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腾讯登录Nature：营养不良相关的肠道炎症
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在贫困国家中超过十亿人正在挨饿，即使在富裕国家，营养不良仍然是一个重大问题，营养不良处于世界领先的死亡原因。一百年多年来，医生们已经知道饮食中缺乏蛋白质或低水平的氨基酸会导致如腹泻、肠道发炎和其他免疫系统疾病，这可能是致命的。
然而，营养不良导致如此严重的症状的分子机制至今不甚明了。现在，奥地利首都维也纳分子生物技术研究所（IMBA）与德国基... |
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在贫困国家中超过十亿人正在挨饿，即使在富裕国家，营养不良仍然是一个重大问题，营养不良处于世界领先的死亡原因。一百年多年来，医生们已经知道饮食中缺乏蛋白质或低水平的氨基酸会导致如腹泻、肠道发炎和其他免疫系统疾病，这可能是致命的。
然而，营养不良导致如此严重的症状的分子机制至今不甚明了。现在，奥地利首都维也纳分子生物技术研究所（IMBA）与德国基尔大学合作，Josef Penninger约瑟夫Penninger领导的一个研究小组发现了营养不良引发肠道炎症易感性增加的分子机制。
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研究人员正在研究一种酶，这种酶有助于控制血压、肾功能衰竭、糖尿病、心脏衰竭和肺损伤，被称为血管紧张素转换酶2或ACE2。ACE2通过氨基酸转运尤其是必需氨基酸色氨酸的吸收控制我们肠子摄取食物氨基酸的方式。
该项研究的第一作者Thomas Perlot表示：研究显示我们吃的食物可直接将我们肠子中的好细菌转变成坏细菌，从而影响我们的健康。研究结果也许可以解释几个世纪以来未知的有关营养不良和生活在我们肠道中细菌之间的分子联系。
这一发现可能有助于将来用一个简单的调节饮食的方法或补充色氨酸的食物治疗患者，而且这几乎没有任何风险。研究人员希望我们的研究结果有助更好的了解营养不良影响人体健康的分子机制。
编译自：<a title="" href="http://medicalxpress.com/news/2012-07-malnutrition-linked-inflammation-gut.html" target="_blank">Malnutrition-linked inflammation of the gut</a>
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<img src="http://www.bioon.com/biology/UploadFiles/201207/2012072720474172.jpg" alt="" width="115" height="150" border="0" />
<a title="" href="http://dx.doi.org/10.1038/nature11228" target="_blank">doi:10.1038/nature11228</a>
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<br/><strong>ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation</strong><br/>
Tatsuo Hashimoto,Thomas Perlot,Ateequr Rehman,Jean Trichereau,Hiroaki Ishiguro,Magdalena Paolino,et al.
Malnutrition affects up to one billion people in the world and is a major cause of mortality<sup>1, 2</sup>. In many cases, malnutrition is associated with diarrhoea and intestinal inflammation, further contributing to morbidity and death<sup>2</sup>. The mechanisms by which unbalanced dietary nutrients affect intestinal homeostasis are largely unknown. Here we report that deficiency in murine angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 (<em>Ace2</em>), which encodes a key regulatory enzyme of the renin-angiotensin system (RAS), results in highly increased susceptibility to intestinal inflammation induced by epithelial damage. The RAS is known to be involved in acute lung failure<sup>3</sup>, cardiovascular functions<sup>4</sup> and SARS infections<sup>5</sup>. Mechanistically, ACE2 has a RAS-independent function, regulating intestinal amino acid homeostasis, expression of antimicrobial peptides, and the ecology of the gut microbiome. Transplantation of the altered microbiota from <em>Ace2</em> mutant mice into germ-free wild-type hosts was able to transmit the increased propensity to develop severe colitis. ACE2-dependent changes in epithelial immunity and the gut microbiota can be directly regulated by the dietary amino acid tryptophan. Our results identify ACE2 as a key regulator of dietary amino acid homeostasis, innate immunity, gut microbial ecology, and transmissible susceptibility to colitis. These results provide a molecular explanation for how amino acid malnutrition can cause intestinal inflammation and diarrhoea.
<br/>来源：生物谷
<em>全球分子诊断网（</em><em><a href="http://www.360zhyx.com">www.zhenduan.org</a></em><em>）</em>
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在贫困国家中超过十亿人正在挨饿，即使在富裕国家，营养不良仍然是一个重大问题，营养不良处于世界领先的死亡原因。一百年多年来，医生们已经知道饮食中缺乏蛋白质或低水平的氨基酸会导致如腹泻、肠道发炎和其他免疫系统疾病，这可能是致命的。
然而，营养不良导致如此严重的症状的分子机制至今不甚明了。现在，奥地利首都维也纳分子生物技术研究所（IMBA）与德国基尔大学合作，Josef Penninger约瑟夫Penninger领导的一个研究小组发现了营养不良引发肠道炎症易感性增加的分子机制。
<!--more-->
研究人员正在研究一种酶，这种酶有助于控制血压、肾功能衰竭、糖尿病、心脏衰竭和肺损伤，被称为血管紧张素转换酶2或ACE2。ACE2通过氨基酸转运尤其是必需氨基酸色氨酸的吸收控制我们肠子摄取食物氨基酸的方式。
该项研究的第一作者Thomas Perlot表示：研究显示我们吃的食物可直接将我们肠子中的好细菌转变成坏细菌，从而影响我们的健康。研究结果也许可以解释几个世纪以来未知的有关营养不良和生活在我们肠道中细菌之间的分子联系。
这一发现可能有助于将来用一个简单的调节饮食的方法或补充色氨酸的食物治疗患者，而且这几乎没有任何风险。研究人员希望我们的研究结果有助更好的了解营养不良影响人体健康的分子机制。
编译自：<a title="" href="http://medicalxpress.com/news/2012-07-malnutrition-linked-inflammation-gut.html" target="_blank">Malnutrition-linked inflammation of the gut</a>
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201207/2012072720474172.jpg" alt="" width="115" height="150" border="0" />
<a title="" href="http://dx.doi.org/10.1038/nature11228" target="_blank">doi:10.1038/nature11228</a>
PMC:
PMID:
</div>
<div>
<br/><strong>ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation</strong><br/>
Tatsuo Hashimoto,Thomas Perlot,Ateequr Rehman,Jean Trichereau,Hiroaki Ishiguro,Magdalena Paolino,et al.
Malnutrition affects up to one billion people in the world and is a major cause of mortality<sup>1, 2</sup>. In many cases, malnutrition is associated with diarrhoea and intestinal inflammation, further contributing to morbidity and death<sup>2</sup>. The mechanisms by which unbalanced dietary nutrients affect intestinal homeostasis are largely unknown. Here we report that deficiency in murine angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 (<em>Ace2</em>), which encodes a key regulatory enzyme of the renin-angiotensin system (RAS), results in highly increased susceptibility to intestinal inflammation induced by epithelial damage. The RAS is known to be involved in acute lung failure<sup>3</sup>, cardiovascular functions<sup>4</sup> and SARS infections<sup>5</sup>. Mechanistically, ACE2 has a RAS-independent function, regulating intestinal amino acid homeostasis, expression of antimicrobial peptides, and the ecology of the gut microbiome. Transplantation of the altered microbiota from <em>Ace2</em> mutant mice into germ-free wild-type hosts was able to transmit the increased propensity to develop severe colitis. ACE2-dependent changes in epithelial immunity and the gut microbiota can be directly regulated by the dietary amino acid tryptophan. Our results identify ACE2 as a key regulator of dietary amino acid homeostasis, innate immunity, gut microbial ecology, and transmissible susceptibility to colitis. These results provide a molecular explanation for how amino acid malnutrition can cause intestinal inflammation and diarrhoea.
<br/>来源：生物谷
<em>全球分子诊断网（</em><em><a href="http://www.360zhyx.com">www.zhenduan.org</a></em><em>）</em>
<em></em>
</div>
</div>
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