Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Address correspondence to: Marie B. Demay, Endocrine Unit, Thier 11, Massachusetts General Hospital, 50 Blossom St., Boston, Massachusetts 02114, USA. Phone: 617.726.3966; Email: firstname.lastname@example.org.
First published August 6, 2018 - More info
While disorders of impaired vitamin D activation and action have long been appreciated, the consequences of abnormalities in pathways leading to the inactivation of vitamin D metabolites have only recently been identified. Two recent articles have shed new light on this area of vitamin D biology. The report by Martineau et al., published in the JCI, describes a pathway in which binding of the vitamin D metabolite 24R,25(OH)2D3 to its effector molecule FAM57B2 plays an important role in endochondral ossification during bone repair. This work follows, and adds to, another recent JCI publication by Roizen et al., showing that rapid inactivation of vitamin D metabolites causes vitamin D deficiency, leading to vitamin D–dependent rickets.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.