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Gut Microbiota, Intestinal Permeability, Obesity-Induced Inflammation, and Liver Injury

机译:肠道菌群,肠道通透性,肥胖引起的炎症和肝损伤

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摘要

Obesity and its metabolic complications are major health problems in the United States and worldwide, and increasing evidence implicates the microbiota in these important health issues. Indeed, it appears that the microbiota function much like a metabolic "organ," influencing nutrient acquisition, energy homeostasis, and, ultimately, the control of body weight. Moreover, alterations in gut microbiota, increased intestinal permeability, and metabolic endotoxemia likely play a role in the development of a chronic low-grade inflammatory state in the host that contributes to the development of obesity and associated chronic metabolic diseases such as nonalcoholic fatty liver disease. Supporting these concepts are the observations that increased gut permeability, low-grade endotoxemia, and fatty liver are observed in animal models of obesity caused by either high-fat or high-fructose feeding. Consistent with these observations, germ-free mice are protected from obesity and many forms of liver injury. Last, many agents that affect gut flora/ permeability, such as probiotics/prebiotics, also appear to affect obesity and certain forms of liver injury in animal model systems. Here the authors review the role of the gut microbiota and metabolic endotoxemia-induced inflammation in the development of obesity and liver injury, with special reference to the intensive care unit setting.
机译:肥胖及其代谢并发症是美国和世界范围内的主要健康问题,越来越多的证据表明微生物群与这些重要的健康问题有关。实际上,似乎微生物群的功能很像新陈代谢的“器官”,它影响营养的获取,能量的动态平衡,并最终影响体重的控制。此外,肠道菌群的变化,肠道通透性的增加和代谢性内毒素血症可能在宿主中慢性低度炎症状态的发展中起作用,从而导致肥胖症和相关慢性代谢性疾病的发展,例如非酒精性脂肪肝。支持这些概念的是在高脂或高果糖喂养引起的肥胖动物模型中观察到的肠道通透性增加,低度内毒素血症和脂肪肝的观察结果。与这些观察结果一致,无菌小鼠免受肥胖和多种形式的肝损伤的保护。最后,许多影响肠道菌群/通透性的药物,例如益生菌/益生元,也似乎在动物模型系统中影响肥胖和某些形式的肝损伤。在这里,作者回顾了肠道菌群和代谢性内毒素血症引起的炎症在肥胖和肝损伤发展中的作用,并特别提到了重症监护病房的设置。

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