美国科罗拉多大学医学院Miguel A. Lanaspa团队发现，肝脏与肠道中的果糖激酶在糖引起的代谢失调中发挥了不同功能。该研究于2020年6月4日在线发表于《细胞—代谢》。
Title: Deletion of Fructokinase in the Liver or in the Intestine Reveals Differential Effects on Sugar-Induced Metabolic Dysfunction
Author: Ana Andres-Hernando, David J. Orlicky, Masanari Kuwabara, Takuji Ishimoto, Takahiko Nakagawa, Richard J. Johnson, Miguel A. Lanaspa
Abstract: Intake of fructose-containing sugars is strongly associated with metabolic syndrome.Compared with other sugars, dietary fructose is uniquely metabolized by fructokinase.However, the tissue-specific role of fructokinase in sugar-induced metabolic syndrome,and the specific roles of glucose and fructose in driving it, is not fully understood.Here, we show that in mice receiving excess fructose-glucose solutions, whole-bodydeletion of fructokinase, and thus full blockade of fructose metabolism, is sufficientto prevent metabolic syndrome. This protection is not only due to reduced fructosemetabolism, but also due to decreased sugar intake. Furthermore, by using tissue-specificfructokinase-deficient mice, we determined that while sugar intake is controlled byintestinal fructokinase activity, metabolic syndrome is driven by fructose metabolismin the liver. Our findings show a two-pronged role for fructose metabolism in sugar-inducedmetabolic syndrome, one arm via the intestine that mediates sugar intake and a secondarm in the liver that drives metabolic dysfunction.