine role for the adipocyte in maintaining glucose homeostasis. Here we report that mice lacking the adipocyte hormone resistin exhibit low blood glucose levels after fasting, due to reduced hepatic glucose production. This is partly mediated by activation of adenosine monophosphate\u2013activated protein kinase and decreased expression of gluconeogenic enzymes in the liver. The data thus support a physiological function for resistin in the maintenance of blood glucose during fasting. Remarkably, lack of resistin diminishes the increase in post-fast blood glucose normally associated with increased weight, suggesting a role for resistin in mediating hyperglycemia associated with obesity.<\/jats:p>","DOI":"10.1126\/science.1092341","type":"journal-article","created":{"date-parts":[[2004,2,19]],"date-time":"2004-02-19T20:53:03Z","timestamp":1077223983000},"page":"1195-1198","source":"Crossref","is-referenced-by-count":569,"title":["Regulation of Fasted Blood Glucose by Resistin"],"prefix":"10.1126","volume":"303","author":[{"given":"Ronadip R.","family":"Banerjee","sequence":"first","affiliation":[{"name":"Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Penn Diabetes Center, 611 CRB, 415 Curie Boulevard, Universityof Pennsylvania School of Medicine, Philadelphia, PA 19104, USA."},{"name":"Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shamina M.","family":"Rangwala","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Penn Diabetes Center, 611 CRB, 415 Curie Boulevard, Universityof Pennsylvania School of Medicine, Philadelphia, PA 19104, USA."},{"name":"Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer S.","family":"Shapiro","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Penn Diabetes Center, 611 CRB, 415 Curie Boulevard, Universityof Pennsylvania School of Medicine, Philadelphia, PA 19104, USA."},{"name":"Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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Mu and M. Birnbaum for AMPK antibodies and advice and D. Zhou and J. Epstein for assistance with embryonic stem (ES) cell injection. Funded by NIDDK (M.A.L. and L.R.) and the American Diabetes Association (S.M.R. and M.A.L.). R.R.B. was supported by Genetics Training Grant NIH T32-GM008216. Cores funded by NIH P30 DK19525 [mouse phenotyping (H. Patel) radioimmunoassay (H. Colins) and transgenic (J. Richa)] NIH P01 DK49210 [morphology(G. Swain) and ES (H. Fu K. 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