INSULIN EFFECT ON VASCULAR REGULATION IN OBESE HUMANS

我的长期目标是探索肥胖和胰岛素之间的联系 人类的抵抗力和高血压。肥胖与 交感神经活动水平增加，这可能是一个危险因素 在高血压的发展过程中。肥胖还与 胰岛素抵抗。因为肥胖并不总是导致 高血压和交感神经活动的增加并不是 总是与高血压相关，这增加了一种可能性，即 交感神经活动增加和胰岛素抵抗相互作用 在肥胖人群中推广高血压。此外，胰岛素是一种有效的 可钝化正常交感神经血管收缩的血管扩张剂 研究对象。因此，胰岛素抵抗的发展与 交感神经活动的增加可能会促进 肥胖者的高血压。在这种情况下，它是 可能交感神经活动与 血管阻力随胰岛素的发展而改变 肥胖个体对血管收缩的抵抗力。 因此，我们推测交感神经血管收缩 肥胖者的血管阻力越大，阻力越高 因为胰岛素抵抗使血管扩张作用减弱。 胰岛素，允许非对抗性的交感神经血管收缩。 如果是这样的话，这可能是将肥胖联系起来的一个关键因素， 交感神经活性和胰岛素抵抗在糖尿病的发生发展中的作用 肥胖人群中的高血压。在这项建议中，我们将提出这个想法 胰岛素抵抗会加剧高血压的影响 内脏肥胖者交感神经活性增加。

My long-term goal is to explore the link between obesity, insulin resistance, and hypertension in humans. Obesity is associated with increased levels of sympathetic activity, which may be a risk factor in the development of hypertension. Obesity is also associated with insulin resistance. Since obesity does not always result in hypertension, and increased levels of sympathetic activity are not always associated with hypertension, this raises the possibility that increased sympatetic activity and insulin resistance interact to promote hypertension in obese humans. Further, insulin is a potent vasodilator that can blunt sympathetic vasoconstriction in normal subjects. Thus, the development of insulin resistance in conjunction with increased sympathetic activity might promote the development of hypertension in the obese individual. In this context, it is possible that the relation between sympathetic nerve activity and vascular resistance is altered by the development of insulin resistance in obese individuals to favor vaso constriction. Therefore, we speculate that sympathetic vasoconstriction will be greater and vascular resistance will be higher in obese individuals because insulin resistance blunts the vasodilatory actions of insulin, permitting unopposed sympathetic vasoconstriction to occur. If so, this might be a key factor which links obesity, augmented sympathetic activity, and insulin resistance in the development of hypertension in obese humans. In this proposal we will tes the idea that insulin resistance exacerbates the hypersive effects of increased sympathetic nerve activity in viscerally obese indviduals.