Given the rising evidence that gut malfunction including changes in the gut microbiota composition, plays a major role in the development of obesity and associated metabolic diseases, the exploring of novel probiotic bacteria with potential health benefits has attracted great attention. Recently Lactobacillus spp., exert potent anti‐obesity effects by regulating key transcriptional and translational factors in adipose tissues. However, the molecular mechanism behind the anti‐obesity effect of probiotics is not yet fully understood. Therefore, we investigated the effect of Lactobacillus plantarum A29 on the expression of adipogenic and lipogenic genes in 3T3‐L1 adipocytes and high‐fat diet (HFD)‐fed mice. We observed that the treatment of 3T3‐L1 adipocytes with the cell‐free metabolites of L plantarum inhibited their differentiation and fat depositions via downregulating the key adipogenic transcriptional factors (PPAR‐γ, C/EBP‐α, and C/EBP‐β) and their downstream targets (FAS, aP2, ACC, and SREBP‐1). Interestingly, supplementation with L plantarum reduced the fat mass and serum lipid profile concurrently with downregulation of lipogenic gene expression in the adipocytes, resulting in reductions in the bodyweight of HFD‐fed obese mice. L plantarum treatment attenuated the development of obesity in HFD‐fed mice via the activation of p38MAPK, p44/42, and AMPK‐α by increasing their phosphorylation. Further analysis revealed that A29 modulated gut‐associated microbiota composition. Thus, A 29 potential probiotic strain may alleviate the obesity development and its associated metabolic disorders via inhibiting PPARγ through activating the p38MAPK and p44/42 signaling pathways.

中文翻译：

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选定的益生菌对饮食诱导的小鼠肥胖的积极代谢作用与肠道菌群失调的改善有关

鉴于越来越多的证据表明，包括肠道微生物群组成变化在内的肠道功能障碍在肥胖和相关代谢疾病的发展中起着重要作用，因此探索具有潜在健康益处的新型益生菌引起了人们的极大关注。最近，乳杆菌属通过调节脂肪组织中的关键转录和翻译因子发挥有效的抗肥胖作用。然而，益生菌抗肥胖作用背后的分子机制尚不完全清楚。因此，我们研究了植物乳杆菌 A29 对 3T3-L1 脂肪细胞和高脂饮食 (HFD) 喂养小鼠脂肪生成和脂肪生成基因表达的影响。我们观察到，用植物乳杆菌的无细胞代谢物处理 3T3-L1 脂肪细胞通过下调关键的脂肪生成转录因子（PPAR-γ、C/EBP-α 和 C/EBP-β）来抑制它们的分化和脂肪沉积。及其下游目标（FAS、aP2、ACC 和 SREBP-1）。有趣的是，补充植物乳杆菌可降低脂肪量和血清脂质谱，同时下调脂肪细胞中的脂肪生成基因表达，导致 HFD 喂养的肥胖小鼠体重减轻。植物乳杆菌处理通过增加磷酸化来激活 p38MAPK、p44/42 和 AMPK-α，从而减轻 HFD 喂养小鼠肥胖的发展。进一步的分析表明，A29 调节了肠道相关微生物群的组成。因此，