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

2010 ◽  
Vol 95 (2) ◽  
pp. 977-977
Author(s):  
Neva J. Fudge ◽  
Christopher S. Kovacs
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Calcium Absorption ◽  
Intestinal Calcium Absorption ◽  
Skeletal Mineralization

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.

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

scholarly journals Intestinal Calcium Absorption and Serum Vitamin D Metabolites in Normal Subjects and Osteoporotic Patients

1979 ◽  
Vol 64 (3) ◽  
pp. 729-736 ◽  
Author(s):  
J. C. Gallagher ◽  
B. Lawrence Riggs ◽  
John Eisman ◽  
Alan Hamstra ◽  
Sara B. Arnaud ◽  
...  
Keyword(s):  
Vitamin D ◽  
Calcium Absorption ◽  
Serum Vitamin ◽  
Normal Subjects ◽  
Intestinal Calcium Absorption ◽  
Vitamin D Metabolites ◽  
Serum Vitamin D

scholarly journals Novel vitamin D analogs that modulate leukemic cell growth and differentiation with little effect on either intestinal calcium absorption or bone mobilization

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 82-93 ◽  
Author(s):  
JY Zhou ◽  
AW Norman ◽  
M Lubbert ◽  
ED Collins ◽  
MR Uskokovic ◽  
...  
Keyword(s):  
Vitamin D ◽  
Mechanism Of Action ◽  
Vitamin D3 ◽  
Clonal Growth ◽  
Calcium Absorption ◽  
Active Form ◽  
Intestinal Calcium Absorption ◽  
Leukemic Cells ◽  
Binding Studies ◽  
Vitamin D Analogs

Abstract Induction of terminal differentiation of leukemic and preleukemic cells is a therapeutic approach to leukemia and preleukemia. The 1 alpha, 25- dihydroxyvitamin D3 [1,25(OH)2D3], the hormonally active form of vitamin D3, can induce differentiation and inhibit proliferation of leukemia cells, but concentrations required to achieve these effects cause life-threatening hypercalcemia. Seven new analogs of 1,25(OH)2D3 were discovered to be either equivalent or more potent than 1,25(OH)2D3 as assessed by: (a) inhibition of clonal proliferation of HL-60, EM-2, U937, and patients' myeloid leukemic cells: and (b) induction of differentiation of HL-60 promyelocytes. Furthermore, these analogs stimulated clonal growth of normal human myeloid stem cells. The most potent analog, 1,25-dihydroxy-16ene-23yne-vitamin D3, was about fourfold more potent than 1,25(OH)2D3. This analog decreased clonal growth and expression of c-myc oncogene in HL-60 cells by 50% within ten hours of exposure. Effects on calcium metabolism of these novel analogs in vivo was assessed by intestinal calcium absorption (ICA) and bone calcium mobilization (BCM). Each of the analogs mediated markedly less (10 to 200-fold) ICA and BCM as compared with 1,25(OH)2D3. To gain insight into the possible mechanism of action of these new analogs, receptor binding studies were done with 1,25(OH)2–16ene-23yne-D3 and showed that it competed only about 60% as effectively as 1,25(OH)2D3 for 1,25(OH)2D3 receptors present in HL-60 cells and 98% as effective as 1,25(OH)2D3 for receptors present in chick intestinal cells. In summary, we have discovered seven novel vitamin D analogs that are more potent than the physiologic 1,25(OH)2D3 as measured by a variety of hematopoietic assays. In contrast, these compounds appear to have the potential to be markedly less toxic (induction of hypercalcemia). These novel vitamin D compounds may be superior to 1,25(OH)2D3 in a number of clinical situations including leukemia/preleukemia; they will provide a tool to dissect the mechanism of action of vitamin D seco-steroids in promoting cellular differentiation.

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