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微血管功能障碍是否将肥胖与胰岛素抵抗及高血压联系起来?

Does microvascular dysfunction link obesity with insulin resistance and hypertension?

作者信息

de Jongh Renate T, Serné Erik H, Eringa Etto C, IJzerman Richard G, Stehouwer Coen DA

机构信息

a VU University Medical Center, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.

b VU University Medical Center, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.

出版信息

Expert Rev Endocrinol Metab. 2006 Mar;1(2):181-187. doi: 10.1586/17446651.1.2.181.

Abstract

Obesity and obesity-associated clinical disorders are becoming an increasing public health burden. In this perspective, we postulate that impairment of microvascular function links obesity with insulin resistance and hypertension. Obesity is characterized by generalized microvascular dysfunction, which is associated with, and may precede, the development of insulin resistance and hypertension. Understanding of mechanisms involved in obesity-associated microvascular dysfunction may reveal new therapeutic targets. In obesity, cellular regulatory mechanisms of vasoreactivity are shifted towards vasoconstriction, with an increased role for endothelin-1 and a decreased role for nitric oxide. In addition, communicative pathways between adipose tissue and the microvasculature comprise increased release of adipokines and increased sympathetic activity. Although one mechanism may dominate, microvascular defects in obesity are probably caused by an integrated response consisting of endocrine, vasocrine and neurogenic mechanisms. This remains a fruitful area for future research.

摘要

肥胖及与肥胖相关的临床疾病正日益成为公共卫生负担。从这个角度来看,我们推测微血管功能受损将肥胖与胰岛素抵抗及高血压联系起来。肥胖的特征是全身性微血管功能障碍,这与胰岛素抵抗和高血压的发生相关,且可能先于它们出现。了解肥胖相关微血管功能障碍所涉及的机制可能会揭示新的治疗靶点。在肥胖状态下,血管反应性的细胞调节机制转向血管收缩,内皮素-1的作用增强,一氧化氮的作用减弱。此外,脂肪组织与微血管之间的通讯途径包括脂肪因子释放增加和交感神经活动增强。虽然可能有一种机制起主导作用,但肥胖中的微血管缺陷可能是由内分泌、血管分泌和神经源性机制组成的综合反应所致。这仍是未来研究的一个富有成果的领域。

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