Premium
Ciglitazone reverses cAMP‐induced post‐insulin receptor resistance in rat adipocytes in vitro
Author(s) -
Kirsch Diethelm M.,
Bachmann Werner,
Häring Hans U.
Publication year - 1984
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(84)80909-6
Subject(s) - ciglitazone , endocrinology , in vitro , insulin resistance , medicine , chemistry , receptor , adipogenesis , insulin , pharmacology , biology , biochemistry , peroxisome proliferator activated receptor
Ciglitazone (cig), a thiazolidine‐dione, lowers glucose and insulin levels in animal models of diabetes type II but not in controls. Since catecholamines given to rat adipocytes in vitro induce insulin resistance similar to that seen in type II diabetes in vivo, we measured the effect of cig on mono‐A14‐[ 125 I]insulin binding and 3‐O‐methyl‐D‐glucose transport (GT) in isolated rat adipocytes treated with isoprenaline (iso, 10 μM). Cig (⩽ 5 μM) reversed (ED 10 nM) the inhibitory effect of iso on insulin stimulation of GT. It had no effect on either basal or insulin stimulated GT. Furthermore, cig did not influence insulin binding either in the presence or absence of iso, which indicates that cig acts only on a post‐insulin receptor level. Cig also reversed the inhibiton of GT by both forskolin, a cyclase activator and RO20‐1724, an imidazolidine phosphodiesterase inhibitor but not that of db‐cAMP. It thus seems that cig does not act within the cAMP system but only neutralizes its inhibitory effect on the insulin stimulation of GT.