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首页> 外文期刊>Cell metabolism >Deletion of Fructokinase in the Liver or in the Intestine Reveals Differential Effects on Sugar-Induced Metabolic Dysfunction
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Deletion of Fructokinase in the Liver or in the Intestine Reveals Differential Effects on Sugar-Induced Metabolic Dysfunction

机译：肝脏缺失肝脏或肠道揭示对糖诱导的代谢功能障碍的差异影响

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摘要

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-body deletion of fructokinase, and thus full blockade of fructose metabolism, is sufficient to prevent metabolic syndrome. This protection is not only due to reduced fructose metabolism, but also due to decreased sugar intake. Furthermore, by using tissue-specific fructokinase-deficient mice, we determined that while sugar intake is controlled by intestinal fructokinase activity, metabolic syndrome is driven by fructose metabolism in the liver. Our findings show a two-pronged role for fructose metabolism in sugar-induced metabolic syndrome, one arm via the intestine that mediates sugar intake and a second arm in the liver that drives metabolic dysfunction.
机译：摄入含果糖的糖与代谢综合征强烈相关。与其他糖相比，膳食果糖由Fructokinase唯一地代谢。然而，Fruceopasease在糖诱导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它的特定作用，尚不完全理解。在这里，我们表明，在接受过量的果糖 - 葡萄糖溶液的小鼠中，果实酶的全身缺失，因此完全阻断果糖新陈代谢足以防止代谢综合征。这种保护不仅是由于果糖新陈代谢降低，而且由于糖摄入量降低。此外，通过使用组织特异性的果糖酶缺陷小鼠，我们确定虽然含糖摄入量由肠果胰蛋白酶活性控制，但代谢综合征被肝脏在肝脏中的果糖代谢驱动。我们的研究结果表明，糖诱导代谢综合征的果糖新陈代谢的两时间作用，一只臂通过肠道介导糖摄入和肝脏中的第二臂，驱动代谢功能障碍。

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