Vitamin K and Osteoporosis.
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ABSTRACT:
SUBMITTER: Fusaro M
PROVIDER: S-EPMC7760385 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
Publications
Vitamin K and Osteoporosis.
Fusaro Maria M Cianciolo Giuseppe G Brandi Maria Luisa ML Ferrari Serge S Nickolas Thomas L TL Tripepi Giovanni G Plebani Mario M Zaninotto Martina M Iervasi Giorgio G La Manna Gaetano G Gallieni Maurizio M Vettor Roberto R Aghi Andrea A Gasperoni Lorenzo L Giannini Sandro S Sella Stefania S M Cheung Angela A
Nutrients 20201125 12
Vitamin K acts as a coenzyme of carboxylase, catalyzing the carboxylation of several vitamin K dependent proteins. Beyond its well-known effects on blood coagulation, it also exerts relevant effects on bone and the vascular system. In this review, we point out the relevance of an adequate vitamin K intake to obtain sufficient levels of carboxylated (active form) vitamin K dependent proteins (such as Osteocalcin and matrix Gla protein) to prevent bone health. Another bone-related action of Vitami ...[more]
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Project description:Osteoporosis is a bone disease leading to an increased fracture risk. It is considered a complex multifactorial genetic disorder with interaction of environmental and genetic factors. As a candidate gene for osteoporosis, we studied vitamin D binding protein (DBP, or group-specific component, Gc), which binds to and transports vitamin D to target tissues to maintain calcium homeostasis through the vitamin D endocrine system. DBP can also be converted to DBP-macrophage activating factor (DBP-MAF), which mediates bone resorption by directly activating osteoclasts. We summarized the genetic linkage structure of the DBP gene. We genotyped two single-nucleotide polymorphisms (SNPs, rs7041 = Glu416Asp and rs4588 = Thr420Lys) in 6,181 elderly Caucasians and investigated interactions of the DBP genotype with vitamin D receptor (VDR) genotype and dietary calcium intake in relation to fracture risk. Haplotypes of the DBP SNPs correspond to protein variations referred to as Gc1s (haplotype 1), Gc2 (haplotype 2), and Gc1f (haplotype3). In a subgroup of 1,312 subjects, DBP genotype was found to be associated with increased and decreased serum 25-(OH)D(3) for haplotype 1 (P = 3 x 10(-4)) and haplotype 2 (P = 3 x 10(-6)), respectively. Similar associations were observed for 1,25-(OH)(2)D(3). The DBP genotype was not significantly associated with fracture risk in the entire study population. Yet, we observed interaction between DBP and VDR haplotypes in determining fracture risk. In the DBP haplotype 1-carrier group, subjects of homozygous VDR block 5-haplotype 1 had 33% increased fracture risk compared to noncarriers (P = 0.005). In a subgroup with dietary calcium intake <1.09 g/day, the hazard ratio (95% confidence interval) for fracture risk of DBP hap1-homozygote versus noncarrier was 1.47 (1.06-2.05). All associations were independent of age and gender. Our study demonstrated that the genetic effect of the DBP gene on fracture risk appears only in combination with other genetic and environmental risk factors for bone metabolism.
| S-EPMC2729412 | biostudies-literature
Project description:Up to 71% of South Korean postmenopausal women have vitamin D deficiency {serum 25-hydroxyvitamin D [25(OH) D] level <50 nmol/L}. Data on vitamin D supplementation was collected during the screening phase of an efficacy/safety study of denosumab in Korean postmenopausal women with osteoporosis. This report describes the effect of vitamin D supplementation on repletion to 25(OH)D levels ?50 nmol/L in Korean postmenopausal women with osteoporosis.Vitamin D levels of Korean postmenopausal women (60-90 years old) were measured by extracting 25(OH)D? and 25(OH)D? from serum samples via protein precipitation and using liquid chromatography with tandem mass spectrometry detection. Calibration curves were constructed from the mass chromatograms to obtain total vitamin D levels. Subjects with serum 25(OH)D levels <50 nmol/L were supplemented with 1000 IU of vitamin D tablets during the 2.5-month-long screening period. Dose, frequency, and duration were determined by the investigator. If repletion was achieved (?50 nmol/L) on retest, subjects were eligible to be rescreened for study entry.Of 371 subjects screened, 191 (52%) required vitamin D supplementation, and 88% (168 of 191) were successfully repleted. More than half of the subjects (58%) who were successfully repleted received doses of 2000 IU daily. The mean time to successful repletion was 31 days (standard deviation 8.4 days; range 11-48 days).Supplementation with daily median doses of 2000 IU vitamin D successfully repleted 88% of Korean postmenopausal women with osteoporosis within 48 days to a serum vitamin D level of 50 nmol/L.
| S-EPMC4951469 | biostudies-literature
Project description:The influence of the vitamin D receptor (VDR) gene for the risk of osteoporosis remains to be elucidated. The aim of the present study was to understand the distribution of various single-nucleotide polymorphisms (SNPs) within the VDR gene and its association with the risk of osteoporosis. In total, 378 subjects without a genetic relationship were recruited to the study between January 2013 and July 2015. The subjects were divided into three groups, which were the normal (n=234), osteoporosis (n=65) and osteoporosis with osteoporotic fracture (n=79) groups. Three pertinent SNPs of the VDR gene rs17879735 (ApaI, Allele A/a, SNP C>A) were examined with polymerase chain reaction-restriction fragment length polymorphism. The bone mineral density (BMD) of the lumbar spine (L2-L4), femoral neck, Ward's and Tro was measured using dual-energy X-ray absorptiometry. The distributions of genotype frequencies aa, AA and Aa were 48.68, 42.86 and 8.46%, separately. Following analysis of each site, BMD, body mass index (BMI) and age, BMD for each site was negatively correlated with age (P<0.01) and positively correlated with BMI (P<0.01). Correction analysis revealed that there were significant differences in the Ward's triangle BMD among each genotype (P<0.05), in which the aa genotype exhibited the lower BMD (P<0.05). No significant difference was identified among the different genotypes in the occurrence of osteoporosis with osteoporotic fracture (P>0.05). In conclusion, these indicated that the VDR gene ApaI polymorphisms had an important role in the osteoporosis risk.
| S-EPMC4950620 | biostudies-literature
Project description:ObjectiveOsteoporosis is the most common type of bone disorder characterized by low bone mineral density (BMD). It is a multifactorial disease and caused by the interaction of environmental and genetic factors. It has been reported that mutations in the vitamin D receptor (VDR) gene highly affect the metabolism of minerals, which reduces bone density. Therefore, this study aimed to determine the association of VDR gene polymorphisms TaqI (rs731236) and ApaI (rs7975232) with osteoporosis risk in the Saudi population.MethodsThis case-control study involved 73 individuals with osteoporosis and 73 healthy controls in Jeddah, KSA. DNA extracted from peripheral blood was used to determine the genotypes and allele frequencies of VDR variants by polymerase chain reaction-restriction fragment length polymorphisms. Osteoporosis was confirmed by measuring BMD using dual-energy X-ray absorptiometry. The results were interpreted using the Hardy-Weinberg equilibrium assumption with P < 0.05 considered as significant.ResultsA significant increase in the genotype frequencies of the ApaI (Aa) and (aa) was observed among osteoporotic patients compared to controls (P = 0.002 and P < 0.0001, respectively). Only the homozygous (tt) genotype of TaqI was significantly higher in those with osteoporosis than in the controls (P = 0.001). The minor "a" allele of ApaI and the "t" allele of TaqI were significantly more common in the patients as compared to controls (P < 0.0001 and P = 0.01, respectively).ConclusionVDR polymorphisms ApaI and TaqI were found to be significantly determinant risk factors for osteoporosis progression in the Saudi population.
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Project description:Vitamin D deficiency further increases the risk of osteoporosis in HIV-positive patients coinfected with hepatitis C virus (HCV); however, it is still unclear whether HCV-related increased fracture risk is a function of the severity of liver disease. The aim of this review was to identify studies on associative vitamin D deficiency patterns in high-risk populations such as HIV/HCV coinfected patients. We did this by searching MEDLINE and EMBASE databases, from inception to August 2014, and included bibliographies. The final 12 articles selected are homogeneous in terms of age but heterogeneous in terms of sample size, participant recruitment, and data source. Most of the HIV/HCV coinfected patients have less than adequate levels of vitamin D. After reviewing the selected articles, we concluded that vitamin D deficiency should be regarded as a continuum and that the lower limit of the ideal range is debatable. We found that vitamin D deficiency might influence liver disease progression in HIV/HCV coinfected patients. Methodological issues in evaluating vitamin D supplementation as a relatively inexpensive therapeutic option are discussed, as well as the need for future research, above all on its role in reducing the risk of HCV-related fracture by modifying liver fibrosis progression.
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