The activation of peroxisome proliferator-activated rece ptor gamma (PPAR-γ) is known to induce the differentiation of adipocytes. This study aimed to investigate the probiotic effect of Leuconostoc mesenteroides (L. mesenteroides) on high-fat diet (HFD)-induced PPAR-γ activation and abdominal fat depots. Incubation of differentiated 3T3-L1 adipocytes with media of L. mesenteroides EH-1, a butyric acid-producing strain, significantly reduced the amounts of lipid droplets. The oral administration of L. mesenteroides EH-1 produced large amounts (>1 mM) of butyric acid in cecum and attenuated the HFD-induced upregulation of PPAR-γ and accumulation of abdominal fats in mice. The combination of 2% glucose with L. mesenteroides EH-1 increased the production of butyric acid and potentiated the probiotic activity of L. mesenteroides EH-1 against the formation of lipid droplets in 3T3-L1 adipocytes as well as abdominal fats in HFD-fed mice. The inhibition of free fatty acid receptor 2 (Ffar2) by its antagonist, GLPG-0974, markedly diminished the probiotic effects of L. mesenteroides EH-1 plus glucose on the suppression of HFD-induced PPAR-γ and abdominal fats. Besides demonstrating the probiotic value of L. mesenteroides EH-1, our results highlight the possible therapy targeting the butyric acid-activated Ffar2 pathway to reduce abdominal fats.

中文翻译：

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产生丁酸的肠膜明串珠菌减少小鼠腹部脂肪库。


已知过氧化物酶体增殖物激活受体γ（PPAR-γ）的激活可诱导脂肪细胞的分化。本研究旨在探讨肠膜明串珠菌( L. mesenteroides ) 的益生菌对高脂饮食 (HFD) 诱导的 PPAR-γ 激活和腹部脂肪库的影响。将分化的 3T3-L1 脂肪细胞与产丁酸菌株L. mesenteroides EH-1 的培养基一起孵育，可显着减少脂滴的量。口服肠系膜乳杆菌EH-1 可在盲肠中产生大量 (>1 mM) 丁酸，并减弱 HFD 诱导的小鼠 PPAR-γ 上调和腹部脂肪积累。 2% 葡萄糖与肠系膜乳杆菌EH-1 的组合增加了丁酸的产生，并增强了肠系膜乳杆菌EH-1 对抗 3T3-L1 脂肪细胞中脂滴以及 HFD 中腹部脂肪形成的益生菌活性。喂老鼠。游离脂肪酸受体 2 (Ffar2) 的拮抗剂 GLPG-0974 对游离脂肪酸受体 2 (Ffar2) 的抑制显着减弱了肠系膜乳杆菌EH-1 加葡萄糖对 HFD 诱导的 PPAR-γ 和腹部脂肪的抑制作用。除了证明肠系膜乳杆菌EH-1 的益生菌价值外，我们的结果还强调了针对丁酸激活 Ffar2 途径以减少腹部脂肪的可能疗法。