Department of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University, Weifang, 261031, China.
Clinical Research Center, Affiliated Hospital of Shandong Second Medical University, Weifang, 261031, China.
Lipids Health Dis. 2024 Jun 29;23(1):207. doi: 10.1186/s12944-024-02198-7.
Ketogenic diets are increasingly popular for addressing obesity, but their impacts on the gut microbiota and metabolome remain unclear. This paper aimed to investigate how a ketogenic diet affects intestinal microorganisms and metabolites in obesity.
Male mice were provided with one of the following dietary regimens: normal chow, high-fat diet, ketogenic diet, or high-fat diet converted to ketogenic diet. Body weight and fat mass were measured weekly using high-precision electronic balances and minispec body composition analyzers. Metagenomics and non-targeted metabolomics data were used to analyze differences in intestinal contents.
Obese mice on the ketogenic diet exhibited notable improvements in weight and body fat. However, these were accompanied by a significant decrease in intestinal microbial diversity, as well as an increase in Firmicutes abundance and a 247% increase in the Firmicutes/Bacteroidetes ratio. The ketogenic diet also altered multiple metabolic pathways in the gut, including glucose, lipid, energy, carbohydrate, amino acid, ketone body, butanoate, and methane pathways, as well as bacterial secretion and colonization pathways. These changes were associated with increased intestinal inflammation and dysbiosis in obese mice. Furthermore, the ketogenic diet enhanced the secretion of bile and the synthesis of aminoglycoside antibiotics in obese mice, which may impair the gut microbiota and be associated with intestinal inflammation and immunity.
The study suggest that the ketogenic diet had an unfavorable risk-benefit trade-off and may compromise metabolic homeostasis in obese mice.
生酮饮食在解决肥胖问题上越来越受欢迎，但它们对肠道微生物群和代谢组的影响仍不清楚。本文旨在研究生酮饮食如何影响肥胖症患者的肠道微生物和代谢物。
雄性小鼠接受以下饮食方案之一：正常饲料、高脂肪饮食、生酮饮食或高脂肪饮食转换为生酮饮食。每周使用高精度电子天平和 minispec 身体成分分析仪测量体重和体脂肪量。使用宏基因组学和非靶向代谢组学数据来分析肠道内容物的差异。
接受生酮饮食的肥胖小鼠体重和体脂肪显著改善。然而，这伴随着肠道微生物多样性显著降低，厚壁菌门丰度增加，厚壁菌门/拟杆菌门比值增加 247%。生酮饮食还改变了肠道中的多个代谢途径，包括葡萄糖、脂质、能量、碳水化合物、氨基酸、酮体、丁酸盐和甲烷途径，以及细菌分泌和定植途径。这些变化与肥胖小鼠的肠道炎症和失调有关。此外，生酮饮食增强了肥胖小鼠胆汁的分泌和氨基糖苷类抗生素的合成，这可能损害肠道微生物群，并与肠道炎症和免疫有关。
该研究表明，生酮饮食存在不利的风险-效益权衡，可能会损害肥胖小鼠的代谢稳态。
