Obesity-induced increases in sympathetic nerve activity: sex matters.

Obesity-induced increases in sympathetic nerve activity: sex matters.
复制标题

DOI:
10.1016/j.autneu.2014.11.006
复制
发表时间:
2015-01
期刊:
Autonomic neuroscience : basic & clinical
影响因子:
--
通讯作者:
Fadel PJ
Fadel PJ
中科院分区:
其他
文献类型:
--
作者:
Brooks VL;Shi Z;Holwerda SW;Fadel PJ

文献摘要

被引文献

相似文献

大量来自男性人类和动物受试者的证据表明,肥胖增加交感神经活动(SNA),这有助于高血压的发展。然而,最近包括女性的研究报告称,男性中发现的肌肉SNA与腰围或体重指数(BMI)之间的密切关系并不存在于超重和肥胖女性中。在肥胖的动物模型中,已经发现肥胖和高血压发展之间的关联存在类似的性别差异。在这篇简短的综述中,我们考虑了这种性别差异的两种可能机制。首先,内脏肥胖、瘦素、胰岛素和血管紧张素II已被确定为肥胖诱导的男性交感神经兴奋的潜在罪魁祸首。我们探讨这些因素是否对女性产生同样的影响。第二,我们考虑血管对交感神经激活的反应性是否存在性别差异。我们的文献调查表明,绝经前女性可能能够抵抗肥胖引起的交感神经兴奋和高血压,部分原因是脂肪分布的差异,以及其静音炎症反应和减少生产的升压与降压成分的肾素-血管紧张素系统。此外,血管对SNA增加的反应性可能降低。然而,更重要的是,我们确定迫切需要进一步研究,不仅性别差异本身,而且机制,可能介导这些差异。这些信息不仅需要改善肥胖绝经前妇女的治疗选择,而且还可能揭示肥胖男性和女性的新治疗途径。
Abundant evidence obtained largely from male human and animal subjects indicates that obesity increases sympathetic nerve activity (SNA), which contributes to hypertension development. However, recent studies that included women reported that the strong relationships between muscle SNA and waist circumference or body mass index (BMI) found in men are not present in overweight and obese women. A similar sex difference in the association between adiposity and hypertension development has been identified in animal models of obesity. In this brief review, we consider two possible mechanisms for this sex difference. First, visceral adiposity, leptin, insulin, and angiotensin II have been identified as potential culprits in obesity-induced sympathoexcitation in males. We explore if these factors wield the same impact in females. Second, we consider if sex differences in vascular reactivity to sympathetic activation contribute. Our survey of the literature suggests that premenopausal females may be able to resist obesity-induced sympathoexcitation and hypertension in part due to differences in adipose disposition as well as its muted inflammatory response and reduced production of pressor versus depressor components of the renin-angiotensin system. In addition, vascular responsiveness to increased SNA may be reduced. However, more importantly, we identify the urgent need for further study, not only of sex differences per se, but also of the mechanisms that may mediate these differences. This information is required not only to refine treatment options for obese premenopausal women but also to potentially reveal new therapeutic avenues in obese men and women.