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科学家发现饥饿"开关"

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2016年03月05日

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无法抵御再来一块甜点的诱惑?德国科学家说,这或许不是因为你的意志力薄弱,而是饥饿“开关”失效之故。

科学家发现饥饿"开关"

It's long been known that two key hormones - ghrelin and leptin - play a key role in the body's appetite and weight management. Ghrelin tells you when you're hungry, while leptin is crucial for telling the brain when you've eaten enough.

研究早就发现,胃饥饿素和瘦素这两种激素对食欲和体重管理起着重要作用,胃饥饿素告诉你什么时候饿了,瘦素则在你吃饱时通知大脑可以停止进食。

For many years, scientists thought obesity could be caused by a shortage of leptin - thinking that without adequate levels, overweight people simply never received the message they had eaten enough.

多年来,科学家认为肥胖是因为人体缺少瘦素,使得大脑无法及时获知吃饱的信息,引起过度进食。

But more recent studies have shown that obese people have plenty of leptin (in fact, the fatter you are, the more of it you appear to have), but are more likely to be 'leptin-resistant'. This means the cells in the brain that should register leptin no longer 'read' the signals saying the body is full, but instead assume it is starving - no matter how much food is eaten.

但近来越来越多的研究显示,肥胖人群体内瘦素充足,而且比正常人更多,因此他们更可能是出现了“瘦素抵抗”,也就是说,无论进食了多少,大脑不再把瘦素当作吃饱的信号,反而认为是饥饿。

Now in a further breakthrough, scientists in Germany have discovered a 'switch' in the brain which regulates the effect of the hunger suppressant leptin. They have discovered an enzyme - histone deacetylase 5 (HDAC5) - has a significant influence on the effect of the hormone.

德国研究人员解开了这个谜。他们发现,大脑中有一个“开关”控制瘦素的作用,它就是一种名为组蛋白去乙酰化酶5(HDAC5)的酶。

In fact, those unable to produce the enzymes, were leptin resistant. Remarkably, activating the hormone reversed the effect - causing weight loss.

如果大脑无法产生这种酶,机体就会出现瘦素抵抗,反转瘦素的作用。


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