Kurakawa Takuto, Kani Koudai, Chudan Seita, Nishikawa Miyu, Tabuchi Yoshiaki, Sakamoto Kazuichi, Nagai Yoshinori, Ikushiro Shinichi, Furusawa Yukihiro
Department of Biotechnology, Faculty of Engineering, Toyama Prefectural University, 5180 Kurokawa, Imizu 939-0398, Toyama, Japan.
Department of Pharmaceutical Engineering, Faculty of Engineering, Toyama Prefectural University, 5180 Kurokawa, Imizu 939-0398, Toyama, Japan.
Microorganisms. 2024 Dec 4;12(12):2495. doi: 10.3390/microorganisms12122495.
Obesity is a global epidemic and a significant risk factor for various diseases. Obesity and dysbiosis are associated, drawing attention to the mechanisms that regulate the gut microbiota. In this study, we focused on the postbiotic effects of rice kefiran (Kef), a functional product of cultured in a rice-based medium, on obesity and its complications. Although Kef has the potential to improve obesity, the underlying mechanisms remain unknown. Therefore, we aimed to elucidate the mechanisms underlying changes in gut microbiota. The administration of Kef significantly suppressed diet-induced body weight gain, reduced liver fat accumulation, and modestly improved insulin resistance. Among the gut bacteria, and , which were positively correlated with obesity, decreased in mice administered Kef. In contrast, and , both reported to ameliorate obesity, were increased. Consistent with the changes in the gut microbiota, Kef increased fecal acetate levels, which ameliorated obesity and hepatic steatosis. Predictive metagenomic analysis suggested that Kef administration increased the abundance of KEGG orthologs, associated with carbohydrate metabolism and improvements in insulin resistance. In conclusion, Kef improves diet-induced obesity, hepatic steatosis, and insulin resistance by regulating the gut microbiota's composition.
肥胖是一种全球性流行病，也是多种疾病的重要风险因素。肥胖与肠道菌群失调相关，这引发了人们对调节肠道微生物群机制的关注。在本研究中，我们聚焦于在大米培养基中培养的功能性产品米凯菲尔（Kef）对肥胖及其并发症的后生元效应。尽管Kef有改善肥胖的潜力，但其潜在机制仍不清楚。因此，我们旨在阐明肠道微生物群变化的潜在机制。给予Kef可显著抑制饮食诱导的体重增加，减少肝脏脂肪堆积，并适度改善胰岛素抵抗。在肠道细菌中，与肥胖呈正相关的 和 ，在给予Kef的小鼠中减少。相反，据报道两者都能改善肥胖，它们的数量增加。与肠道微生物群的变化一致，Kef增加了粪便乙酸盐水平，这改善了肥胖和肝脂肪变性。预测性宏基因组分析表明，给予Kef增加了与碳水化合物代谢和胰岛素抵抗改善相关的KEGG直系同源物的丰度。总之，Kef通过调节肠道微生物群的组成改善饮食诱导的肥胖、肝脂肪变性和胰岛素抵抗。
