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Vol. 59, Issue 4, 765-773, April 2001
Departments of Integrative Biology and Pharmacology (H.S.A.,
P.J.A.D.) and Cardiology (C.D.), University of Texas Medical School,
Houston, Texas; Ligand Pharmaceuticals, San Diego,
California (S.L., D.L.C., M.B., M.D.L., R.A.H.); and The
Salk Institute for Biological Studies, La Jolla, California (L.N.,
P.T.)
Both retinoid X receptor (RXR)-selective agonists (rexinoids) and
thiazolidinediones (TZDs), PPAR (peroxisome proliferator-activated receptor)-
-specific ligands, produce insulin sensitization in diabetic rodents. In vitro studies have demonstrated that TZDs mediate
their effects via the RXR/PPAR- complex. To determine whether
rexinoids lower hyperglycemia by activating the RXR/PPAR- heterodimer in vivo, we compared the effects of a rexinoid (LG100268) and a TZD (rosiglitazone) on gene expression in white adipose tissue,
skeletal muscle, and liver of Zucker diabetic fatty rats (ZDFs). In
adipose tissue, rosiglitazone decreased tumor necrosis factor-
(TNF-) mRNA and induced glucose transporter 4 (GLUT4), muscle
carnitine palmitoyl-transferase (MCPT), stearoyl CoA desaturase (SCD1),
and fatty acid translocase (CD36). In contrast, LG100268 increased
TNF- and had no effect or suppressed the expression of GLUT4, MCPT,
SCD1, and CD36. In liver, the rexinoid increased MCPT, SCD1, and CD36
mRNAs, whereas rosiglitazone induced only a small increase in CD36. In
skeletal muscle, rosiglitazone and LG100268 have similar effects; both
increased SCD1 and CD36 mRNAs. The differences in the pattern of genes
induced by the rexinoids and the TZDs in diabetic animals found in
these studies suggests that these compounds may have independent and
tissue-specific effects on metabolic control in vivo.
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