Fructose-induced hypertension: essential role of chloride and fructose absorbing transporters PAT1 and Glut5
Fructose-induced hypertension: essential role of chloride and fructose absorbing transporters PAT1 and Glut5
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DOI：
10.1038/ki.2008.184
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发表时间：
2008-08-01
影响因子：
19.6
通讯作者：
Soleimani, Manoocher
中科院分区：
文献类型：
--
作者：
Singh, Anurag Kumar;Amlal, Hassane;Soleimani, Manoocher
啮齿类动物饮食中果糖的增加概括了代谢综合征的许多方面，包括高血压、胰岛素抵抗和血脂异常。在这里，我们表明，果糖增加空肠氯化钠和水的吸收，这是显着减少的小鼠，其顶端氯/碱交换Slc 26 a6（PAT 1，CFEX）被敲除。增加饮食中果糖的摄入增强了野生型小鼠小肠中这种转运蛋白以及果糖吸收转运蛋白Slc 2a 5（Glut 5）的表达。果糖喂养减少了肾脏的盐排泄，导致高血压，敲除小鼠的反应几乎消失。在平行研究中，无氯饮食阻断了Sprague道利大鼠果糖诱导的高血压。高血压动物果糖摄入量增加时，血清尿酸保持不变。我们认为果糖诱导的高血压可能是由肠道和肾脏对盐的吸收增加引起的，转运蛋白Slc 26 a6和Slc 2a 5在这个过程中是必不可少的。
Increased dietary fructose in rodents recapitulates many aspects of the Metabolic Syndrome with hypertension, insulin resistance and dyslipidemia. Here we show that fructose increased jejunal NaCl and water absorption which was significantly decreased in mice whose apical chloride/base exchanger Slc26a6 (PAT1, CFEX) was knocked out. Increased dietary fructose intake enhanced expression of this transporter as well as the fructose-absorbing transporter Slc2a5 (Glut5) in the small intestine of wild type mice. Fructose feeding decreased salt excretion by the kidney and resulted in hypertension, a response almost abolished in the knockout mice. In parallel studies, a chloride-free diet blocked fructose-induced hypertension in Sprague Dawley rats. Serum uric acid remained unchanged in animals on increased fructose intake with hypertension. We suggest that fructose-induced hypertension is likely caused by increased salt absorption by the intestine and kidney and the transporters Slc26a6 and Slc2a5 are essential in this process.