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瘦素和中枢神经系统黑皮质素在肥胖性高血压中的作用。

Role of leptin and central nervous system melanocortins in obesity hypertension.

机构信息

Department of Physiology and Biophysics, Center of Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, Jackson, Mississippi, USA.

出版信息

Curr Opin Nephrol Hypertens. 2013 Mar;22(2):135-40. doi: 10.1097/MNH.0b013e32835d0c05.

DOI:10.1097/MNH.0b013e32835d0c05
PMID:23299052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3905446/
Abstract

PURPOSE OF REVIEW

Obesity is a major worldwide health problem. Excess weight gain is the most significant preventable cause of increased blood pressure (BP) in patients with essential hypertension and increases the risk for cardiovascular and renal diseases. Our goal is to review the mechanisms that link obesity with hypertension, with special emphasis on the role of leptin and the brain melanocortin system in driving sympathetic activation in obesity.

RECENT FINDINGS

Despite increased interest in obesity as a major risk for developing hypertension, the precise mechanisms linking excess weight gain with increases in BP are still elusive. Current evidence suggests that increased sympathetic nervous system (SNS) activity contributes to impaired renal-pressure natriuresis and sodium retention in obesity. Recent findings indicate that the adipocyte-derived hormone, leptin, activates brain centers that regulate SNS activity through a melanocortin-system-dependent pathway. The interaction of leptin and the brain melanocortin system represents an important area of research to further our understanding of the mechanisms leading to sympathetic activation in obesity.

SUMMARY

Sympathetic overactivity is an important link between excess weight gain and increased BP. Hormones and cytokines secreted by the adipose tissue that interact with neural pathways (e.g. melanocortin system) appear to play a key role in contributing to sympathetic activation in obesity and represent potential new targets for therapies.

摘要

目的综述

肥胖是一个全球性的健康问题。超重是原发性高血压患者血压升高的最主要可预防原因,增加了心血管和肾脏疾病的风险。我们的目标是综述肥胖与高血压相关的机制,特别强调瘦素和脑黑皮质素系统在驱动肥胖中交感神经激活的作用。

最新发现

尽管人们对肥胖作为高血压的主要危险因素越来越感兴趣,但将体重增加与血压升高联系起来的确切机制仍不清楚。目前的证据表明,增加的交感神经系统(SNS)活动导致肥胖时肾功能受损、压力排钠和钠潴留。最近的研究结果表明,脂肪细胞衍生的激素瘦素通过依赖黑皮质素系统的途径激活调节 SNS 活动的脑中枢。瘦素与脑黑皮质素系统的相互作用是研究的一个重要领域,有助于进一步了解导致肥胖中交感神经激活的机制。

总结

交感神经活动过度是体重增加和血压升高之间的重要联系。脂肪组织分泌的与神经通路(如黑皮质素系统)相互作用的激素和细胞因子似乎在促进肥胖中交感神经激活方面起着关键作用,代表了治疗的潜在新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a08/3905446/b16a114beb9c/nihms-533360-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a08/3905446/6a02c22c84ae/nihms-533360-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a08/3905446/b16a114beb9c/nihms-533360-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a08/3905446/6a02c22c84ae/nihms-533360-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a08/3905446/b16a114beb9c/nihms-533360-f0002.jpg

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