| First Author | Kim YK | Year | 2011 |
| Journal | FASEB J | Volume | 25 |
| Issue | 5 | Pages | 1641-52 |
| PubMed ID | 21285397 | Mgi Jnum | J:172777 |
| Mgi Id | MGI:5008723 | Doi | 10.1096/fj.10-175448 |
| Citation | Kim YK, et al. (2011) beta-Carotene and its cleavage enzyme beta-carotene-15,15'-oxygenase (CMOI) affect retinoid metabolism in developing tissues. FASEB J 25(5):1641-52 |
| abstractText | The mammalian embryo relies on maternal circulating retinoids (vitamin A derivatives) for development. beta-Carotene is the major human dietary provitamin A. beta-Carotene-15,15'-oxygenase (CMOI) has been proposed as the main enzyme generating retinoid from beta-carotene in vivo. CMOI is expressed in embryonic tissues, suggesting that beta-carotene provides retinoids locally during development. We performed loss of CMOI function studies in mice lacking retinol-binding protein (RBP), an established model of embryonic vitamin A deficiency (VAD). We show that, unexpectedly, lack of CMOI in the developing tissues further exacerbates the severity of VAD and thus the embryonic malformations of RBP(-/-) mice. Since beta-carotene was not present in any of the mouse diets, we unveiled a novel action of CMOI independent from its beta-carotene cleavage activity. We also show for the first time that CMOI exerts an additional function on retinoid metabolism by influencing retinyl ester formation via modulation of lecithin:retinol acyltransferase (LRAT) activity, at least in developing tissues. Finally, we demonstrate unequivocally that beta-carotene can serve as an alternative vitamin A source for the in situ synthesis of retinoids in developing tissues by the action of CMOI. |
