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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA6z9I2lQBRqjCw_SqOs6kdBxnlAw1ZYMKQUfhpQYtHY0#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RA6z9I2lQBRqjCw_SqOs6kdBxnlAw1ZYMKQUfhpQYtHY0#_4 http://www.w3.org/ns/prov#value Rosiglitazone treatment also completely normalized the elevated serum RBP4 levels in adipose-Glut4-/- mice (Fig. 2c). The dramatic effect of this insulin-sensitizing anti-diabetic agent on serum RBP4 levels raises the possibility that elevation of RBP4 might play a causative role in insulin resistance and type 2 diabetes. Increased RBP4 causes insulin resistance Transgenic mice expressing human RBP4 driven by the mouse muscle creatine kinase (Mck) promoter (RBP4-Tg) have an ,3-fold increase in serum RBP4 levels compared with non-transgenic mice19, similar to the elevation observed in serum of adipose-Glut4-/- mice (see Supplementary Fig. 2). RBP4-Tg mice develop normally. Growth curves are similar to wild-type mice until at least 16 weeks of age (not shown). Insulin levels are higher in fed RBP4-Tg mice compared with wild-type mice, indicating insulin resistance (see Supplementary Table 2), which is also evident in insulin tolerance tests (Fig. 3a). 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