Bilateral ovariectomy is the best characterized and the most reported animal model of human menopause. Ovariectomized rodents develop insulin resistance (IR) and visceral obesity, the main risk factors in the pathophysiology of metabolic syndrome (MS). These alterations are a consequence of hypoestrogenic status, which produces an augment of visceral fat, high testosterone levels (hyperandrogenism), as well as inflammation, oxidative stress, and metabolic complications, such as dyslipidemia, hepatic steatosis, and endothelial dysfunction, among others. Clinical trials have reported that menopause per se increases the severity and incidence of MS, and causes the highest mortality due to cardiovascular disease in women. Despite all the evidence, there are no reports that clarify the influence of estrogenic deficiency as a cause of MS. In this review, we provide evidence that ovariectomized rodents can be used as a menopausal metabolic syndrome model for evaluating and discovering new, safe, and effective therapeutic approaches in the treatment of cardiometabolic complications associated to MS during menopause.

双侧卵巢切除术是人类更年期特征最充分，报道最多的动物模型。去卵巢的啮齿动物会产生胰岛素抵抗（IR）和内脏肥胖，这是代谢综合征（MS）病理生理的主要危险因素。这些改变是雌激素状态低下的结果，雌激素状态增加会导致内脏脂肪增加，睾丸激素水平升高（高雄激素血症），炎症，氧化应激和代谢并发症，例如血脂异常，肝脂肪变性和内皮功能障碍等。临床试验报告，更年期本身会增加MS的严重程度和发病率，并由于女性的心血管疾病而导致最高的死亡率。尽管有所有证据，但尚无报道阐明雌激素缺乏症是MS病因的影响。在这篇评论中