Metabolic syndrome (MS) is a health problem that is characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated that MS also damages memory processes. The first‐line drug in the treatment of MS and type 2 diabetes mellitus is metformin, which is an antihyperglycemic agent. This drug has been shown to produce neuroprotection and to improve memory processes. However, the mechanism involved in this neuroprotection is unknown. A 90‐day administration of metformin improved the cognitive processes of rats with MS as evaluated by the novel object recognition test, and this finding could be explained by an increase in the neuronal spine density and spine length. We also found that metformin increased the immunoreactivity of synaptophysin, sirtuin‐1, AMP‐activated protein kinase, and brain‐derived neuronal factor, which are important plasticity markers. We conclude that metformin is an important therapeutic agent that increases neural plasticity and protects cognitive processes. The use of this drug is important in the minimization of the damage caused by MS.

中文翻译：

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二甲双胍对代谢综合征大鼠识别记忆和海马神经可塑性的影响。

代谢综合征（MS）是一种以体脂堆积、高血压、血脂异常和高血糖为特征的健康问题；最近，已经证明 MS 也会损害记忆过程。治疗 MS 和 2 型糖尿病的一线药物是二甲双胍，它是一种降糖药。这种药物已被证明可以产生神经保护作用并改善记忆过程。然而，这种神经保护所涉及的机制尚不清楚。根据新型物体识别测试的评估，服用二甲双胍 90 天改善了 MS 大鼠的认知过程，这一发现可以通过神经元脊柱密度和脊柱长度的增加来解释。我们还发现二甲双胍增加了突触素、sirtuin-1、AMP 活化蛋白激酶、和脑源性神经元因子，这是重要的可塑性标志物。我们得出结论，二甲双胍是一种重要的治疗剂，可增加神经可塑性并保护认知过程。使用这种药物对于尽量减少 MS 造成的损害很重要。