scholarly journals Consumption of Vitamin D-and Calcium-Fortified Soft White Cheese Lowers the Biochemical Marker of Bone Resorption TRAP 5b in Postmenopausal Women at Moderate Risk of Osteoporosis Fracture

2012 ◽  
Vol 142 (4) ◽  
pp. 698-703 ◽  
Author(s):  
Jean-Philippe Bonjour ◽  
Valérie Benoit ◽  
Brigitte Rousseau ◽  
Jean-Claude Souberbielle
Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2985
Author(s):  
George Moschonis ◽  
Ellen GHM van den Heuvel ◽  
Christina Mavrogianni ◽  
Yannis Manios

Considering the role of bone metabolism in understanding the pathogenesis of osteoporosis, the aim of the present study was to examine the effects of vitamin D-enriched cheese on the serum concentrations of the parathyroid hormone (PTH) and certain bone remodeling biomarkers in postmenopausal women in Greece. In a randomised, controlled dietary intervention, 79 postmenopausal women (55–75 years old) were randomly allocated either to a control (CG: n = 39) or an intervention group (IG: n = 40), consuming 60 g of either non-enriched or vitamin D3-enriched Gouda-type cheese (5.7 μg of vitamin D3), respectively, daily and for eight weeks during the winter. The serum concentrations of 25-hydroxy vitamin D (25(OH)D), PTH, bone formation (i.e., osteocalcin, P1NP) and bone resorption (i.e., TRAP-5b) biomarkers were measured. Consumption of the vitamin D-enriched cheese led to higher serum 25(OH)D concentrations of 23.4 ± 6.39 (p = 0.022) and 13.4 ± 1.35 (p < 0.001) nmol/L in vitamin D-insufficient women being at menopause for less and more than 5 years, respectively. In vitamin D-insufficient women that were less than 5 years at menopause, consumption of vitamin D-enriched cheese was also associated with lower serum PTH (Beta −0.63 ± 1.11; p < 0.001) and TRAP-5b (Beta −0.65 ± 0.23; p = 0.004) levels at follow-up, compared with the CG. The present study showed that daily intake of 5.7 μg of vitamin D through enriched cheese increased serum 25(OH)D concentrations, prevented PTH increase and reduced bone resorption in vitamin D-insufficient early postmenopausal women, thus reflecting a food-based solution for reducing osteoporosis risk in this susceptible group.


2004 ◽  
Vol 91 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Mary Harrington ◽  
Teresa Bennett ◽  
Jette Jakobsen ◽  
Lars Ovesen ◽  
Christine Brot ◽  
...  

The influence of a high-Na, high-protein (calciuric) diet on Ca and bone metabolism was investigated in postmenopausal women (aged 50–67 years) who were stratified by vitamin D receptor (VDR) genotype. In a crossover trial, twenty-four women were randomly assigned to a diet high in protein (90 g/d) and Na (180 mmol/d) or a diet adequate in protein (70 g/d) and low in Na (65 mmol/d) for 4 weeks, followed by crossover to the alternative dietary regimen for a further 4 weeks. Dietary Ca intake was maintained at usual intakes (about 20 mmol (800 mg)/d). Urinary Na, K, Ca, N and type I collagen cross-linked N-telopeptide (NTx; a marker of bone resorption), plasma parathyroid hormone (PTH), serum 25-hydroxycholecalciferol (25(OH)D3), 1,25-dihydroxycholecalciferol (1,25(OH)2D3), osteocalcin and bone-specific alkaline phosphatase (B-Alkphase) were measured in 24 h urine samples and fasting blood samples collected at the end of each dietary period. The calciuric diet significantly (P<0·05) increased mean urinary Na, N, K, Ca and NTx (by 19 %) compared with the basal diet, but had no effect on circulating 25(OH)D3, 1,25(OH)2D3, PTH, osteocalcin or B-Alkphase in the total group (n 24). There were no differences in serum markers or urinary minerals between the basal and calciuric diet in either VDR genotype groups. While the calciuric diet significantly increased urinary NTx (by 25·6 %, P<0·01) in the f+ VDR group (n 10; carrying one or more (f) Fok I alleles), it had no effect in the f− VDR group (n 14; not carrying any Fok I alleles). It is concluded that the Na- and protein-induced urinary Ca loss is compensated for by increased bone resorption and that this response may be influenced by VDR genotype.


Bone ◽  
1991 ◽  
Vol 12 (4) ◽  
pp. 257-260 ◽  
Author(s):  
J.S. Johansen ◽  
P.D. Delmas ◽  
B.J. Riis ◽  
E. Gineyts ◽  
C. Christiansen

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
T Petelina ◽  
K Avdeeva ◽  
N Musikhina ◽  
L Gapon ◽  
S Bykova ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Aim To investigate the role of markers of vascular inflammation, vitamin D, parathyroid hormone as predictors of increased pulse-wave velocity (PWV) and degenerative bone changes in postmenopausal women with arterial hypertension (AH). Methods 164 females were examined. Gr.1 included 42 healthy individuals, Gr.2 - 58 patients with AH and Gr.3 - 64 postmenopausal women with AH and osteoporosis. Parameters of blood pressure monitoring; PWV, osteodensitometry (T-Score); inflammatory markers: hsCRP, TNFα, homocysteine, IL-1β, 6, 8, endothelin-1; lipid profile parameters; sex and parathyroid hormones, vitamin D  were measured. Results In Gr.3 excess levels of PWV, hsCRP, homocysteine, IL8, total cholesterol, LDL cholesterol, endothelin-1 and parathyroid hormone was detected with decrease in the level of sex hormones and vitamin D. Besides, negative correlations of T-Score with age, PWV, duration of menopause, IL-6, hsCRP were registered; positive correlations between PWV with IL6, LDL cholesterol, hsCRP, endothelin-1, DBP variability were found. The logistic regression method revealed the main markers that affect increase of PWV, such as hsCRP and endothelin-1.Rise of each marker by unit of measurement leads to increase in PWV by 1.3 times and 2.4%, respectively. In Gr.2 increase in PWV level of more than 12.05 m/s was associated with 3.8-fold increase in the risk of osteoporosis. In Gr.3 increase in PWV level on 1 m/s was associated with 6 fold increase in the risk of osteoporosis. Conclusions Elevated levels of PWV are associated with markers of inflammation, levels of parathyroid hormone, vitamin D, T-Score and may be part of the pathogenesis of the cardiovascular continuum in postmenopausal women, which will require an individual approach to the treatment of AH with comorbid metabolic disorders.


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