Relative Activities of Some Metabolites and Analogs of Cholecalciferol in Stimulation of Tibia Ash Weight in Chicks Otherwise Deprived of Vitamin D

1977 ◽  
Vol 107 (2) ◽  
pp. 194-198 ◽  
Author(s):  
Alfred Boris ◽  
James F. Hurley ◽  
Thelma Trmal
Keyword(s):  
Vitamin D ◽  
Ash Weight ◽  
Tibia Ash ◽  
Stimulation Of

scholarly journals Assessment of Vitamin D Status in Patients Suffering from Uncomplicated Malaria in a Health Center in the District of Abidjan (Côte d’Ivoire)

2021 ◽  
pp. 10-17
Author(s):  
Brice Kouakou Bla ◽  
Alexis Gnogbo Bahi ◽  
Juliana Mensah-Akaki ◽  
Souleymane Méité ◽  
Françis Adou Yapo ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parasite Density ◽  
Uncomplicated Malaria ◽  
Parasite Species ◽  
Complete Blood Count ◽  
Vitamin D Status ◽  
25 Oh Vitamin D ◽  
Stimulation Of

Aims: The pathophysiology of Plasmodium falciparum infection is most often associated with anemia and immune deficiency. Given the important role of vitamin D in the synthesis of hemoglobin and in the stimulation of the immune system, it would be essential to assess the vitamin D status of patients with malaria in order to improve the quality of treatment management. Methodology: A thick drop and a blood smear were used to determine parasite density and parasite species respectively. The complete blood count was performed using an automated analyzer labelled Sysmex XN 1000i. Biochemical parameters such as calcium and phosphorus were determined using the Cobas C311 Hitachi. The Vidas was used to determine the concentrations of 25 (OH) -vitamin D. Results: The results showed a decrease in 25 (OH) -vitamin D concentrations in relation to the parasite density and anemia observed in patients with uncomplicated malaria. Conclusion: Vitamin D status in patients with uncomplicated malaria could represent an essential biomarker in the monitoring of antimalarial treatment.

Vitamin D3 and glucose-6-phosphate dehydrogenase in rat duodenal epithelial cells

1989 ◽  
Vol 257 (5) ◽  
pp. G760-G765
Author(s):  
L. B. Nasr ◽  
J. D. Monet ◽  
P. Lucas ◽  
C. A. Bader
Keyword(s):  
Vitamin D ◽  
Intraperitoneal Administration ◽  
Middle Part ◽  
G6pd Activity ◽  
Dihydroxyvitamin D3 ◽  
Rat Duodenum ◽  
High Level ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Stimulation Of

A microdensitometric method was employed to determine enzyme activities in situ in undisrupted tissue rat duodenum. The effect of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] on glucose-6-phosphate dehydrogenase (G6PD) activity and on the two utilization pathways of synthesized NADPH, H1 (mixed function oxidation) and H2 (biosynthesis), was studied. In normal animals, a crypt-to-villus gradient of G6PD activity and of both NADPH utilization pathways was observed. A high level of NADPH utilization occurred predominantly via the H2 pathway. In vitamin D-deficient rat animals, G6PD activity in the middle part of the villus was approximately 60% lower than in normal animals [10.05 +/- 0.35 vs. 3.95 +/- 0.26 (means +/- SE) A585.min-1.micron-3 X 10(5), P less than 0.001] with reduced NADPH utilization via the H2 pathway (8.39 +/- 0.49 vs. 2.73 +/- 0.43 A585.min-1.micron-3 X 10(5), P less than 0.001) but not the H1 pathway (1.65 +/- 0.17 vs. 1.22 +/- 0.19 A585.min-1.micron-3 X 10(5), P = NS). Intraperitoneal administration of 1,25(OH)2D3 (500 pmol) to vitamin D-deficient animals resulted in increased G6PD activity within 30 min (4.09 +/- 0.38 vs. 5.51 +/- 0.39 A585.min-1.micron-3 X 10(5), P less than 0.05), attaining normal levels within 2 h. The H2 but not the H1 pathway of NADPH utilization increased significantly in response to 1,25(OH)2D3. This increase is essentially located in the basal and middle parts of the villus. Thus 1,25(OH)2D3 may influence biosynthesis in the duodenum via stimulation of G6PD activity and the H2 pathway of NADPH utilization.

Stimulation of Calmodulin Binding to Skeletal Muscle Membrane Proteins by 1,25-Dihydroxy-Vitamin D 3

1990 ◽  
Vol 45 (6) ◽  
pp. 663-670 ◽  
Author(s):  
Virginia Massheimer ◽  
Luis M. Fernandez ◽  
Ana R. de Boland
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Membrane Proteins ◽  
Binding Proteins ◽  
Sodium Dodecyl ◽  
Muscle Membrane ◽  
Calmodulin Binding ◽  
Ca Uptake ◽  
Vitamin D 3 ◽  
Stimulation Of

Abstract Previous work has shown that 1,25-dihydroxy-vitamin D 3 rapidly increases calmodulin levels of skeletal muscle membranes without altering the muscle cell calmodulin content. Therefore, the effects of the sterol on the binding of calmodulin to specific muscle membrane proteins were investigated. Soleus muscles from vitamin D-deficient chicks were treated in vitro for short intervals (5-15 min) with physiological concentrations of 1,25-dihydroxy-vitamin D3. Proteins of mitochondria and microsomes isolated by differential centrifugation were separated on sodium dodecyl sulfate polyacrylamide gels. Calmodulin-binding proteins were identified by a [125I]calmodulin gel overlay procedure followed by autoradiography. 1,25-Dihydroxy- vitamin D3 increased the binding of labelled calmodulin to a major, calcium-independent, calmodulin-binding protein of 28 Kda localized in microsomes, and to minor calmodulin- binding proteins of 78 and 130 Kda proteins localized in mitochondria. The binding of [125I]calmodulin to these proteins was abolished by flufenazine or excess non-radioactive calmodulin. 1,25-Dihydroxy-vitamin D3 rapidly increased muscle tissue Ca uptake and cyclic AM P levels and stimulated the phosphorylation of several membrane proteins including those whose calmodulin-binding capacity potentiates. Analogously to the sterol, forskolin increased membrane calmodulin content, calmodulin binding to the 28 Kda microsomal protein and 45Ca uptake by soleus muscle preparations. Forskolin also induced a similar profile of changes in muscle membrane protein phosphorylation as the hormone. These results suggest that 1,25- dihydroxy-vitamin D 3 affects calmodulin distribution in muscle cells through cyclic AMP-dependent phosphorylation of membrane calmodulin-binding proteins. These changes may play a role in the stimulation of muscle Ca uptake by the sterol.

scholarly journals Stimulation of Intestinal Mucosal Proliferation by Vitamin D

1973 ◽  
Vol 64 (5) ◽  
pp. 977-982 ◽  
Author(s):  
Stanley J. Birge ◽  
David H. Alpers
Keyword(s):  
Vitamin D ◽  
Mucosal Proliferation ◽  
Stimulation Of

Stimulation of 24R,25-dihydroxyvitamin D3 synthesis by metabolites of vitamin D3

1983 ◽  
Vol 245 (4) ◽  
pp. E359-E364 ◽  
Author(s):  
G. S. Reddy ◽  
G. Jones ◽  
S. W. Kooh ◽  
D. Fraser ◽  
H. F. DeLuca
Keyword(s):  
Vitamin D ◽  
Vitamin D3 ◽  
The Other ◽  
Hydroxyl Group ◽  
Vitamin D Metabolites ◽  
Structural Requirements ◽  
Dihydroxyvitamin D3 ◽  
Hydroxylated Metabolites ◽  
Perfusion Period ◽  
Stimulation Of

Previously we have shown that the isolated perfused kidney from vitamin D-deficient rats converts [3H]25(OH)D3 into [3H]1 alpha,25(OH)2D3. When certain vitamin D metabolites were added to perfusate the same kidney began to synthesize [3H]24R,25(OH)2D3. In this study we investigated the structural requirements of the vitamin D molecule necessary to stimulate synthesis of [3H]24R,25(OH)2D3 in a 1-hydroxylating kidney. Kidneys were perfused with tracer [3H]25(OH)D3 (450 pM) alone and in the presence of a variety of hydroxylated metabolites and fluorinated analogues of vitamin D3 at concentrations of 450 pM to 25 microM. Tracer [3H]25(OH)D3 alone resulted in synthesis of only [3H]1 alpha,25(OH)2D3 during the 6-h perfusion period. 25-Hydroxylated metabolites [25(OH)D3, 25 nM; 1 alpha,25(OH)2D3, 25 nM; 24R,25(OH)2D3, 25 nM; 24(F)2,25(OH)D3, 50 nM] stimulated [3H]24R,25(OH)2D3 production at 2 h of perfusion. On the other hand, analogues without the 25-hydroxyl group [D3; 1 alpha(OH)D3; 25(F)D3; 1 alpha(OH),25(F)D3; 1 alpha(F)D3; 1 beta(F)D3]; did not stimulate [3H]24R,25(OH)2D3 synthesis. We conclude that the 25-hydroxyl group is an essential determinant of 24-hydroxylation.

Bone changes due to pregnancy and lactation: influence of vitamin D status

1986 ◽  
Vol 251 (4) ◽  
pp. E400-E406 ◽  
Author(s):  
P. J. Marie ◽  
L. Cancela ◽  
N. Le Boulch ◽  
L. Miravet
Keyword(s):  
Vitamin D ◽  
Bone Resorption ◽  
Bone Formation ◽  
Trabecular Bone ◽  
Formation Rate ◽  
Vitamin D Status ◽  
Bone Formation Rate ◽  
Bone Calcium ◽  
Pregnancy And Lactation ◽  
Stimulation Of

The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was mainly impaired in D-depleted rats, resulting in trabecular bone loss, which, in -D mother rats, was associated with decreased bone ash and total bone calcium. Lactation further stimulated bone resorption and reduced the trabecular bone volume; ash weight and bone calcium content were also decreased independently of the vitamin D status and changes in plasma iPTH levels. In presence of vitamin D, the bone formation rate increased fourfold during lactation but was unchanged in -D lactating rats. During lactation, vitamin D-depleted rats lost twofold more calcified bone than +D rats because of impaired mineralization. Thus, the present study shows that both the endosteal bone resorption and formation are stimulated by pregnancy and lactation and that vitamin D is required for normal bone mineralization during the reproductive period.

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