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嗜酸乳杆菌YL01及其胞外多糖通过调节肠道特定菌群和AMPK/ACC信号通路改善肥胖小鼠的肥胖和胰岛素抵抗。

Lactobacillus acidophilus YL01 and its exopolysaccharides ameliorate obesity and insulin resistance in obese mice via modulating intestinal specific bacterial groups and AMPK/ACC signaling pathway.

作者信息

Zhao Chongjie, Xie Linlin, Shen Jing, He Hongpeng, Zhang Tongcun, Hao Lizhuang, Sun Cai, Zhang Xiaoyuan, Chen Mian, Liu Fei, Li Zhongyuan, Wang Nan

机构信息

College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China; Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, Tianjin 300457, China.

Key Laboratory of Plateau Grazing Animal Nutrition and Feed Science of Qinghai Province, State Key Laboratory of Plateau Ecology and Agriculture, The Academy of Animal and Veterinary Science, Qinghai University, Xining 810000, China.

出版信息

Int J Biol Macromol. 2025 Apr;300:140287. doi: 10.1016/j.ijbiomac.2025.140287. Epub 2025 Jan 23.

DOI:10.1016/j.ijbiomac.2025.140287
PMID:39863204
Abstract

Probiotics intervention by Lactobacillus acidophilus has potential effect on alleviating obesity and insulin resistance. However, the limited knowledge of functional substances and potential regulatory mechanisms hinder their widespread application. Herein, L. acidophilus YL01 was firstly isolated from Chinese traditional yogurt, demonstrating inhibitory activities on amylase and glucosidase that are comparable to those of L. rhamnosus LGG. Besides, the oral administration of L. acidophilus YL01 and its EPS significantly reduced body weight in high-fat mice (p < 0.05), as well as fat accumulation in liver and adipocytes. Moreover, they not only reduced fasting blood glucose and glucose/insulin resistance, but also improved dyslipidemia, liver function and inflammation. Further high-performance liquid chromatography analysis and Fourier transform infrared spectroscopy indicated that EPS is an acidic polysaccharide, characterized by a molecular weight of 952 kDa and predominantly composed of glucose. Additionally, the mechanism investigation revealed that the L. acidophilus YL01 and EPS demonstrated limited efficacy in restoring the composition of gut microbiota, but rather exerted an influence on the abundance of specific bacterial groups. The enrichment of the bacterial groups resulted in the increase of acetic acid and butyric acid, which further mediates the gut-liver crosstalk in regulating lipid metabolism by the activation of AMPK/ACC pathway.

摘要

嗜酸乳杆菌的益生菌干预对缓解肥胖和胰岛素抵抗具有潜在作用。然而,对其功能物质和潜在调控机制的了解有限,阻碍了它们的广泛应用。在此,嗜酸乳杆菌YL01首先从中国传统酸奶中分离出来,其对淀粉酶和葡萄糖苷酶的抑制活性与鼠李糖乳杆菌LGG相当。此外,口服嗜酸乳杆菌YL01及其胞外多糖可显著降低高脂小鼠的体重(p<0.05),以及肝脏和脂肪细胞中的脂肪积累。此外,它们不仅降低了空腹血糖和葡萄糖/胰岛素抵抗,还改善了血脂异常、肝功能和炎症。进一步的高效液相色谱分析和傅里叶变换红外光谱表明,胞外多糖是一种酸性多糖,分子量为952 kDa,主要由葡萄糖组成。此外,机制研究表明,嗜酸乳杆菌YL01和胞外多糖在恢复肠道微生物群组成方面的功效有限,而是对特定细菌群的丰度产生影响。这些细菌群的富集导致乙酸和丁酸增加,进而通过激活AMPK/ACC途径介导肠道-肝脏在调节脂质代谢中的串扰。

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Lactobacillus acidophilus YL01 and its exopolysaccharides ameliorate obesity and insulin resistance in obese mice via modulating intestinal specific bacterial groups and AMPK/ACC signaling pathway.嗜酸乳杆菌YL01及其胞外多糖通过调节肠道特定菌群和AMPK/ACC信号通路改善肥胖小鼠的肥胖和胰岛素抵抗。
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