scholarly journals Vitamin K Supplementation Modulates Bone Metabolism and Ultra-Structure of Ovariectomized Mice

2018 ◽  
Vol 51 (1) ◽  
pp. 356-374 ◽  
Author(s):  
Letícia Batista Azevedo Rangel ◽  
Daniel de Siqueira ◽  
Olívia do Rosário Soares ◽  
Higor Scardini Santana ◽  
Emílio de Castro Miguel ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Metabolism ◽  
Vitamin K ◽  
Bone Structure ◽  
Mineral Metabolism ◽  
Bone Matrix ◽  
Complete Analysis ◽  
Ovariectomized Mice ◽  
Bone Ultrastructure

Background/Aims: Osteoporosis is a bone metabolic disease that affects mostly post-menopausal women. There has been shown that vitamin K (VK) supplementation during menopause may decrease bone loss as well as risk of bone breaking. Aiming to clarify the beneficial role of VK in bone metabolism during menopause, we investigated mineral metabolism and bone ultrastructure of ovariectomized (OVX) mice. Methods: To determine the effects chronic use of VK in bone structure and mineral metabolism in OVX mice, we used several methods, such as DXA, µCTScan, and SEM as well as biomolecular techniques, such as ELISA and qRT-PCR. In addition, complete analysis of serum hormonal and other molecules associated to bone and lipid metabolism were evaluated overview the effects of VK in menopause murine model. Results: VK treatment significantly affects Pi metabolism independently of OVX, changing Pi plasma, urinary output, balance, and Pi bone mass. Interestingly, VK also increased VLDL in mice independently of castration. In addition, VK increased compact bone mass in OVX mice when we evaluated it by DXA, histomorphometry, µCTScanning. VK increased bone formation markers, osteocalcin, HYP- osteocalcin, and AP whereas it decreased bone resorption markers, such as urinary DPD/creatinine ratio and plasmatic TRAP. Surprisingly, SEM images revealed that VK treatment led to amelioration of microfractures observed in OVX untreated controls. In addition, SHAM operated VK treated mice exhibited higher number of migrating osteoblasts and in situ secretion of AP. OVX led to decreased to in situ secretion of AP that was restored by VK treatment. Moreover, VK treatment increased mRNA expression of bone Calbindin 28KDa independently of OVX. Conclusion: VK treatment in OVX mice exhibited beneficial effects on bone ultrastructure, mostly by altering osteoblastic function and secretion of organic bone matrix. Therefore, VK could be useful to treat osteopenic/osteoporotic patients.

scholarly journals Bone and Mineral Metabolism Phenotypes in MEN1-Related and Sporadic Primary Hyperparathyroidism, before and after Parathyroidectomy

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1895
Author(s):  
Francesca Marini ◽  
Francesca Giusti ◽  
Federica Cioppi ◽  
Davide Maraghelli ◽  
Tiziana Cavalli ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Bone Mass ◽  
Bone Metabolism ◽  
Mineral Metabolism ◽  
Parathyroid Tissue ◽  
Young Patients ◽  
Surgical Removal ◽  
Mineral Density ◽  
Bone Mass Loss ◽  
Before And After

Primary hyperparathyroidism (PHPT) is the most common endocrinopathy in multiple endocrine neoplasia type 1 (MEN1). Persistent levels of increased parathyroid hormone (PTH) result in a higher incidence of osteopenia and osteoporosis compared to the general population. Surgical removal of hyper-functioning parathyroid tissue is the therapy of choice. This retrospective study evaluated the effect of parathyroidectomy (PTX) on bone metabolism and bone mass in two series of patients with MEN1 PHPT and sporadic PHPT (sPHPT) by comparing bone metabolism-related biochemical markers and bone mineral density (BMD) before and after surgery. Our data confirmed, in a higher number of cases than in previously published studies, the efficacy of PTX, not only to rapidly restore normal levels of PTH and calcium, but also to normalize biochemical parameters of bone resorption and bone formation, and to improve spine and femur bone mass, in both MEN1 PHPT and sPHPT. Evaluation of single-patient BMD changes after surgery indicates an individual variable bone mass improvement in a great majority of MEN1 PHPT patients. In MEN1 patients, PTX is strongly suggested in the presence of increased PTH and hypercalcemia to prevent/reduce the early-onset bone mass loss and grant, in young patients, the achievement of the bone mass peak; routine monitoring of bone metabolism and bone mass should start from adolescence. Therapy with anti-fracture drugs is indicated in MEN1 patients with BMD lower than the age-matched normal values.

Vitamin K status is associated with childhood bone mineral content

2008 ◽  
Vol 100 (4) ◽  
pp. 852-858 ◽  
Author(s):  
Marieke J. H. van Summeren ◽  
Silvia C. C. M. van Coeverden ◽  
Leon J. Schurgers ◽  
Lavienja A. J. L. M. Braam ◽  
Florence Noirt ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Mass ◽  
Bone Mineral Content ◽  
Bone Metabolism ◽  
Vitamin K ◽  
Bone Health ◽  
Mineral Content ◽  
Vitamin D Status ◽  
Time Points ◽  
Total Body

In adult bone, vitamin K contributes to bone health, probably through its role as co-factor in the carboxylation of osteocalcin. In children, the significance of vitamin K in bone-mass acquisition is less well known. The objective of this longitudinal study was to determine whether biochemical indicators of vitamin K status are related to (gains in) bone mineral content (BMC) and markers of bone metabolism in peripubertal children. In 307 healthy children (mean age 11·2 years), BMC of the total body, lumbar spine and femoral neck was determined at baseline and 2 years later. Vitamin K status (ratio of undercarboxylated (ucOC) to carboxylated (cOC) fractions of osteocalcin; UCR) was also measured at both time points. Markers of bone metabolism, sex steroids, vitamin D status and growth hormones were measured at baseline only. Large variations in the levels of the UCR were found at both time-points, indicating a substantial interindividual difference in vitamin K status. Improvement of vitamin K status over 2 years (n281 children) was associated with a marked increase in total body BMC (r− 49·1,P < 0·001). The UCR was associated with pubertal stage, markers of bone metabolism, sex hormones and vitamin D status. A better vitamin K status was associated with more pronounced increase in bone mass in healthy peripubertal children. In order to determine the significance of these findings for childhood bone health, additional paediatric studies are needed.

scholarly journals Vitamin K and Bone Metabolism: A Review of the Latest Evidence in Preclinical Studies

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Solmaz Akbari ◽  
Amir Alireza Rasouli-Ghahroudi
Keyword(s):  
Bone Metabolism ◽  
Vitamin K ◽  
Osteoblast Differentiation ◽  
Positive Impact ◽  
Bone Matrix ◽  
Vitamin K2 ◽  
Preclinical Studies ◽  
Matrix Mineralization ◽  
Shed Light ◽  
Bone Matrix Mineralization

Bone is a metabolically active tissue that renews itself throughout one’s life. Cytokines along with several hormonal, nutritional, and growth factors are involved in tightly regulated bone remodeling. Accordingly, vitamin K as a multifunctional vitamin has been recently deemed appreciable as a topic of research as it plays a pivotal role in maintenance of the bone strength, and it has been proved to have a positive impact on the bone metabolism. Vitamin K exerts its anabolic effect on the bone turnover in different ways such as promoting osteoblast differentiation, upregulating transcription of specific genes in osteoblasts, and activating the bone-associated vitamin k dependent proteins which play critical roles in extracellular bone matrix mineralization. There is also credible evidence to support the effects of vitamin k2 on differentiation of other mesenchymal stem cells into osteoblast. The main objective of the present paper is to comprehensively outline the preclinical studies on the properties of vitamin K and its effects on the bone metabolism. The evidence could shed light on further clinical studies to improve osteogenesis in bone graft surgeries.

scholarly journals Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Xuekun Fu ◽  
Bo Zhou ◽  
Qinnan Yan ◽  
Chu Tao ◽  
Lei Qin ◽  
...  
Keyword(s):  
Bone Mass ◽  
Volume Fraction ◽  
Bone Marrow Cells ◽  
Bone Matrix ◽  
Osteoblastic Cells ◽  
Mineral Density ◽  
Bone Volume Fraction ◽  
Ovariectomized Mice

AbstractIn vertebrates, the type 1 parathyroid hormone receptor (PTH1R) is a critical regulator of skeletal development and homeostasis; however, how it is modulated is incompletely understood. Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone. Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts, but not mesenchymal stem cells, chondrocytes and fibroblasts, in non-hematopoietic bone marrow cells, with concomitant depletion of osteoblasts on the bone surfaces, especially those stimulated by PTH. Furthermore, haploinsufficiency of Kindlin-2 and Pth1r genes, but not that of either gene, in mice significantly decreases basal and, to a larger extent, PTH-stimulated bone mass, supporting the notion that both factors function in the same genetic pathway. Mechanistically, Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα. Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone. Interestingly, PTH promotes Kindlin-2 expression in vitro and in vivo, thus creating a positive feedback regulatory loop. Finally, estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice. Thus, we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis.

scholarly journals Effects of Vitamin K on Bone Mass and Bone Metabolism

1996 ◽  
Vol 126 (suppl_4) ◽  
pp. 1187S-1191S ◽  
Author(s):  
Cees Vermeer ◽  
Birgit L. M. G. Gijsbers ◽  
Alexandra M. Crāciun ◽  
Monique M. C. L. Groenen-van Dooren ◽  
Marjo H. J. Knapen
Keyword(s):  
Bone Mass ◽  
Bone Metabolism ◽  
Vitamin K

scholarly journals Is Preptin a New Bone Metabolism Parameter in Hemodialysis Patients?

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 341
Author(s):  
Małgorzata Kałużna ◽  
Krzysztof Pawlaczyk ◽  
Krzysztof Schwermer ◽  
Krzysztof Hoppe ◽  
Aisha Yusuf Ibrahim ◽  
...  
Keyword(s):  
Lumbar Spine ◽  
Glucose Tolerance ◽  
Bone Metabolism ◽  
Mineral Metabolism ◽  
Peptide Hormone ◽  
Normal Glucose Tolerance ◽  
Indirect Measurement ◽  
Chronic Hemodialysis ◽  
Mineral Density ◽  
Patients With Diabetes

Background: Preptin is a bone-anabolic pancreatic peptide hormone. Its role in bone metabolism has been studied in rats and in patients with diabetes, but its levels and significance in bone metabolism in hemodialyzed (HD) patients is unknown. Methods: The relationships between preptin and anthropometric and biochemical parameters related to bone metabolism were studied in 73 patients on chronic hemodialysis (48 males, 25 females; mean age of 57 years; HD vintage of 69.7 months). Of these subjects, 36 patients had diabetes or impaired glucose tolerance (DM/IGT), and 37 patients had normal glucose tolerance (NGT). Dual-energy X-ray absorptiometry of the femoral neck and lumbar spine were also performed. Results: No differences were observed in preptin levels between DM/IGT and NGT HD patients. Preptin was positively correlated with HD vintage (r = 0.312, p = 0.007). Negative correlations between preptin and bone mineral density (BMD), T-score, and Z-score in the lumbar spine (L2-L4) were observed (r = −0.319, p = 0.009; r = −0.341, p = 0.005; r = −0.375, p = 0.002). Preptin was positively correlated with parathormone (PTH) levels (r = 0.379, p < 0.001) and osteocalcin levels (r = 0.262, p = 0.027). Conclusions: The results indicate that preptin may reflect on bone and mineral metabolism disturbances seen in HD patients. The significant correlation of preptin with PTH and osteocalcin suggests that preptin may be important in indirect measurement of bone turnover in HD patients.

The benefits of a high-intensity aquatic exercise program (HydrOS) for bone metabolism and bone mass of postmenopausal women

2013 ◽  
Author(s):  
Linda Denise Fernandes Moreira ◽  
Fernanda Cerveira A. O. Fronza ◽  
Rodrigo Nolasco dos Santos ◽  
Patrícia Lins Zach ◽  
Ilda S. Kunii ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Metabolism ◽  
Postmenopausal Women ◽  
High Intensity ◽  
Exercise Program ◽  
Aquatic Exercise

scholarly journals Ostm1 from Mouse to Human: Insights into Osteoclast Maturation

2020 ◽  
Vol 21 (16) ◽  
pp. 5600 ◽  
Author(s):  
Jean Vacher ◽  
Michael Bruccoleri ◽  
Monica Pata
Keyword(s):  
Bone Formation ◽  
Bone Mass ◽  
Bone Fractures ◽  
Bone Development ◽  
Bone Matrix ◽  
Adult Life ◽  
Cell Types ◽  
Severe Form ◽  
Isolation And Characterization

The maintenance of bone mass is a dynamic process that requires a strict balance between bone formation and resorption. Bone formation is controlled by osteoblasts, while osteoclasts are responsible for resorption of the bone matrix. The opposite functions of these cell types have to be tightly regulated not only during normal bone development, but also during adult life, to maintain serum calcium homeostasis and sustain bone integrity to prevent bone fractures. Disruption of the control of bone synthesis or resorption can lead to an over accumulation of bone tissue in osteopetrosis or conversely to a net depletion of the bone mass in osteoporosis. Moreover, high levels of bone resorption with focal bone formation can cause Paget’s disease. Here, we summarize the steps toward isolation and characterization of the osteopetrosis associated trans-membrane protein 1 (Ostm1) gene and protein, essential for proper osteoclast maturation, and responsible when mutated for the most severe form of osteopetrosis in mice and humans.

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