Eat More，Weigh Less，Live Longer Clever genetic detective work may have found out the reason why a ne

Eat More，Weigh Less，Live Longer Clever genetic detective work may have found out the reason why a near。starvation diet prolongs the life of many animals. Ronald Kahn at Harvard Medical School in Boston，US，and his colleagues have been able to extend the lifespan(寿命)of mice by 18 per cent by blocking the rodent’s(啮齿动物) increase of fat in specific cells.This suggests that thinness--and hot necessarily diet—-promotes long life in “ calerie (热量卡) restricted” animals. “It’s very cool work.”says aging researcher Cynthia Kenyon of the University of California，San Francisco.“These mice eat all they want，lose weight and live longer.It’s like heaven.” Calorie restriction dramatically extends the lifespan of organisms as different as worms and rodents.Whether this works in humans is still unknown，partly because few people are willing to submit to such a strict diet. But many researchers hope they will be able to trigger the same effect with a drug once they understand how less food leads to a longer life.One theory is that eating less reduces the increase of harmful things that can damage cells.But Kahn’s team wondered whether the animals simply benefit by becoming thin. To find out。they used biology tricks to disrupt the insulin(胰岛素)receptor(受体)gene in lab mice—_but only in their fat cells.“Since insulin is needed to help fat cells store fat，these animals were protected against becoming fat，”explains Kahn. This slight genetic change in a single tissue had dramatic effects.By three months of age，Kahn，s modified mice had up to 70 per cent less body fat than normal control mice，despite the fact that they ate 55per cent more food per gram of body weight. In addition，their lifespan increased.The average control mouse lived 753 days，while the thin rodents averaged a lifespan of 887 days.After three years，all the control mice had died，but one--quarter of the modified rodents were still alive. “That they get these effects by just manipulating t11e fat cells is controversial，”says Leonard Guarente of the Massachusetts Institute of Technology, who studies calorie restriction and aging. But Guarente says Kahn has yet to prove that the same effect is responsible for increased lifespan in calorie.restricted animals.“It might be the same effect or there might be two routes to long life，”he points out，“and that would be very interesting.” 第11题：Ronald Kahn and his colleagues can make mice live longer byA. Ronald B.This C. “It’s D.”says E.“These F.It’s G.” Calorie H.Whether I. But J.One K.But L. To M.“Since N. This O.By P. In Q.The R.After S. “That T. But U.restricted V.“It W.” 第11题：Ronald X.offering Y. B．giving Z. C．disrupting [. D．preventing

Ronald Kahn和他的团队通过特定基因改造让小鼠活得更久。他们采用生物手段，仅在小鼠脂肪细胞中干扰胰岛素受体基因，阻止脂肪细胞储存脂肪，使小鼠保持瘦削并延长寿命。答案为C．disrupting。

这一精准的基因操作极具创新性。通常认为限制热量摄入是延长寿命的关键，但该研究表明，仅改变脂肪细胞的基因就能产生类似效果。实验中小鼠食量增加55%，体脂却减少70%，寿命延长18%，颠覆了“少吃才能长寿”的传统认知。

这种方法与单纯节食有本质区别。节食需长期限制热量，难以坚持；而基因改造能在不改变饮食习惯的前提下，通过调节脂肪存储延长寿命。这为开发延长寿命的药物提供了新思路——或许无需严格控制饮食，只需靶向调节脂肪细胞功能。

该发现也引发争议。部分研究者质疑其是否与热量限制延长寿命的机制相同。若存在两条独立的长寿路径，将为衰老研究开辟新方向。未来还需验证该机制是否适用于人类，以及能否通过药物安全模拟这种基因效应。