The sweetest thing: blocking fructose metabolism to prevent acute kidney injury?
The sweetest thing: blocking fructose metabolism to prevent acute kidney injury?
复制标题
最甜蜜的事情：阻断果糖代谢以预防急性肾损伤？
DOI：
10.1016/j.kint.2017.03.004
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发表时间：
2017
影响因子：
19.6
通讯作者：
Reeves,WBrian
中科院分区：
文献类型：
--
作者：
Wyatt,ChristinaM;Reeves,WBrian
在动物模型和人类研究中，果糖消耗与高血压有关，内源性果糖代谢已被证明会促进小鼠的急性和慢性肾损伤。最近发表在《自然通讯》上的一项研究表明，通过基因敲除或抑制果糖激酶，可以减少缺血性急性肾损伤，果糖激酶催化果糖代谢的第一步。虽然这一途径在人类肾脏疾病中的作用仍不清楚，但最近对几种候选果糖激酶抑制剂的描述可能会使未来的临床研究成为可能。
Fructose consumption has been linked to hypertension in animal models and human studies, and endogenous fructose metabolism has been shown to promote acute and chronic kidney injury in mice. A recent study published inNature Communicationsdemonstrates a reduction in ischemic acute kidney injury with genetic knockout or inhibition of fructokinase, which catalyzes the first step in fructose metabolism. Although the role of this pathway in human kidney disease remains unclear, the recent description of several candidate fructokinase inhibitors may allow for clinical studies in the future.