Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Nutrition. 2018 Mar;47:33-38. doi: 10.1016/j.nut.2017.09.016. Epub 2017 Oct 26.
The biological mechanisms behind the association between vitamin K (Vit K) and glucose metabolism are uncertain. We aimed to analyze the expression of insulin 1 (Ins 1), insulin 2 (Ins 2) and cyclin D2, the expression of adiponectin and UCP-1 . In addition, we aimed to estimate the doses of Vit K2 able to affect various aspects of glucose and energy metabolism in type 2 diabetes.
Thirty adult male rats were allocated equally into five groups: control group, diabetes mellitus group, and groups 3, 4, and 5, which received Vit K at three daily dose levels (10, 15, and 30 mg/kg, respectively) for 8 wk. At the end of the study, blood samples were collected to quantify total osteocalcin, fasting plasma glucose, fasting insulin, and relevant variables. The expression of OC, Ins 1, Ins 2, cyclin D2, adiponectin, UCP-1 genes was analyzed by real-time polymerase chain reaction.
After administration of Vit K, a dose-dependent decrease in fasting plasma glucose, hemoglobin A1c and homeostatic model assessment method insulin resistance, and a dose-dependent increase in fasting insulin and homeostatic model assessment method β cell function levels, when compared with diabetes mellitus rats, were detected. There was significant upregulation of OC, Ins 1, Ins 2, or cyclin D2 gene expression in the three treated groups in a dose-dependent manner when compared with the diabetic rats. However, expression of adiponectin and UCP-1 were significantly increased at the highest dose (30 mg/kg daily) only.
Vit K administration could improve glycemic status in type 2 diabetic rats by induction of OC gene expression. Osteocalcin could increase β-cell proliferation, energy expenditure, and adiponectin expression. Different concentrations of Vit K were required to affect glucose metabolism and insulin sensitivity.
维生素 K（Vit K）与葡萄糖代谢之间关联的生物学机制尚不清楚。我们旨在分析胰岛素 1（Ins 1）、胰岛素 2（Ins 2）和细胞周期蛋白 D2 的表达、脂联素和 UCP-1 的表达。此外，我们旨在评估 Vit K2 的剂量，以影响 2 型糖尿病患者葡萄糖和能量代谢的各个方面。
将 30 只成年雄性大鼠平均分配到 5 组：对照组、糖尿病组和第 3、4、5 组，分别给予 Vit K 每日 3 个剂量（分别为 10、15 和 30mg/kg），持续 8 周。在研究结束时，采集血样以定量测定总骨钙素、空腹血糖、空腹胰岛素和相关变量。通过实时聚合酶链反应分析 OC、Ins 1、Ins 2、细胞周期蛋白 D2、脂联素、UCP-1 基因的表达。
与糖尿病大鼠相比，Vit K 给药后可观察到空腹血糖、糖化血红蛋白和稳态模型评估法胰岛素抵抗呈剂量依赖性下降，空腹胰岛素和稳态模型评估法β细胞功能水平呈剂量依赖性升高。与糖尿病大鼠相比，3 个治疗组的 OC、Ins 1、Ins 2 或细胞周期蛋白 D2 基因表达呈剂量依赖性显著上调。然而，仅在最高剂量（每日 30mg/kg）时，脂联素和 UCP-1 的表达才显著增加。
Vit K 给药可通过诱导 OC 基因表达改善 2 型糖尿病大鼠的血糖状态。骨钙素可增加β细胞增殖、能量消耗和脂联素表达。需要不同浓度的 Vit K 来影响葡萄糖代谢和胰岛素敏感性。
