Abstract
In normal people, induction by FGF23 of renal Cyp24a1, the enzyme that degrades 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, helps to protect from the disorders caused by excessive 1,25-dihydroxyvitamin D. Dai and co-workers report, however, that in human and mouse kidney disease, high FGF23 concurs with low rather than high serum 24,25-dihydroxyvitamin D, a biomarker of Cyp24a1 activity. Their characterization of the underlying mechanisms provides new understanding of how kidney disease impairs the health benefits of vitamin D-FGF23/klotho interactions.
| Original language | English |
|---|---|
| Pages (from-to) | 1046-1049 |
| Number of pages | 4 |
| Journal | Kidney International |
| Volume | 82 |
| Issue number | 10 |
| DOIs |
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| State | Published - Nov 2 2012 |
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