Disclosure: The authors declared no conflict of interest.
Article first published online: 12 MAR 2013
Copyright © 2012 The Obesity Society
Volume 21, Issue 1, pages E22–E25, January 2013
How to Cite
Yoshikawa, O., Ebata, Y., Tsuchiya, H., Kawahara, A., Kojima, C., Ikeda, Y., Hama, S., Kogure, K., Shudo, K. and Shiota, G. (2013), A retinoic acid receptor agonist tamibarotene suppresses iron accumulation in the liver. Obesity, 21: E22–E25. doi: 10.1002/oby.20013
Funding agencies: This work was supported in part by Kyoto Pharmaceutical University Fund for the Promotion of Scientific Research (HT) and by a Grant-in-Aid for Young Scientists B (No. 21790666, HT) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan.
- Issue published online: 12 MAR 2013
- Article first published online: 12 MAR 2013
- Accepted manuscript online: 7 AUG 2012 02:45PM EST
- Manuscript Accepted: 12 JUN 2012
- Manuscript Received: 18 DEC 2011
Hepatic iron overload (HIO) and iron-induced oxidative stress have recently emerged as an important factor for the development and progression of insulin resistance. The aim of this study was to evaluate the effect of tamibarotene, a selective retinoic acid receptor α/β agonist, on hepatic iron metabolism, based on our previous findings that retinoids suppress hepatic iron accumulation by increasing hepatic iron efflux through the regulation of hemojuvelin and ferroportin expression.
Design and Methods:
We quantitated the non-heme iron content and iron metabolism-related gene expression in the liver, and serum lipid and blood glucose levels in KK-Ay mice after dietary administration of tamibarotene.
It was demonstrated that tamibarotene significantly reduced blood glucose and hepatic iron, but not serum lipids, and that hemojuvelin expression significantly decreased while ferroportin increased, as observed previously.
These results suggest that tamibarotene is a promising alternative for the treatment of insulin resistance associated with HIO.