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维生素 K₂ 可预防链脲佐菌素诱导的 1 型糖尿病大鼠的高血糖和松质骨骨质疏松症。

Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes.

机构信息

Institute for Integrated Sports Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.

出版信息

Calcif Tissue Int. 2011 Feb;88(2):162-8. doi: 10.1007/s00223-010-9441-5. Epub 2010 Dec 7.

DOI:10.1007/s00223-010-9441-5
PMID:21136047
Abstract

The purpose of the present study was to examine the effect of vitamin K₂ on cancellous and cortical bone mass in rats with streptozotocin (STZ)-induced type 1 diabetes. Twenty-seven male Sprague-Dawley rats aged 12 weeks were randomized by the weight-stratified method into the following three groups: age-matched control group, STZ + vehicle group, and STZ + vitamin K₂ group. STZ (40 + 50 mg/kg) was administered intravenously twice during the initial 1-week period. Vitamin K₂ (menatetrenone, 30 mg/kg) was administered orally 5 days a week. After 12 weeks of treatment, the serum glucose concentration and femoral length and weight were measured and histomorphometric analysis was performed on the cancellous and cortical bone of the distal femoral metaphysis and femoral diaphysis, respectively. STZ administration induced hyperglycemia and a decrease in femoral weight. The STZ + vehicle group also showed cancellous osteopenia due to a decrease in the number of osteoblasts/bone surface (N.Ob/BS) and the osteoblast surface (ObS)/BS without any significant changes in bone-resorption parameters, but it did not have a significant decrease in cortical bone mass. Administration of vitamin K₂ to STZ-treated rats prevented the development of hyperglycemia and a decrease in femoral weight. Vitamin K₂ also prevented cancellous osteopenia by inhibiting the decrease in N.Ob/BS and ObS/BS without significantly affecting bone-resorption parameters, but it did not significantly increase cortical bone mass. These results suggest that vitamin K₂ has beneficial effects on glucose concentration and cancellous bone mass in rats with STZ-induced type 1 diabetes.

摘要

本研究旨在探讨维生素 K₂ 对链脲佐菌素(STZ)诱导的 1 型糖尿病大鼠松质骨和皮质骨量的影响。27 只 12 周龄雄性 Sprague-Dawley 大鼠采用体重分层法随机分为以下三组:年龄匹配的对照组、STZ+载体组和 STZ+维生素 K₂ 组。在最初的 1 周内,通过静脉注射两次给予 STZ(40+50mg/kg)。每周 5 天给予维生素 K₂(甲萘醌,30mg/kg)口服。治疗 12 周后,测量血清葡萄糖浓度和股骨长度和重量,并分别对股骨远端干骺端和骨干的松质骨和皮质骨进行组织形态计量学分析。STZ 给药诱导高血糖和股骨重量下降。STZ+载体组还因成骨细胞/骨表面(N.Ob/BS)和成骨细胞表面(ObS)/BS 的数量减少而出现松质骨骨质疏松,而骨吸收参数没有明显变化,但皮质骨量没有明显减少。给予维生素 K₂ 可预防 STZ 处理大鼠的高血糖和股骨重量下降。维生素 K₂ 还通过抑制 N.Ob/BS 和 ObS/BS 的减少来预防松质骨骨质疏松,而不显著影响骨吸收参数,但不会显著增加皮质骨量。这些结果表明,维生素 K₂ 对 STZ 诱导的 1 型糖尿病大鼠的血糖浓度和松质骨量具有有益作用。

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