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自主神经系统在胰岛素血症引起的血液动力学反应中的作用。肥胖和胰岛素抵抗的影响。

Role of the Autonomic Nervous System in the Hemodynamic Response to Hyperinsulinemia-Implications for Obesity and Insulin Resistance.

机构信息

Department of Nutrition and Exercise Physiology, University of Missouri, 204 Gwynn Hall, Columbia, MO, 65211, USA.

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA.

出版信息

Curr Diab Rep. 2022 Apr;22(4):169-175. doi: 10.1007/s11892-022-01456-1. Epub 2022 Mar 5.

Abstract

PURPOSE OF REVIEW

Herein, we summarize recent advances which provide new insights into the role of the autonomic nervous system in the control of blood flow and blood pressure during hyperinsulinemia. We also highlight remaining gaps in knowledge as it pertains to the translation of findings to relevant human chronic conditions such as obesity, insulin resistance, and type 2 diabetes.

RECENT FINDINGS

Our findings in insulin-sensitive adults show that increases in muscle sympathetic nerve activity with hyperinsulinemia do not result in greater sympathetically mediated vasoconstriction in the peripheral circulation. Both an attenuation of α-adrenergic-receptor vasoconstriction and augmented β-adrenergic vasodilation in the setting of high insulin likely explain these findings. In the absence of an increase in sympathetically mediated restraint of peripheral vasodilation during hyperinsulinemia, blood pressure is supported by increases in cardiac output in insulin-sensitive individuals. We highlight a dynamic interplay between central and peripheral mechanisms during hyperinsulinemia to increase sympathetic nervous system activity and maintain blood pressure in insulin-sensitive adults. Whether these results translate to the insulin-resistant condition and implications for long-term cardiovascular regulation warrants further exploration.

摘要

目的综述

本文总结了近期的研究进展,这些进展为自主神经系统在高胰岛素血症期间控制血流和血压中的作用提供了新的见解。我们还强调了在将研究结果转化为肥胖症、胰岛素抵抗和 2 型糖尿病等相关人类慢性疾病方面尚存的知识空白。

最新发现

我们在胰岛素敏感成年人中的发现表明,高胰岛素血症时肌肉交感神经活动的增加并不会导致外周循环中更大程度的交感神经介导的血管收缩。在高胰岛素水平下,α-肾上腺素能受体血管收缩的减弱和 β-肾上腺素能血管舒张的增强可能解释了这些发现。在高胰岛素血症期间,外周血管舒张的交感神经介导抑制没有增加的情况下,心脏输出量的增加维持了胰岛素敏感个体的血压。我们强调了高胰岛素血症期间中枢和外周机制之间的动态相互作用,以增加交感神经系统活动并维持胰岛素敏感成年人的血压。这些结果是否适用于胰岛素抵抗状态以及对长期心血管调节的影响,值得进一步探索。

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