The gut microbiota has pivotal roles in metabolic homeostasis and modulation of the intestinal environment. Notably, the administration of Lactobacillus spp. ameliorates diet-induced obesity in humans and mice. However, the mechanisms through which Lactobacillus spp. control host metabolic homeostasis remain unclear. Accordingly, in this study, we evaluated the physiological roles of Lactobacillus fermentum in controlling metabolic homeostasis in diet-induced obesity. Our results demonstrated that L. fermentum-potentiated oxidative phosphorylation in adipose tissue, resulting in increased energy expenditure to protect against diet-induced obesity. Indeed, oral administration of L. fermentum LM1016 markedly ameliorated glucose clearance and fatty liver in high-fat diet-fed mice. Moreover, administration of L. fermentum LM1016 markedly decreased inflammation and increased oxidative phosphorylation in gonadal white adipose tissue, as demonstrated by transcriptome analysis. Finally, metabolome analysis showed that metabolites derived from L. fermentum LM1016-attenuated adipocyte differentiation and inflammation in 3T3-L1 preadipocytes. These pronounced metabolic improvements suggested that the application of L. fermentum LM1016 could have clinical applications for the treatment of metabolic syndromes, such as diet-induced obesity.

肠道微生物群在代谢稳态和调节肠道环境中具有关键作用。值得注意的是，乳酸杆菌属的给药。改善人类和小鼠的饮食引起的肥胖。然而，乳酸杆菌属的机制。控制宿主代谢稳态仍不清楚。因此，在本研究中，我们评估了发酵乳杆菌在控制饮食诱导的肥胖中代谢稳态中的生理作用。我们的研究结果表明，发酵乳杆菌增强了脂肪组织中的氧化磷酸化，导致能量消耗增加，以防止饮食引起的肥胖。事实上，发酵乳杆菌的口服给药LM1016 显着改善了高脂饮食喂养小鼠的葡萄糖清除率和脂肪肝。此外，如转录组分析所示，给予发酵乳杆菌 LM1016 可显着降低性腺白色脂肪组织中的炎症并增加氧化磷酸化。最后，代谢组分析表明，源自发酵乳杆菌 LM1016 的代谢物减弱了 3T3-L1 前脂肪细胞中的脂肪细胞分化和炎症。这些显着的代谢改善表明，发酵乳杆菌 LM1016 的应用可能具有治疗代谢综合征的临床应用，例如饮食引起的肥胖。