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肝脏与肠道中的果糖激酶在代谢失调中发挥不同功能
作者:小柯机器人 发布时间:2020/6/5 16:35:57

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》。

研究人员表明,在接受过量果糖与葡萄糖溶液的小鼠中,果糖激酶的全身性缺失能够完全阻断果糖代谢,从而预防代谢综合征。这种保护不仅是由于果糖代谢减少,而且还因为糖摄入减少。此外,通过使用组织特异性果糖激酶缺陷型的小鼠,研究人员发现,虽然糖摄入量受肠道果糖激酶活性控制,但代谢综合征却由肝脏中的果糖代谢驱动。
 
因此,这些研究结果表明,果糖代谢在糖引起的代谢综合征中起两方面的作用,一方面通过肠道来介导糖的摄入,另一方面通过肝脏引起代谢功能障碍。
 
据了解,含果糖的糖类摄入与代谢综合征密切相关。与其他糖相比,饮食中的果糖只由果糖激酶所代谢。然而,果糖激酶在糖引起的代谢综合征中的组织特异性作用,以及葡萄糖和果糖在驱动糖代谢综合征中的特定作用尚未得到充分了解。
 
附:英文原文

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

Issue&Volume: 2020-06-04

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.

DOI: 10.1016/j.cmet.2020.05.012

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30251-5

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:22.415
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx