科學家發(fā)現饑餓"開關"

無法抵御再來一塊甜點的誘惑？德國科學家說，這或許不是因為你的意志力薄弱，而是饑餓“開關”失效之故。

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.
研究早就發(fā)現，胃饑餓素和瘦素這兩種激素對食欲和體重管理起著重要作用，胃饑餓素告訴你什么時候餓了，瘦素則在你吃飽時通知大腦可以停止進食。

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.
多年來，科學家認為肥胖是因為人體缺少瘦素，使得大腦無法及時獲知吃飽的信息，引起過度進食。

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.
但近來越來越多的研究顯示，肥胖人群體內瘦素充足，而且比正常人更多，因此他們更可能是出現了“瘦素抵抗”，也就是說，無論進食了多少，大腦不再把瘦素當作吃飽的信號，反而認為是饑餓。

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.
德國研究人員解開了這個謎。他們發(fā)現，大腦中有一個“開關”控制瘦素的作用，它就是一種名為組蛋白去乙酰化酶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.
如果大腦無法產生這種酶，機體就會出現瘦素抵抗，反轉瘦素的作用。

（中國日報網英語點津 yaning）