肥胖有损大脑,运动修复智力

Obesity may have harmful effects on the brain, and exercise may counteract many of those negative effects, according to sophisticated new neurological experiments with mice, even when the animals do not lose much weight. While it's impossible to know if human brains respond in precisely the same way to fat and physical activity, the findings offer one more reason to get out and exercise.
科学家们最近在小鼠身上进行了一项复杂的新型神经生物学实验，其结果显示，肥胖会对大脑造成有害影响，而运动可以抵消上述负面影响中的绝大部分，即使在动物的体重并未大幅减轻时也一样有效。虽然我们不可能知道人类大脑是否会以完全相同的方式来应答脂肪和体育活动，但起码这些研究结果为我们走出户外进行运动又提供了一条新的理由。

It's been known for some time that obesity can alter cognition in animals. Past experiments with lab rodents, for instance, have shown that obese animals display poor memory and learning skills compared to their normal-weight peers. They don't recognize familiar objects or recall the location of the exit in mazes that they've negotiated multiple times.
一段时间之前，人们已经发现肥胖可以改变动物的认知。例如，关于实验室啮齿类动物的既往实验表明，肥胖动物的记忆力和学习能力均低于体重正常的同类动物。它们无法辨认出熟悉的物体，而且哪怕已经多次从迷宫中走过，它们仍然记不住出口的位置。

But scientists hadn't understood how excess weight affects the brain. Fat cells, they knew, manufacture and release substances into the bloodstream that flow to other parts of the body, including the heart and muscles. There, these substances jump-start biochemical processes that produce severe inflammation and other conditions that can lead to poor health.
但是，科学家们一直没有弄明白体重超重是如何影响大脑的。据他们所知，脂肪细胞可以制造出某些物质并将其释放入血液。这些物质随着血流来到身体的其他部位，包括心脏和肌肉等，然后在那里迅速启动一系列的生化过程，造成严重的炎症和其他疾病，导致健康状况恶化。

Many thought the brain, though, should be insulated from those harmful effects. It contains no fat cells and sits behind the protective blood-brain barrier that usually blocks the entry of undesirable molecules.
不过人们一直以为大脑应该可以从上述有害影响中幸免于难。因为大脑本身并不包含脂肪细胞，且它安居于血-脑屏障的保护之后，这道屏障通常足以将危险分子阻挡于大脑之外。

However, recent disquieting studies in animals indicate that obesity weakens that barrier, leaving it leaky and permeable. In obese animals, substances released by fat cells can ooze past the barrier and into the brain.
然而，近期的动物研究结果却十分令人不安。这些研究表明，肥胖可削弱血-脑屏障，使它变得具有泄漏性和渗透性。在肥胖动物中，脂肪细胞释放的物质可以突破血-脑屏障，进入大脑。

The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. For the studies, the scientists gathered mice bred to overeat and grow obese, which, after a few weeks of sitting quietly in their cages and eating at will, the animals had obligingly accomplished. As they grew rotund and accumulated more fat cells, the researchers found, their blood showed increasingly hefty doses of a substance called interleukin 1 that is created by fat cells and known to cause inflammation.
乔治亚瑞金斯大学（Georgia Regents University，位于美国奥古斯塔）的研究人员以这种渗漏造成的后果为对象进行了一系列新颖的神经生物学实验，并将其发表于上个月的《神经科学杂志》(The Journal of Neuroscience)上。出于研究需要，科学家们首先搜集了一些容易过食和肥胖的小鼠。这些小鼠可以好几周都安静地坐在笼子里，随心所欲地吃啊吃。等它们长得圆嘟嘟的，并积累了较多的脂肪细胞后，它们差不多就合格了。研究人员对它们进行了检查，并发现在它们的血液中有一种名为白细胞介素1(interleukin 1)的物质浓度日益增加，这种物质由脂肪细胞产生，且目前已知它会引起炎症。

In these mice, as interleukin 1 migrated to the head, it passed the blood-brain barrier and entered areas such as the hippocampus, a part of the brain critical for learning and memory. There, it essentially gummed up the works, the researchers found when they examined tissue from the animals' brains, which had high levels of interleukin 1 together with widespread markers of inflammation. While inflammation can represent a healthy response to invading molecules, it hurts cells if it persists.
当白细胞介素1随着血液来到这些小鼠的头部后，就穿过血脑屏障进入了海马（与学习和记忆有关的关键部位）等脑区，并把这些组织的正常工作搞得一团糟。在检查过这些动物的大脑组织后，研究人员发现其中存在着高水平的白细胞介素1，炎症标志物也有广泛分布。虽说炎症是身体对入侵分子的一种健康反应，但它如果持续不断，就会对细胞造成伤害。

The researchers also noted extremely low levels in these mice brains of a biochemical associated with healthy synapse function. Synapses are the structures that connect one neuron to another and shunt messages between them. Healthy synapses respond to demands on the brain by slowing or speeding messages, keeping the brain's nervous-system traffic manageable. But low levels of the marker of synapse health suggested to the researchers that in these obese animals' inflamed brains, synapses were no longer functioning properly and messages between neurons likely jerked, hiccuped or stalled.
研究人员还指出，在这些小鼠的大脑中，与健康的突触功能相关的生化标志物水平非常低。突触是指连接一个神经元与另一个神经元，并在它们之间传递信息的结构。健康的突触可应大脑的要求做出相应的反应，减慢或加快信息的传递，从而保持大脑的神经系统交通始终处于井然有序的管理之下。肥胖动物发炎的大脑中突触健康的标志物水平偏低，这提示研究人员它们脑中突触的运作已经失常，神经元间的信息传递也不再顺畅，甚至有可能出现停滞。

That possibility was borne out by subsequent tests on the memory and thinking of some of the remaining obese mice. They performed miserably.
这种可能性很快就在后续的实验中得到了证实：研究人员对其余的肥胖小鼠进行了记忆和思维测试，它们的表现惨不忍睹。