Division of Basic & Translational Research, Department of Surgery, University of Minnesota, Minneapolis, MN, United States.
Biotechnology Institute, University of Minnesota, Saint Paul, MN, United States.
Front Cell Infect Microbiol. 2021 Feb 22;11:614218. doi: 10.3389/fcimb.2021.614218. eCollection 2021.
Human microbiota-associated (HMA) mouse models offer a valuable approach to study the role of intestinal microbiota in the development of obesity. In this study, we used an HMA model to evaluate whether engraftment of human obese or lean microbiota, from each of three donors, could recapitulate host phenotypes under conventional and specific-pathogen-free housing. Microbiota engraftment was correlated with donor relative abundances of the class Bacteroidia (Spearman's = 0.73, ≤ 0.001), and one obese donor resulted in significant weight gain ( ≤ 0.003) and compromised insulin sensitivity under conventional housing. SPF housing partially blunted phenotypic response. Results of this study indicate that our HMA model partially recapitulates obese phenotypes under conventional housing and highlights a need to consider donor-specific effects as well as housing conditions when studying the role of the microbiota in obesity.
人肠道微生物相关（HMA）小鼠模型为研究肠道微生物在肥胖发生中的作用提供了一种有价值的方法。在这项研究中，我们使用 HMA 模型来评估来自三个供体的肥胖或瘦人肠道微生物的定植是否可以在常规和特定病原体自由饲养下重现宿主表型。微生物定植与供体厚壁菌门的相对丰度呈正相关（Spearman's = 0.73， ≤ 0.001），一个肥胖供体在常规饲养下导致体重显著增加（ ≤ 0.003）和胰岛素敏感性受损。SPF 饲养部分削弱了表型反应。本研究结果表明，我们的 HMA 模型在常规饲养下部分重现了肥胖表型，并强调在研究微生物在肥胖中的作用时，需要考虑供体特异性效应以及饲养条件。
