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【Diabetes】瘢痕组织形成是肥胖与糖尿病联系的关键

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Scarring Is Key To Link Between Obesity And Diabetes, Study Finds

http://www.sciencedaily.com/releases/2009/08/090813142349.htm

ScienceDaily (Aug. 13, 2009) — Scientists at the University of Liverpool have found that a protein that can cause scarring of fat tissue could be key to understanding the link between obesity and type 2 diabetes.

The team, in collaboration with University Hospital Aintree, the University of Warwick and researchers in Sweden, found that people classified as obese and those with pre-diabetes have raised levels of a protein called SPARC, that can cause tissue scarring. The research revealed that an increase in insulin, a hormone that controls blood sugar levels, and leptin, a hormone that regulates appetite, can trigger an increase in SPARC, which can prevent the proper storage of fat in fat tissue cells.

It is thought that leptin, in an attempt to balance energy levels in the body, could trigger SPARC to limit the storage of fat. SPARC can do this by increasing the formation of scars in fat tissue, which can prevent fat being stored safely in the body. Researchers found that this process could predispose obese patients to type 2 diabetes.

Professor John Wilding, from the University's School of Clinical Science, explains: "We tested fat tissue of patients at University Hospital Aintree and found that an increase in leptin also increases SPARC levels, which reduces the safe storage of fat through the development of abnormal tissue scarring. Scarring of fat tissue is known to increase as we gain weight and we found that this is exacerbated by leptin, as well as an increase in insulin, produced by the pancreas."

Dr Katarina Kos, lead author of the research, added: "Leptin is produced in fat cells to regulate appetite, but the body becomes resistant to the effects of appetite reduction in obese patients. Leptin continues to increase in response to overall fat mass and promotes scarring through increased SPARC levels. Once scarring occurs, the excess nutritional energy from fat cannot be taken up by fat cells and so remains in the blood and begins to gather around organs. As a result, fat cells of people classified as obese, may not fulfil their natural purpose to store fat."

Diabetes is caused by the cells' inability to respond to insulin, which would normally enable uptake of sugar from the blood. To compensate, the pancreas creates more insulin to clear blood sugar from the circulation. The pancreas becomes exhausted and is unable to produce sufficient insulin to keep up with the demands of the body. This results in the development of type 2 diabetes, which can cause problems such as lack of energy to the cells and, over time, damage to the eyes, kidneys and heart.

The research team, working with the Swedish fast food study group at Linkoping University, also found that weight gain, induced by more than doubling calorie intake through eating 'junk food', causes SPARC levels to increase by 33%. In a further study with the University of Gothenburg, scientists found that a reduced calorie diet can decrease SPARC levels and the stimulus for tissue scarring.

Researchers are now investigating why some people are more prone to fat tissue scarring than others and how further understanding of SPARC could contribute to future treatments for diabetes.

The research is published in the journal Diabetes.

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2009-08-15 17:01 浏览 : 766 回复 : 2

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小顾营养编辑于 2009-08-15 17:06

• 广东省人民医院一胸外科80后医生猝死

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本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。

2009-08-15 19:51

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• 医院试工害怕被「白嫖」怎么办？究竟去还是不去？

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Scarring Is Key To Link Between Obesity And Diabetes, Study Finds
瘢痕组织形成是肥胖与糖尿病联系的关键
http://www.sciencedaily.com/releases/2009/08/090813142349.htm

ScienceDaily (Aug. 13, 2009) — Scientists at the University of Liverpool have found that a protein that can cause scarring of fat tissue could be key to understanding the link between obesity and type 2 diabetes.
每日科学（2009年8月13日）利物浦大学的科学家发现一种可导致脂肪组织疤痕的蛋白质可能是了解肥胖及2型糖尿病之间联系的关键。

The team, in collaboration with University Hospital Aintree, the University of Warwick and researchers in Sweden, found that people classified as obese and those with pre-diabetes have raised levels of a protein called SPARC, that can cause tissue scarring. The research revealed that an increase in insulin, a hormone that controls blood sugar levels, and leptin, a hormone that regulates appetite, can trigger an increase in SPARC, which can prevent the proper storage of fat in fat tissue cells.
在与安特里大学医院团队合作的瑞典华威大学和研究人员发现，列为肥胖及有糖尿病前期水平的人群中，有一种可造成组织疤痕称作SPARC蛋白的含量增高。研究表明胰岛素水平的增加可以触发SPARC的增加，这将阻止脂肪在脂肪组织细胞中的适当贮存。胰岛素是一种控制血糖水平和瘦素、调节食欲的激素。

It is thought that leptin, in an attempt to balance energy levels in the body, could trigger SPARC to limit the storage of fat. SPARC can do this by increasing the formation of scars in fat tissue, which can prevent fat being stored safely in the body. Researchers found that this process could predispose obese patients to type 2 diabetes.
瘦素被认为试图平衡体内的能量水平，这可能会引发SPARC限制储存脂肪。 SPARC可以通过脂肪组织中增加瘢痕做到这一点，这样便可以阻止脂肪稳固的储存在体内。研究人员发现这一过程可能使肥胖患者易患2型糖尿病。

Professor John Wilding, from the University's School of Clinical Science, explains: "We tested fat tissue of patients at University Hospital Aintree and found that an increase in leptin also increases SPARC levels, which reduces the safe storage of fat through the development of abnormal tissue scarring. Scarring of fat tissue is known to increase as we gain weight and we found that this is exacerbated by leptin, as well as an increase in insulin, produced by the pancreas."
该大学临床医学院的威尔丁教授解释说： “我们测试了在安特里大学医院病人的脂肪组织发现，瘦素的增加SPARC水平也随之增加，从而降低了脂肪通过发展异常疤痕组织的稳固储存。脂肪组织的结疤是因为我们体重的增加，我们发现这是因为瘦素剧增，以及胰腺产生胰岛素的增加。
Dr Katarina Kos, lead author of the research, added: "Leptin is produced in fat cells to regulate appetite, but the body becomes resistant to the effects of appetite reduction in obese patients. Leptin continues to increase in response to overall fat mass and promotes scarring through increased SPARC levels. Once scarring occurs, the excess nutritional energy from fat cannot be taken up by fat cells and so remains in the blood and begins to gather around organs. As a result, fat cells of people classified as obese, may not fulfil their natural purpose to store fat."
研究的主要作者科斯卡塔琳博士补充说： “瘦素是脂肪细胞产生用来调节食欲的，但肥胖患者的身体抵抗这种减少食欲的作用。通过增加SPARC的水平使整体脂肪聚集和促进脂肪结疤，针对此反应，瘦素继续增加。一旦疤痕发生时，来自脂肪细胞不能吸收的多余营养能量仍然残留在血液中并开始会聚到周围器官中。结果肥胖者的脂肪细胞可能不会履行其让脂肪储存的目的。

Diabetes is caused by the cells' inability to respond to insulin, which would normally enable uptake of sugar from the blood. To compensate, the pancreas creates more insulin to clear blood sugar from the circulation. The pancreas becomes exhausted and is unable to produce sufficient insulin to keep up with the demands of the body. This results in the development of type 2 diabetes, which can cause problems such as lack of energy to the cells and, over time, damage to the eyes, kidneys and heart.
糖尿病是因为细胞不能对胰岛素产生反应，胰岛素可以使身体正常地从血液摄取糖。为了弥补这种缺陷，胰腺产生更多的胰岛素用来清除循环中的血糖。终于胰腺变得枯竭，无法产生跟上身体所需足够多的胰岛素。这样的发展结果是成为2型糖尿病患者，这可能会导致例如细胞缺乏能源的问题，并随着时间的推移损害眼睛、肾脏和心脏。

The research team, working with the Swedish fast food study group at Linkoping University, also found that weight gain, induced by more than doubling calorie intake through eating 'junk food', causes SPARC levels to increase by 33%. In a further study with the University of Gothenburg, scientists found that a reduced calorie diet can decrease SPARC levels and the stimulus for tissue scarring.
在林雪平大学与瑞典快餐研究组工作的科研小组还发现，通过食用'垃圾食品' 摄取了一倍多热量引起了体重增加，导致SPARC的水平增加了33 ％。在进一步与哥德堡大学的研究中科学家发现减少饮食热量可以降低SPARC的水平和对疤痕组织的刺激。

Researchers are now investigating why some people are more prone to fat tissue scarring than others and how further understanding of SPARC could contribute to future treatments for diabetes.

研究人员目前正在调查为什么有些人比其他人更容易产生脂肪组织疤痕以及如何进一步了解SPARC从而有助于未来糖尿病治疗。

The research is published in the journal Diabetes.
这项研究发表在糖尿病杂志上。

编译
瘢痕组织形成是肥胖与糖尿病联系的关键

每日科学（2009年8月13日）利物浦大学的科学家发现一种可导致脂肪组织疤痕的蛋白质可能是了解肥胖及2型糖尿病之间联系的关键。

在与安特里大学医院团队合作的瑞典华威大学和研究人员发现，列为肥胖及有糖尿病前期水平的人群中，有一种可造成组织疤痕称作SPARC蛋白的含量增高。研究表明胰岛素水平的增加可以触发SPARC的增加，这将阻止脂肪在脂肪组织细胞中的适当贮存。胰岛素是一种控制血糖水平和瘦素、调节食欲的激素。

瘦素被认为试图平衡体内的能量水平，这可能会引发SPARC限制储存脂肪。 SPARC可以通过脂肪组织中增加瘢痕做到这一点，这样便可以阻止脂肪稳固的储存在体内。研究人员发现这一过程可能使肥胖患者易患2型糖尿病。

该大学临床医学院的威尔丁教授解释说： “我们测试了在安特里大学医院病人的脂肪组织发现，瘦素的增加SPARC水平也随之增加，从而降低了脂肪通过发展异常疤痕组织的稳固储存。脂肪组织的结疤是因为我们体重的增加，我们发现这是因为瘦素剧增，以及胰腺产生胰岛素的增加。”

研究的主要作者科斯卡塔琳博士补充说：“瘦素是脂肪细胞产生用来调节食欲的，但肥胖患者的身体抵抗这种减少食欲的作用。通过增加SPARC的水平使整体脂肪聚集和促进脂肪结疤，针对此反应，瘦素继续增加。一旦疤痕发生时，来自脂肪细胞不能吸收的多余营养能量仍然残留在血液中并开始会聚到周围器官中。结果肥胖者的脂肪细胞可能不会履行其让脂肪储存的目的。”

糖尿病是因为细胞不能对胰岛素产生反应，胰岛素可以使身体正常地从血液摄取糖。为了弥补这种缺陷，胰腺产生更多的胰岛素用来清除循环中的血糖。终于胰腺变得枯竭，无法产生跟上身体所需足够多的胰岛素。这样的发展结果是成为2型糖尿病患者，这可能会导致例如细胞缺乏能源的问题，并随着时间的推移损害眼睛、肾脏和心脏。

在林雪平大学与瑞典快餐研究组工作的科研小组还发现，通过食用'垃圾食品' 摄取了一倍多热量引起了体重增加，导致SPARC的水平增加了33 ％。在进一步与哥德堡大学的研究中科学家发现减少饮食热量可以降低SPARC的水平和对疤痕组织的刺激。

研究人员目前正在调查为什么有些人比其他人更容易产生脂肪组织疤痕以及如何进一步了解SPARC从而有助于未来糖尿病治疗。

这项研究发表在糖尿病杂志上。（丁香）

2009-08-15 21:35

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mRNA 编辑于 2009-08-15 21:39

• 教育部：今年国家定向培养免费医学生，你会报考吗？——回帖

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