Department of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Institute of Biomedicine, 08028 Barcelona, Spain.
World J Gastroenterol. 2012 Sep 7;18(33):4478-80. doi: 10.3748/wjg.v18.i33.4478.
This short review comments on the recently published work of Ishimoto et al regarding the opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice. The framework for the commentary is the preexisting background of epidemiological and experimental data regarding the association between ingestion of fructose, as present in sweetened beverages, and the development of metabolic syndrome. The work of Ishimoto et al clearly confirms the negative effect of fructose on lipid and glucose metabolism, independently from the amount of energy provided by the ingested sugar. It also confirms the absolute requirement of liver fructose metabolism, driven by fructokinase activity, in order to develop the full spectrum of metabolic syndrome alterations.
这篇简短的综述评论了 Ishimoto 等人最近发表的关于果糖激酶 C 和 A 同工型对小鼠果糖诱导的代谢综合征的相反作用的研究。评论的框架是关于摄入果糖（存在于甜饮料中）与代谢综合征发展之间关联的既有流行病学和实验数据的背景。Ishimoto 等人的工作清楚地证实了果糖对脂质和葡萄糖代谢的负面影响，而与摄入糖提供的能量多少无关。它还证实了肝脏果糖代谢的绝对必要性，这种代谢是由果糖激酶活性驱动的，以便发展出代谢综合征改变的全部特征。
