Vitamin D Receptor Genotypes and Intestinal Calcium Absorption in Postmenopausal Women

1997 ◽  
Vol 61 (6) ◽  
pp. 460-463 ◽  
Author(s):  
L. Gennari ◽  
L. Becherini ◽  
L. Masi ◽  
S. Gonnelli ◽  
C. Cepollaro ◽  
...  
Keyword(s):  
Vitamin D ◽  
Postmenopausal Women ◽  
Vitamin D Receptor ◽  
Calcium Absorption ◽  
Intestinal Calcium Absorption

The CDX2-site polymorphism in the vitamin D receptor gene and expression of genes for intestinal calcium absorption

2003 ◽  
Vol 124 (4) ◽  
pp. A126
Author(s):  
Julian R. Walters ◽  
Mohammed Khanji ◽  
Natalie Barley ◽  
Orli Rhodes-Kendler ◽  
Umma Khair
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Calcium Absorption ◽  
Receptor Gene ◽  
Intestinal Calcium Absorption ◽  
Vitamin D Receptor Gene ◽  
Expression Of Genes

scholarly journals Pregnancy Up-Regulates Intestinal Calcium Absorption and Skeletal Mineralization Independently of the Vitamin D Receptor

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 886-895 ◽  
Author(s):  
Neva J. Fudge ◽  
Christopher S. Kovacs
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Calcium Absorption ◽  
Fold Increase ◽  
Normal Diet ◽  
Intestinal Calcium Absorption ◽  
A Genome ◽  
Pregnancy And Lactation ◽  
Turnover Markers ◽  
Calbindin D

Without the vitamin D receptor (VDR), adult mammals develop reduced intestinal calcium absorption, rickets, and osteomalacia. Intestinal calcium absorption normally increases during pregnancy so that the mother can supply sufficient calcium to her fetuses. The maternal skeleton is rapidly resorbed during lactation to provide calcium needed for milk; that lost bone mineral content (BMC) is completely restored after weaning. We studied Vdr null mice to determine whether these adaptations during pregnancy and lactation require the VDR. Vdr nulls were severely rachitic at 10 wk of age on a normal diet. Pregnancy induced a 158% increase in Vdr null BMC to equal the pregnant wild-type (WT) value. Lactation caused BMC losses that were equal in Vdr nulls and WT. Vdr nulls recovered after weaning to a BMC 50% higher than before pregnancy and equal to WT. Additional analyses showed that during pregnancy, duodenal 45Ca absorption increased in Vdr nulls, secondary hyperparathyroidism lessened, bone turnover markers decreased, and osteoid became fully mineralized. A genome-wide microarray analysis of duodenal RNA found marked reduction of Trpv6 in Vdr nulls at baseline but a 13.5-fold increase during pregnancy. Calbindin D-9K (S100g) and Ca2+-ATPase (Pmca1) were not altered by pregnancy. Several other solute transporters increased during pregnancy in Vdr nulls. In summary, Vdr nulls adapt to pregnancy by up-regulating duodenal Trpv6 and intestinal 45Ca absorption, thereby enabling rapid normalization of BMC during pregnancy. These mice lactate normally and fully restore BMC after weaning. Therefore, VDR is not required for the skeletal adaptations during pregnancy, lactation, and after weaning.

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