上海交大学者找到细菌引起人体肥胖的直接证据 Shanghai jiaotong university scholars found direct evidence of human obesity caused by bacteria

　　上海交通大学教授赵立平领导的实验室12月13日在国际微生物生态学会会刊ISME Journal上发表论文，用一种来自肥胖病人的肠道细菌，在无菌小鼠内引起了严重的肥胖和胰岛素抵抗，为肠道菌群参与人体肥胖、糖尿病发生、发展的“慢性病的肠源性学说”提供了最直接的实验证据。

The leadership of the Shanghai jiaotong university professor ZhaoLiPing laboratory on December 13 in the international society of microbial ecology catalogue ISME: published papers,With a gut bacteria from the obese patients,In sterile in mice caused serious obesity and insulin resistance,For intestinal flora in the human body fat/Diabetes occurs/The development of"Chronic diseases of enterogenic doctrine"Provides the most direct experimental evidence.

　　赵立平教授的实验室在临床研究中发现，有一种可以产生内毒素的条件致病菌，在一个体重达175千克的肥胖患者肠道里过度生长，占到总菌量的三分之一之多。经过一种特殊设计的营养配方干预以后，这种病菌数量很快下降到检测不出来的水平，患者的体重在将近半年里下降了51.4千克，高血糖、高血压和高血脂等症状也恢复正常。赵教授的博士生费娜把这个细菌分离出来，接种到无菌小鼠体内，造成了严重的肥胖症和糖尿病的早期症状——胰岛素抵抗。

ZhaoLiPing the professor's laboratory found in clinical research,There is a kind of conditional pathogenic bacteria can produce endotoxin,At a weight of 175 kg of excessive growth in obese patients with intestinal,Account for more than a third of the total amount of bacteria.After a special design of nutrition formula after the intervention,The number of bacteria quickly dropped to the level of test not to come out,The patient's weight in the half-year dropped by 51.4 kg,High blood sugar/Symptoms such as high blood pressure and high cholesterol is back to normal.Zhao's doctoral FeiNa to separate the bacteria,Vaccination to sterile mice,Has caused severe obesity and the early symptoms of diabetes, insulin resistance.

　　人体肠道里生活着大约1000种细菌，统称为肠道菌群，其总重量大约有1.5千克，其细胞总数量是人体自身细胞总数的10倍，其编码的基因总数量是人体基因总数的100倍。如此庞大的肠道菌群如何影响人体的健康，自1908年的诺贝尔奖获得者梅契尼可夫提出，肠道菌群产生的毒素是人体衰老和得病的主要原因以来，一直是微生物学家关注的问题。

There are about 1000 types of bacteria living in human intestinal tract,Collectively referred to as intestinal flora,The total weight is about 1.5 kg,The total number of cells is 10 times of the total number of cells of human body oneself,The total number of genes encoding is 100 times of the total number of genes in the human body.So huge intestinal flora how to affect the health of human body,Since 1908 the Nobel Prize winner mei qi, to put forward,Intestinal flora of toxin is the main cause of human aging and disease,Microbiologist has always been a concern.

　　2004年，美国华盛顿大学教授戈登领导的实验室，首次报道肠道菌群可以调节小鼠的脂肪代谢，降低消耗脂肪的基因活动，升高合成脂肪的基因活性，令动物过度合成和积累脂肪。他们还发现，肠道菌群是动物肥胖发生的必需条件，因为无菌动物即使吃高脂饲料，也不会肥胖的。

In 2004,,Gordon, a professor at the university of Washington under the leadership of the laboratory,Reported for the first time can be adjusted the fat metabolism of mice intestinal flora,Reduce fat consumption of gene activity,Increased synthesis of fat gene actiity,Animals over the synthesis and accumulation of fat.They also found that,Intestinal flora is the necessary condition of animal fat,Because of the sterile animals even eat high-fat feed,Also won't fat.

　　2007年，比利时天主教卢文大学教授喀尼与其合作者发现，高脂饲料喂成的肥胖小鼠的血液内，病菌产生的内毒素比正常小鼠高2～3倍，而且全身有低度的炎症。他们把提纯的内毒素以同样的低剂量直接皮下注射给吃普通饲料、本来不会胖的小鼠，结果这些小鼠出现全身性的低度炎症，变得肥胖，而且有了胰岛素抵抗，表明肠道病原细菌产生的内毒素如果进入血液，可以引起小鼠肥胖和胰岛素抵抗。但是，对于能调控动物脂肪代谢的基因表达、产生内毒素引起肥胖和炎症的细菌到底是哪些种类，国际上一直没有能“验明正身”。

In 2007,,Belgian Catholic LuWen cascade, a professor at the university and its partners,High-fat fed into fat in the blood of mice,Produced by the bacteria endotoxin 2 ~ 3 times higher than normal mice,And there are low-grade inflammation of the body.Their purification of endotoxin in the same low dose subcutaneously directly to eating the forage of ordinary/Wouldn't fat mice,Results of these mice appeared systemic low-grade inflammation,To become fat,And have insulin resistance,Indicates that the intestinal pathogenic bacteria endotoxin if into the blood,Can cause obesity and insulin resistance in mice.but,To regulate gene expression of animal fat metabolism/Produce endotoxin the bacteria that cause obesity and inflammation what sort it is,Never can in the world"Of a".

　　2004年以来，包括赵教授实验室在内的多个研究组都观察到高脂饲料喂胖的小鼠的肠道里病菌增加，有益菌减少。华大基因近日在自然杂志发表论文，发现条件致病菌的增加和丁酸盐产生菌的减少是糖尿病人菌群的主要特征。但是，由于这些结果都是用相关分析的方法获得，学术界对于人体肠道菌群结构变化是肥胖、糖尿病的原因还是结果，一直存在争议。

Since 2004,Multiple groups, including zhao laboratory are observed high-fat fed fat mice bacteria in the intestine of increase,Beneficial bacterium reduce.Huada gene recently published in the journal nature,Found that the increase of the pathogens and the decrease of butyric acid salt producing strains are the main characteristic of people with diabetes flora.but,Due to these results are obtained with the method of correlation analysis,For human intestinal flora structure change is obese/The cause of diabetes or results,Has been controversial.

　　赵教授实验室找到的这种病菌可以产生内毒素，能够让本来吃高脂饲料吃不胖的无菌小鼠发展出严重的肥胖症，同时能够引起小鼠炎症和胰岛素抵抗，也可以关闭消耗脂肪需要的基因、激活合成脂肪的基因，是国际上一直在寻找的能引起肥胖的细菌。

Zhao lab to find this kind of bacteria can produce endotoxin,Can let it eat high-fat feed to eat not fat of sterile mice developed severe obesity,At the same time can cause inflammation and insulin resistance in mice,Fat consumption can also close the needs of the gene/Activation of synthetic fat gene,Is the world have been looking for the bacteria can cause obesity.

　　赵教授实验室在做这项研究时，遵循了证明某种细菌是引起传染病病因的“科赫法则”的要求，先在人体内发现某种细菌与肥胖相关，然后把这种细菌分离出来，让动物发展出肥胖症，从而证明这种细菌是该病人肥胖的原因而不是结果。这项工作为分离鉴定更多的参与人体肥胖和糖尿病的细菌提供了新的思路和技术方法，沿着这个方向深入下去，可以阐明肠道菌群如何与饮食互作，引起肥胖和糖尿病的机制，有望发展出以肠道菌群为靶点，预防和治疗肥胖、糖尿病的新方法。(记者 周凯)

Professor zhao when doing the research in the laboratory,Follows the prove some bacteria is a cause of infectious diseases"Koch law"The requirements of the,First some bacteria found in the human body is associated with obesity,And then to separate the bacteria,Let the animals to develop obesity,To prove that bacteria are the patient rather than the cause of obesity.This work for more participation of human obesity and diabetes were isolated bacteria provides a new train of thought and method,Further along the way,How can clarify intestinal flora and diet interactions,Cause the mechanism of obesity and diabetes,Is expected to develop target in intestinal flora,Prevention and treatment of obesity/New methods of diabetes.(The reporter chu-kai)