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首页> 外文期刊>Nutrition, metabolism, and cardiovascular diseases: NMCD >Relationship between autonomic dysfunction, insulin resistance and hypertension, in diabetes.
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Relationship between autonomic dysfunction, insulin resistance and hypertension, in diabetes.

机译:糖尿病中植物神经功能紊乱,胰岛素抵抗和高血压之间的关系。

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Sympathovagal imbalance and insulin resistance are the common underlying disorders linking hypertension and diabetes. The role of hyperinsulinemia, however, on sympathovagal balance and blood pressure has never been clearly dissected from that of hyperglycemia. Nevertheless, the study of animal models of hypertension showed that hypertension does not invariably result in the onset of insulin resistance. This suggests that insulin resistance precedes the onset of hypertension and (possibly) contributes to its pathogenesis, mainly through sympathetic activation. To examine this hypothesis, recent studies investigated the relationship between insulin sensitivity and sympathetic activity in subjects with insulin resistance but free of overt hyperglycemia and obesity, i.e., insulin-resistant offspring of type 2 diabetic patients, demonstrating a prevalence of sympathetic over vagal activity. Therefore insulin resistance and sympathovagal imbalance come before hypertension, but a clear causative role cannot be demonstrated since other mechanisms, including an inappropriate lifestyle, must be taken into account to determine clinical hypertension. Finally, several experiments in human healthy volunteers suggest that the modulation of autonomic regulation at the forearm level can regulate insulin sensitivity, tempting us to speculate that it is the primary autonomic imbalance, through vasoconstriction, that results in both insulin resistance and hypertension. In conclusion, the close relationship between autonomic imbalance, insulin resistance and hypertension is unquestionable; although logical hypothesis can be constructed, which of the three is the earliest event is still not understood, and further research is required.
机译:交感神经不平衡和胰岛素抵抗是将高血压和糖尿病联系起来的常见潜在疾病。然而,从未将高胰岛素血症对交感神经平衡和血压的作用与高血糖症清楚地分开。尽管如此,对高血压动物模型的研究表明,高血压不会始终导致胰岛素抵抗的发作。这表明胰岛素抵抗先于高血压发作,并且(可能)主要通过交感神经激活来促进其发病。为了检验这一假设,最近的研究调查了患有胰岛素抵抗但没有明显的高血糖症和肥胖症(即2型糖尿病患者的胰岛素抵抗后代)的受试者的胰岛素敏感性与交感活动之间的关系,表明交感神经活动高于迷走神经活动。因此,胰岛素抵抗和交感神经的失衡先于高血压发生,但由于其他机制(包括不适当的生活方式)必须考虑在内才能确定临床高血压,因此尚无明确的病因。最后,在人类健康志愿者中进行的一些实验表明,前臂水平的自主神经调节可以调节胰岛素敏感性,从而使我们推测是通过血管收缩导致胰岛素抵抗和高血压的主要自主神经失调。总之,自主神经失调,胰岛素抵抗和高血压之间的密切关系是毋庸置疑的。尽管可以建立逻辑假设,但尚不清楚这三个事件中最早的事件,因此需要进一步的研究。

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