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科学家发现缺乏酶Scd-1可能增进新陈代谢
http://www.100md.com 2002年7月12日 医业网
     【医业网据路透社2002年7月11日纽约讯】新研究结论表明,酶SCD-1可能是加速或减慢新陈代谢的开关。缺乏该酶的小鼠倾向于瘦削,即使是吃得很多。详见近期的《自然》杂志(Science 2002;297:240-243)。

    本研究可帮助科学家研制肥胖的治疗方法,作者之一、美国威斯康辛大学的生化兼营养学教授兰比(James M. Ntambi)告诉路透社记者,机体SCD-1的数量似乎可以由勒帕茄碱调节,至少可调节部分。随着该激素的增多,SCD-1减少。

    勒帕茄碱由脂肪细胞释放,脂肪细胞越多,该物质分泌越多。正常情况下,当大脑感受到较多勒帕茄碱时,它就认为机体脂肪储存量安全,就发出信号抑制食欲。此外,勒帕茄碱也能调节新陈代谢,但原因不明。1994年,研究者发现了该激素,认为可用它来治疗肥胖。但当他们试着给超重者更多勒帕茄碱想借此抑制食欲减少体重时,实验失败了。“许多胖人体内的勒帕茄碱水平都很高”,另一位作者、纽约洛克菲勒大学赫华德休斯医学院的弗瑞德曼(Jeffrey M. Friedman)说,“出于某些我们不太明白的原因,勒帕茄碱对他们效果不好”。他们推测SCD-1能跳过勒帕茄碱重新指出一条道路。
, http://www.100md.com
    在新研究中,科学家们对只缺乏勒帕茄碱和同时缺乏勒帕茄碱及SCD-1的小鼠进行了比较,发现没有或有很少勒帕茄碱的小鼠有发胖倾向。而缺乏SCD-1的小鼠比正常者更瘦,于是研究者检查是否这种小鼠吃得不多,但令人吃惊的是,它们实际上吃得更多。很明显,机体要贮存脂肪需要SCD-1。没有该酶,多数脂肪被燃烧了。但同时该酶又是维持健康的皮肤和皮毛所必须的。完全缺乏该酶的小鼠有掉毛的倾向。这样,科学家需要寻找只是减少该酶生成而不是完全停掉的方法。

    Scientists May Have Found Way to Boost Metabolism

    Thu Jul 11, 5:55 PM ET

    By Linda Carroll

    NEW YORK (Reuters Health) - An enzyme called SCD-1 may act as a switch to turn metabolism up or down, new study findings suggest.
, 百拇医药
    Researchers found that mice that were missing the enzyme tended to stay thin, even if they overate, according to the report published in Science.

    The research may help scientists devise treatments for obesity, study co-author Dr. James M. Ntambi, a professor of biochemistry and nutritional sciences at the University of Wisconsin, Madison, said in an interview with Reuters Health.

    The amount of SCD-1 in an animal's body appears to be regulated, at least in part, by the hormone leptin, Ntambe said. When levels of leptin increase, levels of SCD-1 decrease.
, 百拇医药
    Leptin is released by fat cells. And the larger fat cells get, the more leptin they release. Normally, when the brain gets a surge of leptin, it concludes that the body has a safe store of fat and it sends out a message to dampen appetite. The hormone also appears to regulate metabolism, but until now, nobody knew how.

    In 1994, when researchers discovered leptin, they thought they might have come up with a cure for obesity. But when scientists tried giving overweight people more leptin to see if it would kill appetite and cause weight loss, the experiments were a dismal failure.
, 百拇医药
    "Most obese people already have high levels of leptin," study co-author Dr. Jeffrey M. Friedman, an investigator with the Howard Hughes Medical Institute at The Rockefeller University in New York City, said in an interview with Reuters Health. "For reasons we don't completely understand, leptin doesn't seem to work well enough for them."

    But Friedman and his colleagues suspect that SCD-1 may give obesity researchers a way to skip past leptin and turn up metabolism, allowing people to lose weight.
, 百拇医药
    In the new study, researchers compared mice that were deficient in leptin to mice that were deficient in both leptin and SCD-1. Mice with no or low levels of leptin tend to be obese.

    The first thing the scientists noticed was that the SCD-1-deficient mice were thinner than those with normal levels of the enzyme. When they checked to see whether the SCD-1-deficient mice were eating less, there was a surprise. These mice, though thinner than their counterparts, were actually consuming more food.
, 百拇医药
    Apparently, the body needs SCD-1 in order to store fat. Without the enzyme, most fat is burned instead of being stashed away.

    There is a catch, however. The enzyme is necessary for maintenance of healthy hair and skin. Mice that were completely deficient in SCD-1 tended to lose their hair, Ntambe said.

    So scientists would need to design a therapy that only cut back production of SCD-1, instead of completely knocking it out, he added.

    SOURCE: Science 2002;297:240-243., 百拇医药