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饮食中钠的限制可预防高果糖喂养的大鼠肾脏损伤。

Dietary sodium restriction prevents kidney damage in high fructose-fed rats.

机构信息

Groupe Rein et Hypertension, FRE3400 CNRS/University, Montpellier, France.

出版信息

Kidney Int. 2013 Apr;83(4):674-83. doi: 10.1038/ki.2012.478. Epub 2013 Jan 23.

DOI:10.1038/ki.2012.478
PMID:23344470
Abstract

Sodium depletion has a protective effect on target-organ damage in hypertension independent of blood pressure. Here we tested whether chronic dietary sodium restriction may prevent the development of renal alterations associated with insulin resistance by reducing the inflammatory and oxidant state. Rats were fed normal-salt-60% fructose, low-salt-60% fructose, or control normal-salt diet for 12 weeks. Insulin resistance induced by high-fructose diet was associated with an increase in albuminuria, tubular and glomerular hypertrophy, and inflammation of kidney and adipose tissue. The low-salt diet improved insulin sensitivity and prevented kidney damage. These beneficial effects of sodium depletion were associated with a decrease in renal inflammation (macrophage infiltration, IL-6, TNF-α) and oxidative stress (NADPH oxidase activity), and a prevention of histologic changes in retroperitoneal fat induced by high fructose. Thus, dietary salt depletion has beneficial effects on renal and metabolic alterations associated with a high-fructose diet in rats.

摘要

钠耗竭对高血压靶器官损伤具有保护作用,与血压无关。在这里,我们通过降低炎症和氧化状态来测试慢性饮食钠限制是否可以通过减少炎症和氧化应激来预防与胰岛素抵抗相关的肾脏改变。大鼠喂食正常盐-60%果糖、低盐-60%果糖或对照正常盐饮食 12 周。高果糖饮食引起的胰岛素抵抗与白蛋白尿、肾小管和肾小球肥大以及肾脏和脂肪组织炎症增加有关。低盐饮食可改善胰岛素敏感性并预防肾脏损伤。钠耗竭的这些有益作用与肾脏炎症(巨噬细胞浸润、IL-6、TNF-α)和氧化应激(NADPH 氧化酶活性)的降低以及高果糖引起的腹膜后脂肪组织组织学变化的预防有关。因此,饮食盐耗竭对大鼠高果糖饮食相关的肾脏和代谢改变具有有益作用。

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