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运动训练可预防雄性达尔盐敏感大鼠高果糖诱导的高血压和肾脏损伤。

Exercise Training Prevents High Fructose-Induced Hypertension and Renal Damages in Male Dahl Salt-Sensitive Rats.

机构信息

Department of Molecular Physiology and Biological Physics, School of Medicine, University of Virginia, Charlottesville, VA.

Department of Internal Medicine and Rehabilitation Science, Tohoku University Graduate School of Medicine, Sendai, JAPAN.

出版信息

Med Sci Sports Exerc. 2023 May 1;55(5):803-812. doi: 10.1249/MSS.0000000000003100. Epub 2022 Dec 9.

Abstract

INTRODUCTION

High-fructose diet (HFr) causes metabolic syndrome, and HFr-induced hypertension and renal damage are exaggerated in Dahl salt-sensitive (DS) rats. Exercise training (Ex) has antihypertensive and renal protective effects in rats fed HFr; however, there has been little discussion about the DS rats, which exhibit metabolic disturbances. This study thus examined the effects of Ex on DS rats fed HFr.

METHODS

Male DS rats were divided into three groups. The control group was fed a control diet, and both the HFr group and the HFr-Ex group were fed an HFr (60% fructose). The HFr-Ex group also underwent treadmill running (20 m·min -1 , 60 min·d -1 , 5 d·wk -1 ). After 12 wk, renal function, histology, and renin-angiotensin system were examined.

RESULTS

HFr increased blood pressure, urinary albumin, and creatinine clearance, and Ex inhibited these increases. HFr induced glomerular sclerosis, podocyte injury, afferent arteriole thickening, and renal interstitial fibrosis, and Ex ameliorated them. HFr reduced plasma renin activity, and Ex further reduced the activity. HFr also increased the expression of angiotensinogen, renin, angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor, and Ex restored the ACE expression to the control levels. HFr decreased the expression of ACE2, angiotensin II type 2 receptor, and Mas receptor, and Ex restored the ACE2 and Mas receptor expressions to the control levels and further decreased the angiotensin II type 2 receptor expression. HFr increased the ACE activity and decreased the ACE2 activity, and Ex restored these activities to the control levels.

CONCLUSIONS

Ex prevents HFr-induced hypertension and renal damages in DS rats. The changes in renal renin-angiotensin system may be involved in the mechanism of the antihypertensive and renal protective effects of Ex.

摘要

简介

高果糖饮食(HFr)会导致代谢综合征,而 HFr 诱导的高血压和肾脏损伤在达尔盐敏感(DS)大鼠中更为明显。运动训练(Ex)在 HFr 喂养的大鼠中具有降压和肾脏保护作用;然而,对于表现出代谢紊乱的 DS 大鼠,讨论较少。因此,本研究探讨了 Ex 对 HFr 喂养的 DS 大鼠的影响。

方法

雄性 DS 大鼠分为三组。对照组喂养对照饮食,HFr 组和 HFr-Ex 组均喂养 HFr(60%果糖)。HFr-Ex 组还进行跑步机跑步(20 m·min -1 ,60 min·d -1 ,5 d·wk -1 )。12 周后,检查肾功能、组织学和肾素-血管紧张素系统。

结果

HFr 升高血压、尿白蛋白和肌酐清除率,Ex 抑制这些升高。HFr 诱导肾小球硬化、足细胞损伤、入球小动脉增厚和肾间质纤维化,Ex 改善了这些情况。HFr 降低了血浆肾素活性,Ex 进一步降低了活性。HFr 还增加了血管紧张素原、肾素、血管紧张素转换酶(ACE)和血管紧张素 II 型 1 受体的表达,Ex 将 ACE 表达恢复到对照水平。HFr 降低了 ACE2、血管紧张素 II 型 2 受体和 Mas 受体的表达,Ex 将 ACE2 和 Mas 受体的表达恢复到对照水平,并进一步降低了血管紧张素 II 型 2 受体的表达。HFr 增加了 ACE 活性,降低了 ACE2 活性,Ex 将这些活性恢复到对照水平。

结论

Ex 可预防 DS 大鼠 HFr 诱导的高血压和肾脏损伤。肾素-血管紧张素系统的变化可能参与了 Ex 的降压和肾脏保护作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f691/10090347/1f4b2f6190b3/msse-55-803-g001.jpg

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