Pan Ruirong, Wang Tingwei, Bai Juan, Zhang Jiayan, Gu Yaoguang, Zhao Zhicong, Tang Ruixue, Qian Zifan, Yan Lirong, Xiao Xiang, Liang Shuang, Dong Ying
Department of Geriatric Medicine, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
School of Food and Biological Engineering, Jiangsu University, Zhenjiang, China.
Lipids. 2025 Jul;60(4):237-248. doi: 10.1002/lipd.12435. Epub 2025 Mar 7.
Lactobacillus plantarum fermented barley extract (LFBE) has a potent anti-obesity effect on high-fat-diet fed (HFD) obese rats. However, the underlying mechanism remains unclear. Herein, we investigated the anti-obesity effect and mechanism of LFBE in 3 T3-L1 preadipocytes and HFD-induced obese rats. LFBE significantly inhibited lipid accumulation by decreasing the expression of adipogenesis-related transcription factors, including peroxisome proliferator-activated receptor (PPAR-γ) and CCAAT/enhancer binding protein (C/EBP-α) in differentiated 3 T3-L1 cells. The expression levels of adiponectin, acetyl CoA carboxylase (ACC), and fatty acid synthase (FAS) were also suppressed in differentiated three T3-L1 cells. Administration of LFBE significantly reduced insulin resistance, blood lipid profiles, and improved metabolic hormones in HFD-induced obese rats. Furthermore, the serum pro-inflammatory cytokines including CRP, IL-6, TNFα, and INFγ in HFD-induced obese rats were significantly decreased after LFBE administration. LFBE treatment also attenuated oxidative stress in HFD-induced obese rats by decreasing MDA production and restoring SOD and catalase enzymatic activity. Administration of LFBE could modulate gut microbiota imbalance by increasing the abundance of Lactobacillus and Ruminococcaceae UCG-014 and decreasing Prevotella-9 at the genus level and restoring intestinal barrier dysfunction in HFD-induced obesity rats. Taken together, our study indicated that LFBE is a promising candidate for treating obesity through multiple mechanisms.
植物乳杆菌发酵大麦提取物（LFBE）对高脂饮食喂养（HFD）的肥胖大鼠具有显著的抗肥胖作用。然而，其潜在机制仍不清楚。在此，我们研究了LFBE在3T3-L1前脂肪细胞和HFD诱导的肥胖大鼠中的抗肥胖作用及机制。LFBE通过降低分化的3T3-L1细胞中脂肪生成相关转录因子的表达，包括过氧化物酶体增殖物激活受体（PPAR-γ）和CCAAT/增强子结合蛋白（C/EBP-α），显著抑制脂质积累。在分化的3T3-L1细胞中，脂联素、乙酰辅酶A羧化酶（ACC）和脂肪酸合酶（FAS）的表达水平也受到抑制。给予LFBE可显著降低HFD诱导的肥胖大鼠的胰岛素抵抗、血脂水平，并改善代谢激素。此外，给予LFBE后，HFD诱导的肥胖大鼠血清中的促炎细胞因子，包括CRP、IL-6、TNFα和INFγ显著降低。LFBE治疗还通过降低丙二醛生成并恢复超氧化物歧化酶和过氧化氢酶的酶活性，减轻了HFD诱导的肥胖大鼠的氧化应激。给予LFBE可通过增加乳杆菌属和瘤胃球菌科UCG-014的丰度，在属水平上降低普雷沃氏菌属9的丰度，并恢复HFD诱导的肥胖大鼠的肠道屏障功能障碍，从而调节肠道微生物群失衡。综上所述，我们的研究表明LFBE是一种通过多种机制治疗肥胖的有前景的候选物。
