High leptin levels relay the opposite signal.
高消瘦素水平传递相反的信号。
Leptin ACTS like a natural appetite suppressant.
瘦素就好像是一种天然的“食欲抑制剂”。
And mice without leptin are sluggish balls of blubber.
没有瘦素小鼠简直就是又懒又肥的绒毛球。
Because of the mutation, the mice could not make functional leptin.
由于这一突变，老鼠不能生产功能性瘦素。
The gene produced a protein called leptin that is made in fat cells.
这种制造瘦素的基因存在于老鼠细胞中。
They then added the leptin receptor to one small group of brain cells.
因为缺乏受体，原先瘦蛋白对小白鼠不起作用，科学家们就给其中一小组小白鼠的丘脑细胞中添加了瘦蛋白受体。
Leptin is a hormone made by fat cells that tells you when you're full.
脂肪细胞为了告诉你已经吃饱了，会产生一种激素——瘦素。
Those neurons get their message from hormones, including insulin and leptin.
这些神经元通过激素得到信息，这些激素包括胰岛素和瘦素。
The researchers dubbed the new hormone leptin, afterleptos, which is Greek for thin.
研究人员复制了这种新的激素——瘦素（leptin），延用了希腊语中表示瘦的词“leptos”。
Leptin decides whether fat should be stored or used, resulting in lethargy or energy.
瘦素决定身体要储存或者消耗脂肪，困倦无力还是精神抖擞。
The less sleep you get, the lower your leptin levels-and the higher your ghrelin.
你睡得越少，你的致轻素越少——同时生长素升高。
Too much ghrelin and too little leptin have been shown to result in a larger appetite.
太多的生长素，和太少的瘦素已被证明导致更大的胃口。
Obese people have been found to have an abnormally high level of leptin in their bloodstream.
胖人的血液中的瘦素含量异常的高。
The virus also increases lipid sensitivity and decreases leptin secretion of the new fat cells.
该病毒还会增加新脂肪细胞的脂肪灵敏度，并降低其瘦素分泌。
"Our study is the first success in sensitizing obese mice on a high-fat diet to leptin," he said.
“我们的研究是第一次成功地通过高脂肪膳食使肥胖小鼠的瘦素敏化。”他结着说。
The scientists then traced the leptin decline to a pathway that originates in the brain's hypothalamus.
随后，科学家跟踪瘦素下降原因，找到通路的源头——大脑下丘脑部。
Does obesity disrupt the action of leptin, or does a malfunction in leptin signaling make people obese?
是肥胖扰乱了瘦素的作用，还是瘦素信号失常导致人们变得肥胖？
Lack of sleep causes more ghrelin and less leptin to be produced; therefore increased appetite overall.
Leptin分泌越少，食欲越强。睡眠不足会导致Ghrelin分泌增多和Leptin分泌减少，因此会增强食欲。
When treated with leptin, their appetites decreased and metabolism increased, causing them to lose weight.
当瘦素执行功能时，老鼠食欲减退，代谢加强，导致体重减少。
The hypothalamus is the primary brain region that responds to leptin, sending a signal that curbs appetite.
下丘脑是对瘦素起反应的最主要的大脑区域，通过传递信号来抑制食欲。
To find out, scientists took mice that don’t respond to leptin because they lack the receptor to which it binds.
为了研究清楚，科学家们用一群缺乏瘦蛋白受体的小白鼠进行了实验。
Because humans also produce leptin, researchers hoped giving the hormone to obese people would result in weight loss.
因为人类同样制造瘦素，研究者希望这一激素能减少肥胖人群的体重。
Maas blames two hormones: leptin, which helps the brain sense when you're full, and ghrelin, which triggers hunger.
Maas将其归咎于两种激素：致轻素——帮助大脑意识到你已经饱了；生长素——诱发饥饿感。
Researchers soon found that in addition to leptin, a whole host of chemicals signal the brain to trigger hunger or fullness.
研究者很快发现，除了瘦素之外，还有一整套的化学物质给大脑发送信号，引发饥饿和饱腹的感觉。
If you skimp on sleep, ghrelin levels rise, making you hungry, and leptin levels dip, which signals a need for calories.
如果你克扣了睡眠时间，胃促生长素水平升高，使你饥饿，并且消瘦素下降，标志着需求热量。
Researchers originally thought leptin signaled the body to stop eating and hoped that it might be harnessed as a weight-loss drug.
研究人员最初认为，瘦素能向人体发出停止进食的信号，并希望将其用作减肥药。
Leptin, a hormone produced by fat cells, decreases appetite and boosts metabolism: low leptin levels can lead to an increased appetite.
Leptin由脂肪细胞分泌，能够抑制食欲同时增强新陈代谢的水平。
When they were given replacement leptin, those changes were reversed and brain activity returned to what it had been before they lost weight.
当研究对象摄入瘦素替代品后，这类变化就被逆转，脑部活动重新回到减肥之前的状态。
They are resistant to the effects of leptin in much the same way that people with type 2 diabetes are resistant to the effects of insulin.
但是他们的身体却对瘦素有极大的抗性，就如同第二型糖尿病患者抵抗胰岛素的作用一样。
They are resistant to the effects of leptin in much the same way that people with type 2 diabetes are resistant to the effects of insulin.
但是他们的身体却对瘦素有极大的抗性，就如同第二型糖尿病患者抵抗胰岛素的作用一样。
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