Phylloquinone (vitamin K1) concentration, polymorphism of biotransformation genes, vitamin K-oxidoreductase in the population of Nenets ethnos in Arctic region of Russian Federation

Author(s):  
Н.А. Воробьева ◽  
А.И. Воробьева ◽  
Н.И. Белова ◽  
С.Б. Неманова

Введение. Несмотря на то что выраженный дефицит витамина К встречается достаточно редко, клиническое значение данного нутриента значимо. Следует учитывать, что роль витамина К не ограничивается только процессами коагуляции крови это и регуляция обмена кальция, витамина Д, созревание белка костной ткани остеокальцина. Основной путь поступления филлохинона алиментарный. Отдельного внимания, на наш взгляд, заслуживает изучение данного вопроса в популяциях постоянно проживающих в труднодоступных регионах с алиментарным дефицитом данного нутриента. Цель исследования: анализ возможной зависимости концентрации витамина К1 в сыворотке крови от полиморфизма генов биотрансформации и витамин Коксидоредуктазы у коренного населения (ненцы) в условиях постоянного островного проживания в Арктическом регионе России. Материалы и методы. Проведено поперечное популяционное исследование коренного населения (ненцы), проживающего в Арктической зоне России на острове Вайгач (7001 с. ш. 5933 в. д.). Использованы методы молекулярногенетического исследования полиморфизма генов биотрансформации и витамин Коксидоредуктазы анализ концентрации витамина К1 проводили методом высокоэффективной жидкостной хроматографии с детектированием сигнала на тандемном массспектрометре. Результаты. Выявлен значимый субклинический дефицит витамина К1 (филлохинона) при отсутствии зависимости от полиморфизма генов биотрансформации и витамин Коксидоредуктазы. Заключение. Выявленный нами факт субклинического дефицита витамина К1 может иметь неблагоприятное влияние на развитие остеопороза детерминированным дополнительным присутствием гомозиготного аллеля VKORC1 1173Т, что требует дополнительного изучения. Introduction. Despite the fact that expressed vitamin K deficiency is quite rare, the clinical significance of this nutrient is important. Vitamin K (phylloquinone) is involved in blood coagulation, in regulation of calcium and vitamin D metabolism, in maturation of osteocalcin bone protein. The main route of phylloquinone intake is alimentary. Special mention should be made of alimentary deficiency of this nutrient in populations of permanently residing in difficulttoreach regions. Aim: to analyze the possible dependence of vitamin K1 concentration in serum from polymorphism of genes biotransformation and vitamin Koxidoreductase in indigenous population (Nenets) permanently living on an island in Russian Arctic region. Materials and methods. We conducted a crosspopulation study of the indigenous population (Nenets) living in Russian Arctic zone on Vaigach Island (7001 north latitude 5933 east longitude). We used the methods of molecular genetic studies of genes biotransformation polymorphism and vitamin Koxidoreductase vitamin K1 concentration was analyzed by highperformance liquid chromatography with detection of signal on a tandem mass spectrometer. Results. We revealed a significant subclinical deficiency of vitamin K1 (phylloquinone) with the absence of dependence from genes biotransformation polymorphism and vitamin Koxidoreductase. Conclusion. Revealed subclinical vitamin K1 deficiency may have an adverse effect on osteoporosis development by the deterministic additional presence of homozygous VKORC1 1173T allele that requires additional study.

1988 ◽  
Vol 60 (01) ◽  
pp. 039-043 ◽  
Author(s):  
L Mandelbrot ◽  
M Guillaumont ◽  
M Leclercq ◽  
J J Lefrère ◽  
D Gozin ◽  
...  

SummaryVitamin K status was evaluated using coagulation studies and/ or vitamin IQ assays in a total of 53 normal fetuses and 47 neonates. Second trimester fetal blood samples were obtained for prenatal diagnosis under ultrasound guidance. Endogenous vitamin K1 concentrations (determined by high performance liquid chromatography) were substantially lower than maternal levels. The mean maternal-fetal gradient was 14-fold at mid trimester and 18-fold at birth. Despite low vitamin K levels, descarboxy prothrombin, detected by a staphylocoagulase assay, was elevated in only a single fetus and a single neonate.After maternal oral supplementation with vitamin K1, cord vitamin K1 levels were boosted 30-fold at mid trimester and 60 fold at term, demonstrating placental transfer. However, these levels were substantially lower than corresponding supplemented maternal levels. Despite elevated vitamin K1 concentrations, supplemented fetuses and neonates showed no increase in total or coagulant prothrombin activity. These results suggest that the low prothrombin levels found during intrauterine life are not due to vitamin K deficiency.


2009 ◽  
Vol 95 (2) ◽  
pp. F104-F108 ◽  
Author(s):  
A. Chuansumrit ◽  
T. Plueksacheeva ◽  
S. Hanpinitsak ◽  
S. Sangwarn ◽  
S. Chatvutinun ◽  
...  

1993 ◽  
Vol 16 (3) ◽  
pp. 301-305 ◽  
Author(s):  
E. A. M. Cornelissen ◽  
L. A. A. Kollée ◽  
T. G. P. J. van Lith ◽  
K. Motohara ◽  
L. A. H. Monnens

2007 ◽  
Vol 49 (3) ◽  
pp. 432-439 ◽  
Author(s):  
Rachel M. Pilkey ◽  
A. Ross Morton ◽  
Michael B. Boffa ◽  
Curtis Noordhof ◽  
Andrew G. Day ◽  
...  

2012 ◽  
Vol 25 (9) ◽  
pp. 1660-1663 ◽  
Author(s):  
F. Dituri ◽  
G. Buonocore ◽  
A. Pietravalle ◽  
F. Naddeo ◽  
M. Cortesi ◽  
...  

2017 ◽  
Vol 31 (5) ◽  
pp. 495-505 ◽  
Author(s):  
Yan-ni Mi ◽  
Na-na Ping ◽  
Bo Li ◽  
Xue Xiao ◽  
Yan-bing Zhu ◽  
...  

Folia Medica ◽  
2020 ◽  
Vol 62 (2) ◽  
pp. 378-384
Author(s):  
Silvia Gancheva ◽  
Martina Kitanova ◽  
Peter Ghenev ◽  
Maria Zhelyazkova-Savova

Introduction: Vitamin K (VK) is a co-factor in the post-translational gamma glutamic carboxylation of Gla-proteins. VK-dependent coagulation factors are carboxylated in the liver by VK1. Osteocalcin and Matrix-Gla protein (MGP) are carboxylated in extrahepatic tissues by VK2. A model of VK deficiency would be suitable for studying extrahepatic Gla-proteins provided that severe bleeding is prevented. Aim: The aim of this work was to adapt an established protocol of vascular calcification by warfarin-induced inactivation of MGP as a calcification inhibitor, in an attempt to create a broader state of subclinical VK deficiency and to verify its safety. Materials and methods: Two consecutive experiments, each lasting 4 weeks, were required to modify the dosing schedule of warfa­rin and VK1 and to adapt it to the Wistar rats used. The original high doses of warfarin used initially had to be halved and the protective dose of VK1 to be doubled, in order to avoid treatment-induced hemorrhagic deaths. The second experiment aimed to confirm the efficacy and safety of the modified doses. To verify the VK deficiency, blood vessels were examined histologically for calcium deposits and serum osteocalcin levels were mea­sured. Results: The original dosing schedule induced VK deficiency, manifested by arterial calcifications and dramatic changes in carboxyl­ated and uncarboxylated osteocalcin. The modified dosing regimen caused similar vascular calcification and no bleeding. Conclusion: The modified protocol of carefully balanced warfarin and VK1 doses is an effective and safe way to induce subclinical VK deficiency that can be implemented to investigate VK-dependent proteins like osteocalcin.


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