Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAr29SoHMyMljOVcBH7ZQNTRWacBfrgT41-PJvpJKi8Pc#provenance>. }

Showing items 1 to 11 of 11 with 100 items per page.

_4 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "1.4" provenance.
large_corpus.bel authoredBy _4 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _3 provenance.
assertion hadPrimarySource 16034410 provenance.
_3 wasQuotedFrom 16034410 provenance.
_3 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). There are no differences in glucose, free fatty acid, leptin, adiponectin or resistin levels in fed RBP4-Tg mice compared with controls (see Supplementary Table 2)." provenance.