State Key Laboratory of Microbial Metabolism, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
Front Endocrinol (Lausanne). 2024 Sep 27;15:1446287. doi: 10.3389/fendo.2024.1446287. eCollection 2024.
The ketogenic diet (KD) is a popular option for managing body weight, though its influence on glucose and lipid metabolism was still inconclusive. Gut microbiota is modulated by dietary pattens and has been associated with the changes of metabolic homeostasis induced by KD. Here, we found that two types of KDs, KD1 (8.8% carbohydrate, 73.4% fat, 17.9% protein, 5.7 kcal/g) and KD2 (0.4% carbohydrate, 93.2% fat, 6.4% protein, 6.7 kcal/g), induced changes of gut microbiota and its metabolites, contributing to glucose intolerance but not lipid accumulation in mice. Following a 2-week intervention with KDs, mice fed on KD1 displayed symptoms related to obesity, whereas KD2-fed mice exhibited a decrease in body weight but had severe hepatic lipid accumulation and abnormal fatty acid metabolism, while both KDs led to significant glucose intolerance. Compared to the mice fed on a standard chow diet, the conventional mice fed on both KD1 and KD2 had significant shifted gut microbiota, lower levels of short chain fatty acids (SCFAs) and composition alteration of cecal bile acids. By using an antibiotic cocktail (ABX) to deplete most of the gut microbiota in mice, we found the disturbances induced by KDs in lipid metabolism were similar in the ABX-treated mice to their conventional companions, but the disturbances in glucose metabolism were absent in the ABX-treated mice. In conclusion, these findings suggest that ketogenic diets disrupted glucose and lipid metabolism, at least in mice, and highlight the gut microbial culprits associated with KD induced glucose intolerance rather than lipid accumulation.
生酮饮食(KD)是控制体重的一种流行选择,但其对葡萄糖和脂质代谢的影响仍不确定。饮食模式会调节肠道微生物群,并且与 KD 诱导的代谢稳态变化有关。在这里,我们发现两种类型的 KD,KD1(8.8%碳水化合物,73.4%脂肪,17.9%蛋白质,5.7 kcal/g)和 KD2(0.4%碳水化合物,93.2%脂肪,6.4%蛋白质,6.7 kcal/g),导致肠道微生物群及其代谢物发生变化,导致葡萄糖不耐受,但不会导致小鼠脂质积累。用 KD 干预 2 周后,喂食 KD1 的小鼠表现出与肥胖相关的症状,而喂食 KD2 的小鼠体重下降,但肝脂质积累严重,脂肪酸代谢异常,同时两种 KD 都导致明显的葡萄糖不耐受。与喂食标准饲料的常规小鼠相比,喂食 KD1 和 KD2 的常规小鼠的肠道微生物群明显移位,短链脂肪酸(SCFAs)水平降低,盲肠胆汁酸组成改变。通过使用抗生素鸡尾酒(ABX)耗尽小鼠的大部分肠道微生物群,我们发现 KD 对脂质代谢的干扰在 ABX 处理的小鼠中与常规同伴相似,但在 ABX 处理的小鼠中不存在葡萄糖代谢紊乱。总之,这些发现表明生酮饮食会破坏葡萄糖和脂质代谢,至少在小鼠中是这样,并强调了与 KD 诱导的葡萄糖不耐受而不是脂质积累相关的肠道微生物群罪魁祸首。