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.