生酮饮食以不同于高脂饮食的方式改变肠道菌群。
生酮饮食中肠道微生物的变化一部分是受酮体宿主生成而驱动。
β-羟基丁酸酯能选择性抑制双歧杆菌生长。
生酮饮食相关的肠道菌群降低了肠道Th17细胞水平。
极低碳水化合物、高脂肪的生酮饮食会引起代谢能源利用率的显着变化，从而加速酮体循环。然而，这些化合物对宿主-微生物相互作用的影响尚不明确。本研究中，美国加州大学旧金山分校（UCSF）的Qi Yan Ang、Margaret Alexander和Peter J. Turnbaugh*等人表明生酮饮食会以不同于高脂饮食的方式改变人和小鼠的肠道菌群。
一项为期8 周的住院病人粪便样本的宏基因组和代谢组学分析显示，生酮饮食期间肠道微生物群落结构和功能发生了明显变化。对小鼠进行的梯度饮食实验证实了生酮饮食相对于高脂饮食的独特影响在于双歧杆菌出现重复性消耗。体外和体内实验表明，酮体可选择性抑制双歧杆菌的生长。
最后，将单菌落和人类微生物组移植到无菌小鼠中发现，与生酮饮食相关的肠道菌群降低了肠道促炎Th17细胞的水平。总之，这些结果强调了不同物种（宿主-微生物）间的化学对话在宿主对饮食干预反应中的重要性。
Abstract
Ketogenic Diets Alter the Gut Microbiome Resulting in Decreased Intestinal Th17 Cells
Qi Yan Ang, Margaret Alexander, John C. Newman, Michael Rosenbaum, Andrew D. Patterson, Peter J. Turnbaugh*
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA
Very low-carbohydrate, high-fat ketogenic diets (KDs) induce a pronounced shift in metabolic fuel utilization that elevates circulating ketone bodies; however, the consequences of these compounds for host-microbiome interactions remain unknown. Here, we show that KDs alter the human and mouse gut microbiota in a manner distinct from high-fat diets (HFDs). metagenomic and metabolomic analyses of stool samples from an 8-week inpatient study revealed marked shifts in gut microbial community structure and function during the KD. Gradient diet experiments in mice confirmed the unique impact of KDs relative to HFDs with a reproducible depletion of bifidobacteria. In vitro and in vivo experiments showed that ketone bodies selectively inhibited bifidobacterial growth. Finally, mono-colonizations and human microbiome transplantations into germ-free mice revealed that the KD-associated gut microbiota reduces the levels of intestinal pro-inflammatory Th17 cells. Together, these results highlight the importance of trans-kingdom chemical dialogs for mediating the host response to dietary interventions.
