Department of Endocrinology and Metabolism, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Chariteplatz 1, 10117, Berlin, Germany.
Berlin Institute of Health (BIH), Berlin, Germany.
Microbiome. 2022 Apr 4;10(1):57. doi: 10.1186/s40168-022-01249-4.
Caloric restriction can delay the development of metabolic diseases ranging from insulin resistance to type 2 diabetes and is linked to both changes in the composition and metabolic function of the gut microbiota and immunological consequences. However, the interaction between dietary intake, the microbiome, and the immune system remains poorly described.
We transplanted the gut microbiota from an obese female before (AdLib) and after (CalRes) an 8-week very-low-calorie diet (800 kcal/day) into germ-free mice. We used 16S rRNA sequencing to evaluate taxa with differential abundance between the AdLib- and CalRes-microbiota recipients and single-cell multidimensional mass cytometry to define immune signatures in murine colon, liver, and spleen. Recipients of the CalRes sample exhibited overall higher alpha diversity and restructuring of the gut microbiota with decreased abundance of several microbial taxa (e.g., Clostridium ramosum, Hungatella hathewayi, Alistipi obesi). Transplantation of CalRes-microbiota into mice decreased their body fat accumulation and improved glucose tolerance compared to AdLib-microbiota recipients. Finally, the CalRes-associated microbiota reduced the levels of intestinal effector memory CD8 T cells, intestinal memory B cells, and hepatic effector memory CD4 and CD8 T cells.
Caloric restriction shapes the gut microbiome which can improve metabolic health and may induce a shift towards the naïve T and B cell compartment and, thus, delay immune senescence. Understanding the role of the gut microbiome as mediator of beneficial effects of low calorie diets on inflammation and metabolism may enhance the development of new therapeutic treatment options for metabolic diseases.
NCT01105143 , "Effects of negative energy balance on muscle mass regulation," registered 16 April 2010. Video Abstract.
热量限制可以延缓从胰岛素抵抗到 2 型糖尿病等代谢疾病的发展，与肠道微生物组的组成和代谢功能以及免疫后果的变化有关。然而，饮食摄入、微生物组和免疫系统之间的相互作用仍描述不足。
我们将一位肥胖女性在进行为期 8 周的极低热量饮食（每天 800 卡路里）前后（AdLib 和 CalRes）的肠道微生物组移植到无菌小鼠中。我们使用 16S rRNA 测序来评估 AdLib-和 CalRes-微生物组接受者之间具有差异丰度的分类群，并使用单细胞多维质谱细胞术来定义鼠结肠、肝脏和脾脏中的免疫特征。CalRes 样本的接受者表现出总体上更高的α多样性和肠道微生物组的重构，几个微生物分类群的丰度降低（例如，Clostridium ramosum、Hungatella hathewayi、Alistipi obesi）。与 AdLib 微生物组接受者相比，CalRes 微生物组的移植降低了小鼠的体脂肪积累并改善了葡萄糖耐量。最后，CalRes 相关的微生物组降低了肠道效应记忆 CD8 T 细胞、肠道记忆 B 细胞和肝效应记忆 CD4 和 CD8 T 细胞的水平。
热量限制塑造了肠道微生物组，这可以改善代谢健康，并可能诱导向幼稚 T 和 B 细胞区室的转变，从而延缓免疫衰老。了解肠道微生物组作为低热量饮食对炎症和代谢有益影响的介导物的作用可能会增强代谢疾病新治疗方法的开发。
NCT01105143，“负能平衡对肌肉质量调节的影响”，于 2010 年 4 月 16 日注册。视频摘要。
