Yue Fangfang, Han Haoyue, Xu Jiaxin, Yao Xinyue, Qin Yanting, Zhang Libing, Sun Xin, Huang Jihong, Zhang Fan, Lü Xin
College of Food Science and Engineering, Northwest A&F University, Yangling 712100, Shaanxi, China.
Xijing Hospital, the Fourth Military Medical University. No. 127, Changle West Road, Xi'an, Shaanxi 710032, China.
Int J Biol Macromol. 2025 Feb;289:138803. doi: 10.1016/j.ijbiomac.2024.138803. Epub 2024 Dec 17.
Lactobacillus plantarum KX041 is a probiotics obtained from early screening, which can relieve inflammation and enrich the anti-obesity intestinal flora, and produce high yield of exopolysaccharides (EPS). The extraction, structure and physicochemical properties of EPS have been completed earlier. However, whether the functional activity of L. plantarum KX041 is related to the EPS is still unclear. In this study, combined in vivo and in vitro tests explored the effects of EPS on inflammatory obesity. In vitro tests, EPS relieased inflammation by inhibiting TLR4/p-NFκB, and inhibited adipocyte differentiation and reduced the transcriptional level of inflammation and lipid-synthesis genes (especially CD36 and peroxisome proliferators-activated receptors-γ PPARγ). In vivo tests demonstrated that EPS could alleviate weight gain, white adipocyte expansion, organ damage, insulin resistance, hyperlipidemia, and inflammatory response caused by high fat diet. Combined with in vitro tests, the transcription level of inflammation and lipid-synthesis genes in adipose tissue identified that IL-1β and PPARγ were the key genes for the effect of EPS on inflammatory obesity. Moreover, EPS increased the abundance of Akkermansia and Lachnospiraceae_NK4A136_group, and intestinal levels of isobutyrate, which is one of the key factors in alleviating inflammatory obesity. These insights may inform the development of functionalized dietary interventions in obesity.
植物乳杆菌KX041是一种通过早期筛选获得的益生菌，它可以减轻炎症、丰富抗肥胖肠道菌群，并高产胞外多糖（EPS）。EPS的提取、结构和理化性质已较早完成。然而，植物乳杆菌KX041的功能活性是否与EPS有关仍不清楚。在本研究中，通过体内和体外试验相结合的方式，探讨了EPS对炎症性肥胖的影响。体外试验中，EPS通过抑制TLR4/p-NFκB释放炎症，并抑制脂肪细胞分化，降低炎症和脂质合成基因（尤其是CD36和过氧化物酶体增殖物激活受体γ，PPARγ）的转录水平。体内试验表明，EPS可以减轻高脂饮食引起的体重增加、白色脂肪细胞扩张、器官损伤、胰岛素抵抗、高脂血症和炎症反应。结合体外试验，脂肪组织中炎症和脂质合成基因的转录水平表明，IL-1β和PPARγ是EPS对炎症性肥胖产生作用的关键基因。此外，EPS增加了阿克曼氏菌和毛螺菌科_NK4A136_组的丰度，以及肠道中异丁酸的水平，而异丁酸是减轻炎症性肥胖的关键因素之一。这些见解可能为肥胖的功能化饮食干预的发展提供参考。
