A low-carbohydrate ketogenic diet induces the expression of very-low-density lipoprotein receptor in liver and affects its associated metabolic abnormalities.,npj Science of Food

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A low-carbohydrate ketogenic diet induces the expression of very-low-density lipoprotein receptor in liver and affects its associated metabolic abnormalities.
npj Science of Food ( IF 6.3 ) Pub Date : 2019-12-02 , DOI: 10.1038/s41538-019-0058-4
Tetsuya Okuda ₁

Affiliation

A low-carbohydrate ketogenic diet (LCKD) promotes the progression of hepatic steatosis in C57BL/6 wild-type mice, but improves the condition in leptin-deficient obese (ob/ob) mice. Here, we show a novel effect of LCKD associated with the conflicting effects on these mice. Gene expression microarray analyses showed that expression of the Vldlr gene, which encodes the very-low-density lipoprotein receptor (VLDLR), was induced in LCKD-fed ob/ob mice. Although the VLDLR is not normally expressed in the liver, the LCKD led to VLDLR expression in both ob/ob and wild-type mice. To clarify this effect on VLDL dynamics, we analyzed the lipid content of serum lipoproteins and found a marked decrease in VLDL-triglycerides only in LCKD-fed wild-type mice. Further analyses suggested that transport of triglycerides via VLDL from the liver to extrahepatic tissues was inhibited by LCKD-induced hepatic VLDLR expression, but rescued under conditions of leptin deficiency.

中文翻译：

低碳水化合物生酮饮食会诱导肝脏中极低密度脂蛋白受体的表达，并影响其相关的代谢异常。

低碳水化合物生酮饮食（LCKD）可以促进C57BL / 6野生型小鼠肝脂肪变性的进展，但可以改善瘦素缺乏型肥胖（ob / ob）小鼠的状况。在这里，我们显示了LCKD的新颖作用与对这些小鼠的冲突作用有关。基因表达微阵列分析表明，在LCKD喂养的ob / ob小鼠中诱导了编码极低密度脂蛋白受体（VLDLR）的Vldlr基因的表达。尽管VLDLR在肝脏中通常不表达，但LCKD在ob / ob和野生型小鼠中均导致VLDLR表达。为了阐明这种对VLDL动力学的影响，我们分析了血清脂蛋白的脂质含量，发现仅在LCKD喂养的野生型小鼠中VLDL-甘油三酯显着降低。

更新日期：2019-12-02

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