scholarly journals Influence of Secondary Hyperparathyroidism Induced by Low Dietary Calcium, Vitamin D Deficiency, and Renal Failure on Circulating Rat PTH Molecular Forms

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Pierre D'Amour ◽  
Louise Rousseau ◽  
Stephen Hornyak ◽  
Zan Yang ◽  
Tom Cantor
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Secondary Hyperparathyroidism ◽  
Time Course ◽  
Normal Diet ◽  
Molecular Forms ◽  
Vitamin D Metabolites ◽  
Short Time ◽  
The Relationship ◽  
Normal Calcium

Rats(r) with secondary hyperparathyroidism were studied to define the relationship between vitamin D metabolites and rPTH levels measured by 3 different rat ELISAs. Controls and renal failure (RF) rats were on a normal diet, while 2 groups on a low-calcium (-Ca) or a vitamin D-deficient (-D) diet. RF was induced surgically. Mild RF rats had normal calcium and 25(OH)D but reduced 1,25(OH)2D levels (P<.001) with a 2.5-fold increased in rPTH (P<.001). Severe RF rats and those on a -Ca or -D diet had reduced calcium (P<.01) and 25(OH)D levels (P<.05), with rPTH increased by 2 (-Ca diet;P<.05), 4 (-D diet;P<.001), and 20-folds (RF;P<.001) while 1,25(OH)2D was high (-Ca diet:P<.001) or low (-D diet, RF:P<.001). 25(OH)D and 1,25(OH)2D were positively and negatively related on the -Ca and -D diets, respectively. rPTH molecular forms behaved as expected in RF and on -Ca diet, but not on -D diet with more C-rPTH fragments when less were expected. This may be related to the short-time course of this study compared to prior studies.

Stable Strontium Absorption as a Measure of Intestinal Calcium Absorption: Comparison with the Double-Radiotracer Calcium Absorption Test

1994 ◽  
Vol 87 (3) ◽  
pp. 363-368 ◽  
Author(s):  
Aubrey Blumsohn ◽  
Brian Morris ◽  
Richard Eastell
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Time Course ◽  
Calcium Absorption ◽  
Quadratic Term ◽  
The Mean ◽  
Stable Strontium ◽  
The Relationship ◽  
Dual Tracer ◽  
Fractional Absorption

1. Stable strontium (Sr) has been proposed as an alternative to calcium (Ca) isotopes for the measurement of intestinal Ca absorption. The aim of this study was to compare the time course and fractional absorption of Ca and Sr, when both are measured using dual-tracer techniques. 2. 45Ca and Sr absorption tests were carried out on consecutive days in patients with osteoporosis (n = 10) or chronic renal failure (n = 7). Both tests were repeated in four patients with chronic renal failure after treatment with calcitriol (1 μg daily for 10 days). 3. The time course of Ca absorption was determined using the 85Sr (intravenous)/45Ca (oral) dual-tracer technique, and the time course of Sr absorption using 85Sr (intravenous)/stable Sr (oral). Oral tracers were administered on consecutive days with a test meal containing 5.3 mmol of Ca and 2.5 mmol of either stable Sr or Ca carrier. The fractional absorption of 45Ca and Sr at 6 h (FA360) and the absorption rate as a function of time were calculated by deconvolution. 4. The mean FA360 for Sr (20.2%) was lower than the mean FA360 for 45Ca (37.8%, P < 0.001, paired t-test), but the time course of Sr absorption was similar to that of Ca. There was a significant correlation between the FA360 for 45Ca and Sr, although the relationship was improved by including a quadratic term (R2 = 0.89, P < 0.001, significance of quadratic term, P < 0.05). After 1,25-dihydroxyvitamin D treatment, the FA360 of stable Sr increased 4.29-fold, whereas the FA360 of 45Ca increased only 2.4-fold. 5. Although the fractional absorption of Sr determined by dual-tracer deconvolution was the best predictor of FA360 for 45Ca, little was lost by confining the analysis to a single serum Sr measurement taken 3 h or more after oral administration. 6. We conclude that Sr absorption is qualitatively similar to that of Ca, although absorption of Sr is much lower than that of Ca. Furthermore, the relationship does not appear to be linear. Stable Sr may be useful in place of Ca isotopes in the routine clinical evaluation of Ca absorption.

scholarly journals The Relationship between Vitamin D Metabolites and Androgens in Women with Polycystic Ovary Syndrome

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1219
Author(s):  
Jakub Mesinovic ◽  
Helena J. Teede ◽  
Soulmaz Shorakae ◽  
Gavin W. Lambert ◽  
Elisabeth A. Lambert ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin D ◽  
Polycystic Ovary ◽  
Total Testosterone ◽  
Body Fat Percentage ◽  
Vitamin D Metabolites ◽  
Fat Percentage ◽  
Ovary Syndrome ◽  
Hs Crp ◽  
The Relationship

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women of reproductive age, with hyperandrogenism present in up to 90% of affected women. Some evidence suggests a link between vitamin D deficiency and PCOS features via insulin resistance and inflammation. Our aim was to explore the relationship between biochemical markers of vitamin D status and androgens in women with PCOS. This cross-sectional study used bio-banked samples from 46 pre-menopausal women with PCOS (mean ± SD: age 30 ± 6 years; BMI 29 ± 6 kg/m2). We measured 25-hydroxyvitamin D (25[OH]D), vitamin D-binding protein (DBP), total testosterone, sex hormone-binding globulin (SHBG), and calculated the free androgen index (FAI) and bioavailable and free 25(OH)D. Fasting glucose and insulin were used to calculate the homeostatic model assessment of insulin resistance (HOMA-IR) and body fat percentage was determined via dual energy x-ray absorptiometry. High-sensitivity C-reactive protein (hs-CRP) was measured as a marker of inflammation. DBP was positively associated with total 25(OH)D and expectedly, negatively associated with free 25(OH)D. There were no associations between vitamin D metabolites and total testosterone, SHBG or FAI, even after adjusting for age, body fat percentage, HOMA-IR and hs-CRP. We found no associations between vitamin D metabolites and androgens in women with PCOS. Studies that have identified a vitamin D–androgen link have largely relied on methodology with numerous pitfalls; future studies should exclusively use gold-standard measures to confirm these findings in this population.

scholarly journals Age-Related Changes in the 25-Hydroxyvitamin D Versus Parathyroid Hormone Relationship Suggest a Different Reason Why Older Adults Require More Vitamin D

2003 ◽  
Vol 88 (1) ◽  
pp. 185-191 ◽  
Author(s):  
Reinhold Vieth ◽  
Yasmin Ladak ◽  
Paul G. Walfish
Keyword(s):  
Older Adults ◽  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Age Groups ◽  
The Elderly ◽  
Age Group ◽  
Hydroxyvitamin D ◽  
Age Related ◽  
25 Hydroxyvitamin D ◽  
The Relationship

Vitamin D requirements are thought to vary with age, but there is little comparative evidence for this. One goal in establishing a vitamin D requirement is to avoid secondary hyperparathyroidism. We studied 1741 euthyroid, thyroid clinic outpatients without evidence of calcium abnormalities, ranging in age from 19 to 97 yr, whose serum and urine had been analyzed for calcium, vitamin D, and parathyroid status. We found no effect of age on the 25-hydroxyvitamin D [25(OH)D] concentration associated with specific vitamin D intakes, and there was no relationship between 25(OH)D and 1,25hydroxyvitamin D [1,25(OH)2D]. In every age group, serum 1,25(OH)2D declined with increasing creatinine (P &lt; 0.001). What changed with age included creatinine, which correlated with 25(OH)D (r = 0.146, P &lt; 0.001) only in the youngest age group (19–50 yr) but not in the older age groups (P &gt; 0.1). Creatinine did not correlate with PTH in the youngest age group, but the relationship became significant as age increased (e.g. for the elderly, r = 0.365, P &lt; 0.001). Linear regression of log PTH vs. log 25(OH)D agreed with the natural shape of the relationship observed with scatterplot smoothing, and this showed no plateau in PTH as 25(OH)D increased. We compared PTH concentrations among age groups, based on 20 nmol/liter increments in 25(OH)D. Mean PTH in adults older than 70 yr was consistently higher than in adults younger than 50 yr (P &lt; 0.05 by ANOVA and Dunnett’s t test). PTH levels of the elderly who had 25(OH)D concentrations greater than 100 nmol/liter matched PTH of younger adults having 25(OH)D concentrations near 70 nmol/liter. This study shows that all age groups exhibit a high prevalence of 25(OH)D insufficiency and secondary hyperparathyroidism. Older adults are just as efficient in maintaining 25(OH)D, but they need more vitamin D to produce the higher 25(OH)D concentrations required to overcome the hyperparathyroidism associated with their diminishing renal function.

scholarly journals Vitamin D Metabolism Is Significantly Impaired in COVID-19 Inpatients

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A281-A282
Author(s):  
Alexandra Povaliaeva ◽  
Liudmila Ya Rozhinskaya ◽  
Ekaterina A Pigarova ◽  
Larisa K Dzeranova ◽  
Nino N Katamadze ◽  
...  
Keyword(s):  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Serum Calcium ◽  
Vitamin D Supplementation ◽  
Vitamin D Metabolites ◽  
Lung Involvement ◽  
Hydroxylase Activity ◽  
Vitamin D Metabolism ◽  
Vitamin D Levels

Abstract Objective: to assess the state of vitamin D metabolism in patients hospitalized with COVID-19 infection. Materials and methods: We examined 49 patients, which were hospitalized for inpatient treatment of COVID-19 infection from May to June 2020. Study group included 24 men (49%) and 25 women (51%), median age 58 years [48; 70], BMI 26.4 kg/m2 [24.3; 30.5]. All patients were diagnosed with pneumonia due to SARS-CoV-2 with median percent of lung involvement equal to 29% [14; 37], 22 patients (45%) required oxygen support upon admission. Median SpO2 was equal to 95% (92; 97), median NEWS score was equal to 3 [2; 6]. Participants were tested for vitamin D metabolites (25(OH)D3, 1,25(OH)2D3, 3-epi-25(OH)D3, 24,25(OH)2D3 and D3) by UPLC-MS/MS, free 25(OH)D and vitamin D-binding protein by ELISA, as well as PTH by electrochemiluminescence immunoassay and routine biochemical parameters of blood serum (calcium, phosphorus, albumin) at the time of admission. Results: patients had in general very low 25()D3 levels - median 10.9 ng/mL [6.9; 15.6], corresponding to a pronounced vitamin D deficiency in half of the patients. Levels of 24,25(OH)2D3 were also low – 0.5 ng/mL [0.2; 0.9], and resulting vitamin D metabolite ratios (25(OH)D3/24,25(OH)2D3) were high-normal or elevated in most patients – 24.1 [19.0; 39.2], indicating decreased activity of 24-hydroxylase. Levels of 1,25(OH)2D3, on the contrary, were high-normal or elevated - 57 pg/mL [46; 79], which, in accordance with 25(OH)D3/1,25(OH)2D3 ratio (219 [134; 266]) suggests an increase in 1α-hydroxylase activity. Median level of 3-epi-25(OH)D3 was 0.7 ng/mL [0.4; 1.0] and D3 metabolite was detectable only in 6 patients. Median DBP level was 432 mg/L [382; 498], median free 25(OH)D was 5.6 pg/mL [3.3; 6.7], median calculated free 25(OH)D was 2.0 pg/mL [1.4; 3.3]. Most patients had albumin-adjusted serum calcium level in the lower half of reference range (median 2.24 mmol/L [2.14; 2.34]). Seven patients had secondary hyperparathyroidism and one patient had primary hyperparathyroidism, the rest of the patients had PTH levels within the normal range.25(OH)D3 levels showed significant negative correlation with percent of lung involvement (r = -0.36, p&lt;0.05) and positive correlation with SpO2 (r = 0.4, p&lt;0.05). 1,25(OH)2D3 levels correlated positively with 25(OH)D3 levels (r = 0.38, p&lt;0.05) and did not correlate significantly with PTH levels (p&gt;0.05). Conclusion: Our data suggests that hospitalized patients with COVID-19 infection have significant impairment of vitamin D metabolism, in particular, an increase in 1α-hydroxylase activity, which cannot be fully explained by pre-existing conditions such as vitamin D deficiency and secondary hyperparathyroidism. The observed profound vitamin D deficiency and association of vitamin D levels with markers of disease severity indicate the importance of vitamin D supplementation in these patients.

Effect of Vitamin D Deficiency on Aminoaciduria and Intestinal Transport of Amino Acids in the Rat

1974 ◽  
Vol 52 (5) ◽  
pp. 972-977
Author(s):  
Claude L. Morin ◽  
Jean Léveillé ◽  
Victor Ling
Keyword(s):  
Amino Acids ◽  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Intestinal Transport ◽  
Calcium Content ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Normal Calcium

Generalized hyperaminoaciduria and hyperphosphaturia are associated with human vitamin D deficiency rickets and the effect has been reproduced in animals. The basis for the renal transport impairment was attributed to secondary hyperparathyroidism resulting from hypocalcemia.In this study we attempted over a 16-week period to induce hyperaminoaciduria in Holtzman rats with vitamin D deficient diets of varying calcium content (0.4% and 0.04%) so as to investigate the possibility of a concomitant defect in intestinal transport of amino acids. Despite signs of secondary hyperparathyroidism, generalized hyperaminoaciduria was not in evidence in any of the groups. However, increased urinary excretion of lysine and taurine was demonstrated in rats fed a low calcium diet without vitamin D (LCa−D). The same observation was also made for taurine in rats deprived of vitamin D and on a normal calcium diet (NCa−D) and in animals fed a low calcium diet with vitamin D (LCa+D). The results failed to show any effect of vitamin D deficiency, hypocalcemia, or secondary hyperparathyroidism on the intestinal transport of lysine, alanine, and cycloleucine.

scholarly journals Secondary hyperparathyroidism and vitamin D receptor binding to vitamin D response elements in rats with incipient renal failure.

1997 ◽  
Vol 8 (2) ◽  
pp. 271-278 ◽  
Author(s):  
B P Sawaya ◽  
N J Koszewski ◽  
Q Qi ◽  
M C Langub ◽  
M C Monier-Faugere ◽  
...  
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Receptor ◽  
Receptor Binding ◽  
Mobility Shift ◽  
Compensatory Renal Growth ◽  
Response Elements ◽  
Calcium Phosphorus

The pathogenesis of secondary hyperparathyroidism in early renal failure is poorly understood. In the study presented here, parathyroid hormone and GFR in rats with mild renal failure of various durations are evaluated. Parathyroid hormone increased significantly 3 days after nephrectomy and peaked at 2 wk, despite reduction in GFR of < 50%. Parathyroid hormone remained elevated, but there was no difference in serum levels of calcium, phosphorus, and calcitriol between the nephrectomized and sham-operated rats. There were also no differences in both intestinal and kidney vitamin D receptor concentrations between the two groups. Histomorphometric analysis of bone at 6 wk revealed significant increase in osteoid thickness, osteoblast number, erosion surface with osteoclasts, and erosion depth. Employing electrophoretic mobility shift assay, we consistently observed a significant reduction in kidney calcitriol-receptor complex binding to mouse osteopontin vitamin D response element (-70.2 +/- 4.9%, P < 0.001). Western blot analysis also revealed a significant reduction in at least one retinoid X receptor isoform. In conclusion, biochemical and histological evidence of secondary hyperparathyroidism develops in rats with mild renal failure, despite normal calcium, phosphorus, calcitriol, and vitamin D receptor concentrations. These rats also have evidence of reduced renal vitamin D receptor binding to nuclear response elements. This finding, possibly an important early factor in the pathogenesis of secondary hyperparathyroidism, could also play a role in the development of compensatory renal growth of the remnant kidney.

scholarly journals The localization of 1,25-dihydroxycholecalciferol in bone cell nuclei of rachitic chicks

1971 ◽  
Vol 125 (1) ◽  
pp. 147-153 ◽  
Author(s):  
J. C. Weber ◽  
V. Pons ◽  
E. Kodicek
Keyword(s):  
Vitamin D ◽  
Subcellular Distribution ◽  
Time Course ◽  
Supernatant Fraction ◽  
Intestinal Cell ◽  
Nuclear Fraction ◽  
Vitamin D Metabolites ◽  
Cell Nuclei ◽  
Polar Metabolite ◽  
25 Hydroxycholecalciferol

1. A simple technique has been developed to obtain subcellular fractions of chick bone. The method yielded 60–70% of total DNA in the nuclear debris fraction and 80–90% of total 14C recovered in bone after a dose of radioactive vitamin D. 2. After a dose of [4-14C,1,2-3H2]cholecalciferol (0.5μg) was given to vitamin D-deficient chicks, the time-course of total 14C radioactivity in the epiphysis, metaphysis and diaphysis of proximal tibiae was measured. The maximum concentrations were reached at 6h, corresponding to a similar peak of radioactivity in blood, decreasing until 24h and indicating the dependence on the circulating 14C and on the blood supply of the three bone components. 3. The 14C radioactivity of cholecalciferol and 25-hydroxycholecalciferol (expressed per mg of DNA) followed the pattern of incorporation of total 14C radioactivity in all three bone components. The more polar metabolite fraction reached a peak of radioactivity at 6–9h and maintained its concentration over the 24h period studied in all anatomical bone components. 4. After a dose of [4-14C,1-3H]cholecalciferol (0.5μg) was given to vitamin D-deficient chicks, the subcellular distribution was studied. At 24h after dosing, the nuclear fraction contained 27% and the supernatant fraction had 67% of total 14C recovered in the bone filtrate. When the 14C in the residual bone fragments was included, the nuclear fraction contained up to 35% of the total radioactivity in the bone. 5. The subcellular distribution pattern of individual vitamin D metabolites indicated that the purified nuclear fraction concentrated the polar metabolite, which lost 3H at C-1, so that 77% of the radioactivity could be accounted for by 1,25-dihydroxycholecalciferol. The supernatant fraction contained smaller amounts of 1,25-dihydroxycholecalciferol (9%), with 66% of 25-hydroxycholecalciferol forming the major metabolite, corresponding to its concentration found in blood at 24h. 6. The preferential accumulation of 1,25-dihydroxycholecalciferol in the nuclear fraction and the overall pattern of other metabolites, found previously in intestinal tissue, suggests a similar mechanism of action in bone to that postulated for the intestinal cell in calcium translocation.

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