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【资讯翻译】为什么内脏脂肪比皮下脂肪更糟糕
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【认 领 须 知】1、认领翻译的战友请跟帖注明“认领本文翻译，48小时内未完成，请其他战友认领！”2、请根据自己专业背 景选择认领，如使用翻译软件翻译，被发现者扣分1-2分3、经常认领而不能及时提供优质稿件者将被列入黑名单，取消认领资格，请大家注意！4、翻译时请参照版规： 点击查看5、在首位认领战友未超过规定时间的其他任何认领属违规认领，将不会给予丁当或加分！6、翻译完成后加分（或丁当）的时限为三日，请耐心等待，若超过时限未加者可进行申诉：点击进入7、本文题目仅供译者参考，篇幅较长者可申请适当延时8、翻译前请查一下有无重复帖9、为保证翻译质量，每人每天最多只能认领两篇原文链接： Why Is Visceral Fat Worse Than Subcutaneous Fat?Researchers have long-known that visceral fat – the kind that wraps around the internal organs – is more dangerous than subcutaneous fat that lies just under the skin around the belly, thighs and rear. But how visceral fat contributes to insulin resistance and inflammation has remained unknown.A study led by researchers at the University of Illinois at Chicago points blame at a regulatory molecule in cells called TRIP-Br2 that is produced in response to overeating’s stress on the machinery cells use to produce proteins.The findings are published in the journal Nature Communications.All body fat is not created equal in terms of associated health risks. Visceral fat is strongly linked to metabolic disease and insulin resistance, and an increased risk of death, even for people who have a normal body mass index. Subcutaneous fat doesn’t carry the same risks — some subcutaneous fat may even be protective.In previous studies, Chong Wee Liew, assistant professor of physiology and biophysics in the UIC College of Medicine, and his colleagues found that in obese humans TRIP-Br2 was turned-up in visceral fat but not in subcutaneous fat. When the researchers knocked out TRIP-Br2 in mice and fed them a high-calorie, high-fat diet that would make the average rodent pack on the grams, the knockout mice stayed relatively lean and free from insulin resistance and inflammation.“TRIP-Br2 appears to block or prevent normal lipolysis,” Liew explained. Lipolysis is the breakdown of fat in fat cells, for use as fuel, and ongoing lipolysis can prevent the buildup of excess fat in those cells, Liew said.“Without TRIP-Br2, lipolysis and oxidative metabolism take place at an increased rate, so fat is broken down and quickly used as energy and does not have a chance to build up in organs like the liver,” he said.But Liew and his colleagues still didn’t know why TRIP-Br2 was found in higher amounts in visceral fat than in subcutaneous fat.Their search for answers led them to a cellular structure called the endoplasmic reticulum, or ER, which is responsible for producing all the proteins in the cell. Nutrients from a meal enter the ER, but an excess due to overeating can significantly stress it. In obesity, a stressed ER in visceral fat cells leads to production of inflammatory molecules called cytokines — but exactly how was unclear.Liew and coworkers found that in the absence of TRIP-Br2, ER stress could no longer trigger cytokine production and inflammation in obesity. They also found that the up-regulation of TRIP-Br2 in visceral fat depends on an intermediary factor called GATA 3 that turns on TRIP-Br2.“Together, our findings indicate that these molecular regulators, TRIP-Br2 and GATA3, could be viable targets for small drug molecules that could serve as potential therapeutic agents against obesity,” Liew said.
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初译：Why Is Visceral Fat Worse Than Subcutaneous Fat?为什么内脏脂肪比皮下脂肪更糟糕？Researchers have long-known that visceral fat – the kind that wraps around the internal organs – is more dangerous than subcutaneous fat that lies just under the skin around the belly, thighs and rear. But how visceral fat contributes to insulin resistance and inflammation has remained unknown.科研人员早已知道内脏脂肪（围绕着内脏器官的脂肪）比皮下脂肪（腹部、大腿、臀部周围皮肤以下的脂肪）更危险，但内脏脂肪如何促成胰岛素抵抗和炎症仍不得而知。A study led by researchers at the University of Illinois at Chicago points blame at a regulatory molecule in cells called TRIP-Br2 that is produced in response to overeating’s stress on the machinery cells use to produce proteins.一项由芝加哥伊利诺大学的科研人员主导的研究指出，这归咎于细胞内一种叫做TRIP-Br2的调控分子，这一分子是在与过度饱食压力的应答过程中，在用于制造蛋白质的机械细胞上产生。The findings are published in the journal Nature Communications.该发现发表于《自然通讯》杂志上。All body fat is not created equal in terms of associated health risks. Visceral fat is strongly linked to metabolic disease and insulin resistance, and an increased risk of death, even for people who have a normal body mass index. Subcutaneous fat doesn’t carry the same risks — some subcutaneous fat may even be protective.并不是所有体脂对健康都有相同的危害性。内脏脂肪与代谢性疾病、胰岛素抵抗以及死亡风险的增高有着紧密的联系，即使是身体质量指数正常的人。皮下脂肪不会带来同样的风险，某些皮下脂肪甚至可能具有保护作用。In previous studies, Chong Wee Liew, assistant professor of physiology and biophysics in the UIC College of Medicine, and his colleagues found that in obese humans TRIP-Br2 was turned-up in visceral fat but not in subcutaneous fat. When the researchers knocked out TRIP-Br2 in mice and fed them a high-calorie, high-fat diet that would make the average rodent pack on the grams, the knockout mice stayed relatively lean and free from insulin resistance and inflammation.在前期的研究中，芝加哥伊利诺大学医学院生理学和生物物理学助理教授Chong Wee Liew和他的同事发现，在肥胖人群中，内脏脂肪中发现了TRIP-Br2，而皮下脂肪中没有。当研究者敲除小鼠的TRIP-Br2基因，并给予它们会使得普通啮齿动物体重增加的高卡路里高脂肪饮食，结果发现基因敲除小鼠保持相对瘦小，而且没有发生胰岛素抵抗和炎症。“TRIP-Br2 appears to block or prevent normal lipolysis,” Liew explained. Lipolysis is the breakdown of fat in fat cells, for use as fuel, and ongoing lipolysis can prevent the buildup of excess fat in those cells, Liew said.Liew解释道：“TRIP-Br2似乎能阻止或预防正常脂解作用。“Liew说，脂解即脂肪在脂肪细胞中的分解，供细胞作燃料用，持续的脂解可防止过量脂肪在这些细胞中的积累。“Without TRIP-Br2, lipolysis and oxidative metabolism take place at an increased rate, so fat is broken down and quickly used as energy and does not have a chance to build up in organs like the liver,” he said.他说：“在没有TRIP-Br2的情况下，脂解和氧化代谢以越来越快的速度进行，所以脂肪被分解并很快用作能量，而没有机会在类似肝脏的器官中累积。”But Liew and his colleagues still didn’t know why TRIP-Br2 was found in higher amounts in visceral fat than in subcutaneous fat.但是Liew和他的同事仍然不知道为什么在内脏脂肪中比皮下脂肪中发现更大量的TRIP-Br2。Their search for answers led them to a cellular structure called the endoplasmic reticulum, or ER, which is responsible for producing all the proteins in the cell. Nutrients from a meal enter the ER, but an excess due to overeating can significantly stress it. In obesity, a stressed ER in visceral fat cells leads to production of inflammatory molecules called cytokines — but exactly how was unclear.为寻求答案他们关注到一个叫做内质网（Endoplasmic Reticulum ，ER）的细胞结构，主要负责为细胞制造所有的蛋白质。饮食中的营养素进入内质网，但是因过度饱食摄入的多余营养素会显著的对它施加压力。在肥胖人群中，内脏脂肪细胞中因内质网压力导致产生叫做细胞因子的炎性分子，但是具体机制不明。Liew and coworkers found that in the absence of TRIP-Br2, ER stress could no longer trigger cytokine production and inflammation in obesity. They also found that the up-regulation of TRIP-Br2 in visceral fat depends on an intermediary factor called GATA 3 that turns on TRIP-Br2.Liew和同事发现不存在TRIP-Br2时，内质网压力不再触发细胞因子的产生和肥胖人群的炎症，他们还发现内脏脂肪中TRIP-Br2的上调依赖于一种叫做GATA 3的中介物质，这一物质可触发TRIP-Br2的产生。“Together, our findings indicate that these molecular regulators, TRIP-Br2 and GATA3, could be viable targets for small drug molecules that could serve as potential therapeutic agents against obesity,” Liew said.Liew说：“综上所述，我们的发现表明这些调节分子（TRIP-Br2和GATA3），可作为潜在能够治疗肥胖的小分子药物的可行靶点。”
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编译：为什么内脏脂肪比皮下脂肪更糟糕？科研人员早已知道内脏脂肪（围绕着内脏器官的脂肪）比皮下脂肪（腹部、大腿、臀部周围皮肤以下的脂肪）更危险，但内脏脂肪如何促成胰岛素抵抗和炎症仍不得而知。一项由芝加哥伊利诺大学的科研人员主导的研究指出，这归咎于细胞内一种叫做TRIP-Br2的调控分子，这一分子是在与过度饱食压力的应答过程中，在用于制造蛋白质的机械细胞上产生。该发现发表于《自然通讯》杂志上。并不是所有体脂对健康都有相同的危害性。内脏脂肪与代谢性疾病、胰岛素抵抗以及死亡风险的增高有着紧密的联系，即使是身体质量指数正常的人。皮下脂肪不会带来同样的风险，某些皮下脂肪甚至可能具有保护作用。在前期的研究中，芝加哥伊利诺大学医学院生理学和生物物理学助理教授Chong Wee Liew和他的同事发现，在肥胖人群中，内脏脂肪中发现了TRIP-Br2，而皮下脂肪中没有。当研究者敲除小鼠的TRIP-Br2基因，并给予它们会使得普通啮齿动物体重增加的高卡路里高脂肪饮食，结果发现基因敲除小鼠保持相对瘦小，而且没有发生胰岛素抵抗和炎症。Liew解释道：“TRIP-Br2似乎能阻止或预防正常脂解作用。“Liew说，脂解即脂肪在脂肪细胞中的分解，供细胞作燃料用，持续的脂解可防止过量脂肪在这些细胞中的积累。他说：“在没有TRIP-Br2的情况下，脂解和氧化代谢以越来越快的速度进行，所以脂肪被分解并很快用作能量，而没有机会在类似肝脏的器官中累积。”但是Liew和他的同事仍然不知道为什么在内脏脂肪中比皮下脂肪中发现更大量的TRIP-Br2。为寻求答案他们关注到一个叫做内质网（Endoplasmic Reticulum ，ER）的细胞结构，主要负责为细胞制造所有的蛋白质。饮食中的营养素进入内质网，但是因过度饱食摄入的多余营养素会显著的对它施加压力。在肥胖人群中，内脏脂肪细胞中因内质网压力导致产生叫做细胞因子的炎性分子，但是具体机制不明。Liew和同事发现不存在TRIP-Br2时，内质网压力不再触发细胞因子的产生和肥胖人群的炎症，他们还发现内脏脂肪中TRIP-Br2的上调依赖于一种叫做GATA 3的中介物质，这一物质可触发TRIP-Br2的产生。Liew说：“综上所述，我们的发现表明这些调节分子（TRIP-Br2和GATA3），可作为潜在能够治疗肥胖的小分子药物的可行靶点。”（字数统计：856字）
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关于丁香园是否能够降低内脏脂肪而保持皮下脂肪？如果... | 问答 | 问答 | 果壳网 科技有意思
是否能够降低内脏脂肪而保持皮下脂肪？如果可以需要怎么做？
肥胖对身体的危害主要来自于超标的内脏脂肪皮下脂肪的分布则主要取决于基因（有人胳膊肥、有人腿肥）我面部的皮下脂肪特别少，一瘦下去就很难看，但是胖起来肚子就会大（内脏脂肪增多）是否能够降低内脏脂肪而保持皮下脂肪？如果可以需要怎么做？
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脂肪分解是先分解内脏再分解皮下吗？还是先皮下后内脏？还是同时？
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应该是同时分解的
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发布于： 12:44阅读量：419
长期以来，研究人员知道内脏脂肪（内脏周围包裹的脂肪）比皮下脂肪（位于腹部、大腿或背部）更加危险。但内脏脂肪如何导致胰岛素抵抗和炎症仍然未知。&芝加哥伊利诺斯州立大学的研究人员将焦点放在一种细胞内调节分子TRIP-Br2上，它是影响脂肪储存和代谢的重要因子。&本次的研究结果发表在《自然通讯》期刊上。&身体脂肪的存在会对健康造成不同程度的风险。内脏脂肪通常与代谢性疾病和胰岛素抵抗的发生相关，以及可能造成死亡率的上升，这对于BMI（身高体重指数）正常的人来说亦是如此。而皮下脂肪就没有这些风险，甚至一定程度上还具有保护作用。&之前的研究中，芝加哥伊利诺州立大学的生理学助教Chong Wee Liew和他的同事们发现，肥胖人内脏脂肪中TRIP-Br2含量升高，但是在皮下脂肪中却没有这种趋势。当研究者对小鼠敲除TRIP-Br2基因并喂食高脂食物后发现，这些小鼠体重并未增加，胰岛素抵抗和炎症情况也没有恶化。&Liew说道，“TRIP-Br2似乎能够阻止或妨碍正常的脂类分解。正常的脂类分解能够防止细胞内过量的脂肪堆积。敲除TRIP-Br2后，脂类氧化和代谢速率大增，并迅速转换为能量，内脏脂肪含量减少。”&但是Liew和他的同事们并没有弄清楚为何TRIP-Br2在内脏脂肪中含量高于皮下脂肪。&他们的研究结果导致他们关注到内质网的细胞结构，这是一种负责产生细胞内蛋白质的场所。饮食后的营养物质流入内质网，但是暴饮暴食可以使内质网产生应激反应。在肥胖者中，受到应激的内脏脂肪内质网导致炎症因子分泌的增加，但是具体机制仍然有待探索。&Liew和他的同事们发现，缺失TRIP-Br2后，内质网应激不能够再促使炎症因子的增加。他们发现内脏脂肪中TRIP-Br2的上调依靠一种称为GATA3的中间物质的作用。&Liew说道，“总之，我们的发现预示着TRIP-Br2和GATA3可能成为治疗肥胖的关键靶点。”
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1楼皮下脂肪还可以通过锻炼减去，内脏脂肪.....[0]
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