2017•Scripta Scientifica PharmaceuticaOpen access

THE NEW FACE OF VITAMIN K - MORE THAN BLOOD CLOTTING FACTOR

D. S. Ivanov, M. I. Bliznakova, Е. Б. Петрова, Neli Petkova, Bistra Tzaneva Galunska

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Abstract

Introduction:  Twenty years ago, the metabolism of vitamin K was connected with its role in hemostasis. Since that time, it has been shown that vitamin K exerts multiple functions mediated by the Gla-proteins, having vitamin K as a cofactor. Numerous publications affirm that these Gla-proteins are related to physiological processes beyond coagulations, such as bone metabolism, vascular health and energy homeostasis. Aim:  The aim of this research is to provide new data for the role of vitamin K in a myriad of physiological processes beyond blood clotting. Additionally, it aims to assess the potential new applications of vitamin K as a supplement for the prevention of bone and vascular diseases. Materials and Methods:  Using the online databases Scopus, PubMed and Google Scholar, a search with the keywords: `vitamin K2`, `bone metabolism`, `cardiovascular diseases`, `osteocalcin` and `MGP` was conducted. Information regarding the effects of vitamin K on bone and vascular health was referred to in this work. Results:  Vitamin K and vitamin K-dependent proteins play pivotal roles in the physiology of bone mineralization and in preventing ectopic calcification. Osteocalcin, a Gla protein located in bone and dentin, is important for bone mineralization. Following the posttranslational carboxylation of Glu-residues with a cofactor vitamin K2 (menaquinone), rather than vitamin K1 (phylloquinone), osteocalcin shows increased affinity for calcium. Osteocalcin is believed to be involved in osteoblast regulation and hydroxyapatite crystal growth. Matrix GLa-protein (MGP), sharing some sequences with osteocalcin, is a local inhibitor of arterial calcification. Vitamin K deficiency impairs the function of osteocalcin and MGP and, therefore, presumably contributes to bone demineralization and vascular calcification, the so-called calcium paradox. Conclusions:  Vitamin K deficiencies, traditionally regarded as a cause for internal hemorrhages and blood clotting disorders, apparently can be linked to cardiovascular calcification and abnormal bone modelling. Appropriate treatment of vitamin K deficiency may improve bone and arterial health.

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Introduction:  Twenty years ago, the metabolism of vitamin K was connected with its role in hemostasis. Since that time, it has been shown that vitamin K exerts multiple functions mediated by the Gla-proteins, having vitamin K as a cofactor. Numerous publications affirm that these Gla-proteins are related to physiological processes beyond coagulations, such as bone metabolism, vascular health and energy homeostasis. Aim:  The aim of this research is to provide new data for the role of vitamin K in a myriad of physiological processes beyond blood clotting. Additionally, it aims to assess the potential new applications of vitamin K as a supplement for the prevention of bone and vascular diseases. Materials and Methods:  Using the online databases Scopus, PubMed and Google Scholar, a search with the keywords: `vitamin K2`, `bone metabolism`, `cardiovascular diseases`, `osteocalcin` and `MGP` was conducted. Information regarding the effects of vitamin K on bone and vascular health was referred to in this work. Results:  Vitamin K and vitamin K-dependent proteins play pivotal roles in the physiology of bone mineralization and in preventing ectopic calcification. Osteocalcin, a Gla protein located in bone and dentin, is important for bone mineralization. Following the posttranslational carboxylation of Glu-residues with a cofactor vitamin K2 (menaquinone), rather than vitamin K1 (phylloquinone), osteocalcin shows increased affinity for calcium. Osteocalcin is believed to be involved in osteoblast regulation and hydroxyapatite crystal growth. Matrix GLa-protein (MGP), sharing some sequences with osteocalcin, is a local inhibitor of arterial calcification. Vitamin K deficiency impairs the function of osteocalcin and MGP and, therefore, presumably contributes to bone demineralization and vascular calcification, the so-called calcium paradox. Conclusions:  Vitamin K deficiencies, traditionally regarded as a cause for internal hemorrhages and blood clotting disorders, apparently can be linked to cardiovascular calcification and abnormal bone modelling. Appropriate treatment of vitamin K deficiency may improve bone and arterial health.

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Available abstract

Introduction:  Twenty years ago, the metabolism of vitamin K was connected with its role in hemostasis. Since that time, it has been shown that vitamin K exerts multiple functions mediated by the Gla-proteins, having vitamin K as a cofactor. Numerous publications affirm that these Gla-proteins are related to physiological processes beyond coagulations, such as bone metabolism, vascular health and energy homeostasis. Aim:  The aim of this research is to provide new data for the role of vitamin K in a myriad of physiological processes beyond blood clotting. Additionally, it aims to assess the potential new applications of vitamin K as a supplement for the prevention of bone and vascular diseases. Materials and Methods:  Using the online databases Scopus, PubMed and Google Scholar, a search with the keywords: `vitamin K2`, `bone metabolism`, `cardiovascular diseases`, `osteocalcin` and `MGP` was conducted. Information regarding the effects of vitamin K on bone and vascular health was referred to in this work. Results:  Vitamin K and vitamin K-dependent proteins play pivotal roles in the physiology of bone mineralization and in preventing ectopic calcification. Osteocalcin, a Gla protein located in bone and dentin, is important for bone mineralization. Following the posttranslational carboxylation of Glu-residues with a cofactor vitamin K2 (menaquinone), rather than vitamin K1 (phylloquinone), osteocalcin shows increased affinity for calcium. Osteocalcin is believed to be involved in osteoblast regulation and hydroxyapatite crystal growth. Matrix GLa-protein (MGP), sharing some sequences with osteocalcin, is a local inhibitor of arterial calcification. Vitamin K deficiency impairs the function of osteocalcin and MGP and, therefore, presumably contributes to bone demineralization and vascular calcification, the so-called calcium paradox. Conclusions:  Vitamin K deficiencies, traditionally regarded as a cause for internal hemorrhages and blood clotting disorders, apparently can be linked to cardiovascular calcification and abnormal bone modelling. Appropriate treatment of vitamin K deficiency may improve bone and arterial health.

Key concepts: Osteocalcin, Matrix gla protein, Ectopic calcification, Vitamin K2, Endocrinology, Vitamin, Bone remodeling, Internal medicine

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