吃8个星期高脂肪饮食也不见胖!这究竟是如何做到的?
2017/12/11
在人类中,饮食中脂肪过多是导致肥胖的常见原因。但在最近发表的一项的研究中,吃8个星期高脂肪饮食的小鼠体重却能不增加。这究竟是如何做到的呢?


图片来源:网络

12月5日,发表在eLife杂志上的这项研究中,来自美国华盛顿大学的研究人员鉴定出了一种防止脂肪细胞变得更大(这一过程导致了体重增加和肥胖)的方法。通过激活小鼠脂肪细胞中的一个通路,研究人员发现,即便给小鼠喂以高脂肪饮食,也不会使小鼠变得肥胖。

具体来说,这一研究调查的是Hedgehog蛋白质通路。该通路在机体很多组织中都很活跃。研究中,科学家们改造了在小鼠吃高脂肪饮食时会激活脂肪细胞中Hedgehog通路的基因。

研究结果显示,在吃了8个星期的高脂肪饮食后,Hedgehog通路没有被激活的对照组小鼠变得肥胖了,而经基因改造激活了Hedgehog通路的小鼠并没有比“吃正常饮食的对照组小鼠”获得更多的体重。


Washington University researchers activated the Hedgehog protein pathway in the fat cells of mice. After eight weeks of eating a high-fat diet, mice that had been engineered with genes to activate the pathway didn't gain weight (left), but control animals whose Hedgehog pathways were not activated became obese (right).Credit: Washington University School of Medicine

论文的通讯作者Fanxin Long教授解释道:“我们体重增加主要是由于脂肪细胞变得更大,而不是拥有更多的脂肪细胞。Hedgehog通路通过抑制脂肪细胞的大小阻止了肥胖。更重要的是,当我们进行代谢研究,我们发现,拥有激活Hedgehog通路的小鼠不仅更瘦,而且具有更低的血糖水平,且对胰岛素更敏感。”

Long教授表示,将这一研究成果转化到人类中是比较困难的。任何激活Hedgehog通路的药物都需要被仔细研究,以避免潜在的副作用。在人类中,一些癌症与太强的Hedgehog活性有关。不过,由于Hedgehog通路被认为在人类和小鼠中以相似的途径工作,因此,靶向脂肪组织中的Hedgehog通路可能会成为治疗肥胖的一种方法。

参考资料:

Obesity prevented in mice fed high-fat diet

Hedgehog signaling via Gli2 prevents obesity induced by high-fat diet in adult mice

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  • Hedgehog signaling via Gli2 prevents obesity induced by high-fat diet in adult mice

    Obesity poses a significant risk of developing type II diabetes and other diseases. Hedgehog (Hh) signaling has been shown to inhibit adipose tissue development, but its effect on diet-induced obesity during postnatal life is not known. Here by inducing expression of constitutively active Smoothened (SmoM2) or Gli2 (ΔNGli2) in the adipocyte lineage of postnatal mice, we show that targeted activation of Hh signaling suppresses high-fat-diet-induced obesity and improves whole-body glucose tolerance and insulin sensitivity. Both SmoM2 and ΔNGli2 induce the expression of Wnt6, a known anti-adipogenic factor, in fat depots of the mouse. Hh-Gli2 signaling inhibits not only adipocyte differentiation but also lipogenesis in adipocytes in vitro. Finally, pharmacological inhibition of Porcupine, an acyltransferase essential for Wnt secretion, alleviates both anti-adipogenic and anti-lipogenic effects of Hh in cell culture models. Overall, targeted activation of Hh signaling ameliorates diet-induced obesity and may be explored for pharmaceutical development.

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