Laboratory of Nutrition, Graduate School of Agricultural Science, Tohoku University, Sendai, 981-8555, Japan.
Food Funct. 2011 Jul;2(7):406-11. doi: 10.1039/c1fo10058k. Epub 2011 Jun 13.
Vitamin K is essential for the posttranslational modifications of blood coagulation factors and proteins present in the bone matrix. Vitamin K is distributed not only in the liver and bones but is also abundant in the brain, kidney, and gonadal tissues. However, the function of extra-hepatic/bone vitamin K has not been fully elucidated. Previously, we observed that dietary supplementation with vitamin K suppresses inflammation, and vitamin K deficiency decreases testicular testosterone production in rats. Here, we examined whether the dietary vitamin K state affects testicular steroidogenesis in lipopolysaccharide (LPS)-treated rats because vitamin K has anti-inflammatory activity. Male Wistar rats were fed either vitamin K-free or control diets for 35 d, and then intraperitoneally administered LPS (0.5 mg kg(-1) body weight) to induce inflammation for 6 h. Vitamin K deficiency symptoms were not observed in the vitamin K-free diet group; however, the vitamin K levels in the testis were significantly lower in the vitamin K-free diet group than in the control diet group. After LPS treatment, plasma testosterone levels were significantly reduced in the vitamin K-free diet group compared with the control diet group. Testicular mRNA and protein levels of Cyp11a, a rate-limiting enzyme in steroidogenesis, corresponded to plasma testosterone levels. However, plasma luteinizing hormone levels were unaffected by diet and LPS. Phosphorylated nuclear factor κB p65 in the testis was significantly increased in the LPS-treated, vitamin K-free diet group compared with control. These results indicate that dietary vitamin K affects testicular vitamin K levels and ameliorates the LPS-induced reduction in testicular testosterone synthesis. Testicular vitamin K might facilitate the inhibition of inflammation signal transduction and maintain steady levels of testosterone.
维生素 K 对于血液凝血因子和骨基质中存在的蛋白质的翻译后修饰至关重要。维生素 K 不仅分布在肝脏和骨骼中，而且在大脑、肾脏和性腺组织中也很丰富。然而，肝外/骨维生素 K 的功能尚未完全阐明。先前，我们观察到饮食补充维生素 K 可抑制炎症，维生素 K 缺乏会降低大鼠睾丸中的睾丸激素产生。在这里，我们研究了饮食中维生素 K 状态是否会影响脂多糖 (LPS) 处理的大鼠的睾丸类固醇生成，因为维生素 K 具有抗炎活性。雄性 Wistar 大鼠连续 35 天分别喂食维生素 K 缺乏或对照饮食，然后腹膜内注射 LPS（0.5mg/kg 体重）以诱导炎症 6 小时。在维生素 K 缺乏饮食组中未观察到维生素 K 缺乏症状；然而，维生素 K 缺乏饮食组睾丸中的维生素 K 水平明显低于对照饮食组。在 LPS 处理后，与对照饮食组相比，维生素 K 缺乏饮食组的血浆睾丸激素水平显著降低。睾丸 Cyp11a（类固醇生成的限速酶）的 mRNA 和蛋白水平与血浆睾丸激素水平相对应。然而，饮食和 LPS 对血浆促黄体生成素水平没有影响。与对照饮食组相比，LPS 处理、维生素 K 缺乏饮食组的睾丸核因子 κB p65 磷酸化显著增加。这些结果表明，饮食中的维生素 K 影响睾丸中的维生素 K 水平，并改善 LPS 诱导的睾丸睾丸激素合成减少。睾丸中的维生素 K 可能有助于抑制炎症信号转导并维持稳定的睾丸激素水平。
