(1) Background: Ellagic acid (EA) acts as a product of gut microbiota transformation to prevent insulin resistance, which is limited by high-fat diet (HFD)-induced dysbiosis. The aim of this study was to investigate the synergistic effects and mechanisms of supplementation with the probiotic Weizmannia coagulans (W. coagulans) on the prevention of insulin resistance by EA; (2) Methods: C57BL/6J mice were divided into five groups (n = 10/group): low-fat-diet group, high-fat-diet group, EA intervention group, EA + W. coagulans BC77 group, and EA + W. coagulans BC2000 group; (3) Result: W. coagulans BC2000 showed a synergistic effect on EA’s lowering insulin resistance index and inhibiting high-fat diet-induced endotoxemia. The combined effect of BC2000 and EA activated the autophagy pathway in the mouse liver, a urolithin-like effect. This was associated with altered β-diversity of gut microbiota and increased Eggerthellaceae, a potential EA-converting family. Ellagic acid treatment alone and the combined use of ellagic acid and W. coagulans BC77 failed to activate the hepatic autophagy pathway; (4) Conclusions: W. coagulans BC2000 can assist EA in its role of preventing insulin resistance. This study provides a basis for the development of EA-rich functional food supplemented with W. coagulans BC2000.

中文翻译：

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Weizmannia coagulans BC2000 Plus 鞣花酸通过重塑小鼠肠道微生物群和激活肝脏自噬途径抑制高脂肪诱导的胰岛素抵抗

(1) 背景：鞣花酸 (EA) 作为肠道微生物群转化的产物，可预防胰岛素抵抗，而胰岛素抵抗受到高脂饮食 (HFD) 引起的菌群失调的限制。本研究的目的是探讨补充益生菌Weizmannia coagulans ( W. coagulans)对于通过EA预防胰岛素抵抗的协同作用和机制；（2）方法：C57BL/6J小鼠分为5组（n=10/组）：低脂饮食组、高脂饮食组、EA干预组、EA+ W. coagulans BC77组、EA组+ W. coagulans BC2000 组；(3)结果：W. coagulans BC2000对EA降低胰岛素抵抗指数和抑制高脂饮食引起的内毒素血症具有协同作用。BC2000 和 EA 的联合作用激活了小鼠肝脏中的自噬途径，具有类似尿石素的作用。这与肠道微生物群 β 多样性的改变和潜在 EA 转化家族Eggerthellaceae的增加有关。单独使用鞣花酸以及结合使用鞣花酸和凝结W. coagulans BC77均未能激活肝脏自噬途径；(4)结论：凝结球菌BC2000可辅助EA发挥预防胰岛素抵抗的作用。该研究为开发补充了W. coagulans BC2000的富含EA的功能性食品提供了基础。