Gancheva Silvia M, Zhelyazkova-Savova Maria D
Department of Preclinical and Clinical Pharmacology, Medical University of Varna, Varna, Bulgaria
Folia Med (Plovdiv). 2016 Dec 1;58(4):264-272. doi: 10.1515/folmed-2016-0032.
The metabolic syndrome is a socially important disorder of energy utilization and storage, recognized as a factor predisposing to the development of depression, anxiety and cognitive impairment in humans.
In the present study we examined the effects of vitamin K2 on the behavior of rats with metabolic syndrome and looked for relationships with the effects on blood sugar.
Male Wistar rats were divided in four groups: a control group on a regular rat chow, a metabolic syndrome (MS) group fed a high-fat high-fructose diet, a control group treated with vitamin K2 and a MS group treated with vitamin K2. Vitamin K2 was given by gavage. At the end of the study (after 10 weeks) behavioral tests were performed and fasting blood glucose was measured. Anxiety was determined using the social interaction test and depression was assessed by the Porsolt test. Memory effects were estimated by the object recognition test. Correlations between fasting blood glucose and behavioral performance were analyzed.
The rats from the MS group had elevated blood glucose. They had anxiety, depression and memory deficit. Vitamin K2 normalized blood glucose, reduced anxiety and depression, but did not improve memory. Time of social interaction (inverse index of anxiety) and memory recognition were negatively correlated with blood glucose in the untreated rats but the immobility time (measure of depression) was not. When vitamin K2-treated rats were added, the correlation of blood glucose with the time of social interaction was kept, but the one with the recognition memory was lost. It might be that the anxiolytic effect of vitamin K2 in this setting is at least partly due to its effects on blood glucose, while the anti-depressant effect is glucose-independent.
The present study demonstrated that vitamin K2 prevented the development of anxiety and depression, but did not improve the memory deficit caused by the dietary manipulation in an experimental model of metabolic syndrome. It might be that the anxiolytic effect of vitamin K2 is at least partly due to its effects on blood glucose, while the antidepressant effect is glucose-independent.
代谢综合征是一种在社会层面具有重要意义的能量利用和储存紊乱疾病，被认为是人类患抑郁症、焦虑症和认知障碍的一个易感因素。
在本研究中，我们检测了维生素K2对患有代谢综合征大鼠行为的影响，并探寻其与血糖影响之间的关系。
雄性Wistar大鼠被分为四组：一组喂食常规大鼠饲料作为对照组，一组喂食高脂肪高果糖饮食作为代谢综合征（MS）组，一组用维生素K2治疗作为对照组，另一组用维生素K2治疗作为MS组。维生素K2通过灌胃给药。在研究结束时（10周后）进行行为测试并测量空腹血糖。使用社交互动测试测定焦虑程度，通过波索尔特测试评估抑郁情况。通过物体识别测试评估记忆效果。分析空腹血糖与行为表现之间的相关性。
MS组大鼠血糖升高。它们存在焦虑、抑郁和记忆缺陷。维生素K2使血糖恢复正常，减轻了焦虑和抑郁，但未改善记忆。社交互动时间（焦虑的反向指标）和记忆识别在未治疗的大鼠中与血糖呈负相关，但不动时间（抑郁指标）与血糖无相关性。当加入用维生素K2治疗的大鼠后，血糖与社交互动时间的相关性得以保持，但与识别记忆的相关性消失。可能在这种情况下，维生素K2的抗焦虑作用至少部分归因于其对血糖的影响，而抗抑郁作用则与血糖无关。
本研究表明，在代谢综合征实验模型中，维生素K2可预防焦虑和抑郁的发生，但不能改善因饮食干预导致的记忆缺陷。维生素K2的抗焦虑作用可能至少部分归因于其对血糖的影响，而抗抑郁作用与血糖无关。
