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Literature summary for 1.1.1.146 extracted from

  • Bhat, B.G.; Younis, H.; Herrera, J.; Palacio, K.; Pascual, B.; Hur, G.; Jessen, B.; Ogilvie, K.M.; Rejto, P.A.
    Antisense inhibition of 11betahydroxysteroid dehydrogenase type 1 improves diabetes in a novel cortisone-induced diabetic KK mouse model (2008), Biochem. Biophys. Res. Commun., 365, 740-745.
    View publication on PubMed

Application

Application Comment Organism
medicine inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity reduces the availability of cortisol to activate the glucocorticoid receptor, down regulates gluconeogenesis and thus reduces plasma glucose levels in cortisone-induced diabetic KK mice. In mice treated with 11beta-hydroxysteroid dehydrogenase type 1-antisense oligonucleotide, plasma blood glucose levels are significantly reduced by up to 54% upon induction of diabetes. Cortisol and other diabetes end products are also reduced, and hepatic 11beta-hydroxysteroid dehydrogenase type 1 mRNA is suppressed by up to 84% Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
antisense oligonucleotide in mice treated with 11beta-hydroxysteroid dehydrogenase type 1-antisense oligonucleotide, plasma blood glucose levels are significantly reduced by up to 54% upon induction of diabetes. Cortisol and other diabetes end products are also reduced, and hepatic 11beta-hydroxysteroid dehydrogenase type 1 mRNA is suppressed by up to 84% Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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