四烯甲萘醌

四烯甲萘醌，又稱維他命K₂，為一群相似的化合物，可分為短鏈四烯甲萘醌（如MK-4）和長鏈四烯甲萘醌（如MK-7、MK-8、MK-9）。維生素K₂未有已知的毒性，因維生素K不會在肝臟中過量殘留。

構造

維生素K皆有醌結構，而維生素K₂的命名取決於上圖化學式中n的數目。例如當n為4，名稱就是MK-4。維生素K₂於身體中的傳輸會受其結構影響。

作用機制

維生素K₂的作用機制與維生素K₁類似，能夠輔助γ-穀氨酰羧化酶（英语：Gamma-glutamyl carboxylase）將穀氨酸（Glu）轉化成γ-羧化穀氨酸（Gla）。這過程對生成Gla-蛋白質（含有Gla的蛋白質）有幫助，例子如下：

骨鈣素：骨骼礦化
GAS6：細胞增殖
凝血酶、抗凝蛋白：血液穩態

吸收

維生素K於小腸中被吸收，藉乳糜微粒運輸。維生素K₁和MK-4能夠被肝臟快速處理，但低密度脂蛋白（LDL）會帶走較多長鏈四烯甲萘醌。由於LDL壽命較長，長鏈四烯甲萘醌能夠被肝以外的組織（骨、軟骨、血管等）吸收，對達致維生素K部分功效有幫助。^[1]

攝入

除了肝臟外，蘊含長鏈四烯甲萘醌最豐富的是以細菌發酵的食品，如乳酪（MK-8、MK-9）、納豆（MK-7）等，當中納豆為維生素K₂含量最豐富的食品^[2]。根據對荷蘭人飲食習慣的研究，估計維生素K的攝取由約 90% 維生素K₁、約 7.5 % MK-5至MK-9及約 2.5% MK-4組成。另外根據對完全不飽和四烯甲萘醌的研究，乳酪含有10–20 μg/100g 的MK-8和35–55 μg/100 g 的MK-9。^[3]

另外人體腸道中的細菌亦可製造維生素K₂，可以滿足每日對維生素K的部分需求。

抗凝劑及維生素K的補充

研究指出長期口服抗凝劑減少體內正常骨鈣素，從而影響骨骼健康。這可能導致骨骼礦化不足（骨質減少）、容易骨折等^[4]。另外長期口服抗凝劑亦相信會令小童、成人出現不良的軟組織鈣化^[5]^[6]，這是由於缺乏維生素K導致正常基質Gla蛋白偏少。在動物實驗中血管鈣化可出現於服用華法林兩週內^[7]。另外長期口服抗凝劑的病人被發現其動脈鈣化的程度為其他病人的一倍^[8]^[9]。動脈鈣化亦可能導致收縮期高血壓、心室肥大等^[10]^[11]。雖然大量維生素K降低抗凝劑的效用，但現在正研究將抗凝劑療程及維生素K結合。

参考文献

^ Martin J. Shearer, Paul Newman. Metabolism and cell biology of vitamin K. Thromb Haemost 2008
^ Kaneki M, Hodges SJ, Hosoi T, Fujiwara S, Lyons A, Crean SJ, Ishida N, Nakagawa M, Takechi M, Sano Y, Mizuno Y, Hoshino S, Miyao M, Inoue S, Horiki K, Shiraki M, Ouchi Y, Orimo H; Japanese fermented soybean food as the major determinant of the large geographic difference in circulating levels of K vitamins2: possible implications for hip-fracture risk; Nutrition; 2001; 17(4): 315-321.
^ Shearer N, Metabolism and cell biology of vitamin K. Thromb Haemost. 2008
^ Caraballo PJ, Gabriel SE, Castro MR, Atkinson EJ, Melton LJ 3rd. Changes in bone density after exposure to oral anticoagulants: a meta-analysis.Osteoporos Int. 1999;9(5):441-8.
^ Barnes C, Newall F, Ignjatovic V, Wong P, Cameron F, Jones G, Monagle P. Reduced bone density in children on long-term warfarin. Pediatr Res. 2005;57(4):578-81.
^ Hawkins D, Evans J. Minimising the risk of heparin-induced osteoporosis during pregnancy. Expert Opin Drug Saf. 2005;4(3):583-90
^ Price PA, Faus SA, Williamson MK. Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves. Arterioscler Thromb Vasc Biol. 1998;18(9):1400-7.
^ Schurgers LJ, Aebert H, Vermeer C, Bültmann B, Janzen J. Oral anticoagulant treatment: friend or foe in cardiovascular disease? Blood. 2004 15;104(10):3231-2.
^ Koos R, Mahnken AH, Mühlenbruch G, Brandenburg V, Pflueger B, Wildberger JE, Kühl HP. Relation of oral anticoagulation to cardiac valvular and coronary calcium assessed by multislice spiral computed tomography. Am J Cardiol. 2005;96(6):747-9.
^ Zieman SJ, Melenovsky V, Kass DA. Mechanisms, pathophysiology, and therapy of arterial stiffness. Arterioscler Thromb Vasc Biol. 2005;25(5):932-43.
^ Raggi P, Shaw LJ, Berman DS, Callister TQ. Prognostic value of coronary artery calcium screening in subjects with and without diabetes. J Am Coll Cardiol. 2004;43(9):1663-9.

外部連結

Vitak BV
VitaminK2.org（页面存档备份，存于互联网档案馆）

[1] Martin J. Shearer, Paul Newman. Metabolism and cell biology of vitamin K. Thromb Haemost 2008

[2] Kaneki M, Hodges SJ, Hosoi T, Fujiwara S, Lyons A, Crean SJ, Ishida N, Nakagawa M, Takechi M, Sano Y, Mizuno Y, Hoshino S, Miyao M, Inoue S, Horiki K, Shiraki M, Ouchi Y, Orimo H; Japanese fermented soybean food as the major determinant of the large geographic difference in circulating levels of K vitamins2: possible implications for hip-fracture risk; Nutrition; 2001; 17(4): 315-321.

[3] Shearer N, Metabolism and cell biology of vitamin K. Thromb Haemost. 2008

[4] Caraballo PJ, Gabriel SE, Castro MR, Atkinson EJ, Melton LJ 3rd. Changes in bone density after exposure to oral anticoagulants: a meta-analysis.Osteoporos Int. 1999;9(5):441-8.

[5] Barnes C, Newall F, Ignjatovic V, Wong P, Cameron F, Jones G, Monagle P. Reduced bone density in children on long-term warfarin. Pediatr Res. 2005;57(4):578-81.

[6] Hawkins D, Evans J. Minimising the risk of heparin-induced osteoporosis during pregnancy. Expert Opin Drug Saf. 2005;4(3):583-90

[7] Price PA, Faus SA, Williamson MK. Warfarin causes rapid calcification of the elastic lamellae in rat arteries and heart valves. Arterioscler Thromb Vasc Biol. 1998;18(9):1400-7.

[8] Schurgers LJ, Aebert H, Vermeer C, Bültmann B, Janzen J. Oral anticoagulant treatment: friend or foe in cardiovascular disease? Blood. 2004 15;104(10):3231-2.

[9] Koos R, Mahnken AH, Mühlenbruch G, Brandenburg V, Pflueger B, Wildberger JE, Kühl HP. Relation of oral anticoagulation to cardiac valvular and coronary calcium assessed by multislice spiral computed tomography. Am J Cardiol. 2005;96(6):747-9.

[10] Zieman SJ, Melenovsky V, Kass DA. Mechanisms, pathophysiology, and therapy of arterial stiffness. Arterioscler Thromb Vasc Biol. 2005;25(5):932-43.

[11] Raggi P, Shaw LJ, Berman DS, Callister TQ. Prognostic value of coronary artery calcium screening in subjects with and without diabetes. J Am Coll Cardiol. 2004;43(9):1663-9.

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