Research Institute of Oil Tea Camellia, Hunan Academy of Forestry, Shao Shan South Road, No. 658, Changsha 410004, China.
National Engineering Research Center for Oil Tea Camellia, Changsha 410004, China.
Nutrients. 2024 Oct 4;16(19):3379. doi: 10.3390/nu16193379.
obesity is a worldwide problem that seriously endangers human health. Canola oil (Col) has been reported to regulate hepatic steatosis by influencing oxidative stress and lipid metabolism in Kunming mice. However, whether Col exhibits an anti-obesity effect by altering the gut microbiota remains unknown.
in this study, we observed that a high-fat diet increased lipogenesis and gut microbiota disorder in C57BL/6J male mice, while the administration of Col suppressed lipogenesis and improved gut microbiota disorder.
the results show that Col markedly reduced the final body weight and subcutaneous adipose tissue of C57BL/6J male mice fed a high-fat diet (HFD) after 6 weeks of administration. However, although Col did not effectively increase the serum concentration of HDL, we found that treatment with Col notably inhibited the low-density lipoprotein (LDL), total cholesterol (TC), and triglycerides (TGs) in HFD mice. Furthermore, Col ameliorated obesity in the liver compared to mice that were only fed a high-fat diet. We also found that Col significantly inhibited the relative expression of sterol regulatory element binding protein (SREBP1/2), peroxisome proliferator-activated receptor γ (PPARγ), and insulin-induced genes (Insig1/2) that proved to be closely associated with lipogenesis in HFD mice. In addition, the concentration of acetic acid was significantly increased in Col-treatment HFD mice. Further, we noted that Col contributed to the reprogramming of the intestinal microbiota. The relative abundances of , , and were enhanced under treatment with Col in HFD mice. The results also imply that Col markedly elevated the phosphorylation level of the AMP-activated protein kinase (AMPK) pathway in HFD mice.
the results of our study show that Col ameliorates obesity and suppresses lipogenesis in HFD mice. The underlying mechanisms are possibly associated with the reprogramming of the gut microbiota, in particular, the acetic acid-mediated increased expression of via the AMPK signaling pathway.
肥胖是一个全球性的问题，严重危害人类健康。菜籽油（Col）已被报道通过影响昆明小鼠的氧化应激和脂质代谢来调节肝脂肪变性。然而，Col 是否通过改变肠道微生物群表现出抗肥胖作用尚不清楚。
在这项研究中，我们观察到高脂肪饮食增加了 C57BL/6J 雄性小鼠的脂肪生成和肠道微生物群紊乱，而 Col 的给药抑制了脂肪生成并改善了肠道微生物群紊乱。
结果表明，Col 显著降低了 6 周高脂肪饮食（HFD）喂养的 C57BL/6J 雄性小鼠的最终体重和皮下脂肪组织。然而，尽管 Col 不能有效增加 HDL 血清浓度，但我们发现 Col 显著抑制了 HFD 小鼠的低密度脂蛋白（LDL）、总胆固醇（TC）和甘油三酯（TGs）。此外，Col 改善了与仅喂食高脂肪饮食的小鼠相比肥胖的肝脏。我们还发现，Col 显著抑制了与脂肪生成密切相关的固醇调节元件结合蛋白 1/2（SREBP1/2）、过氧化物酶体增殖物激活受体 γ（PPARγ）和胰岛素诱导基因 1/2（Insig1/2）在 HFD 小鼠中的相对表达。此外，Col 处理 HFD 小鼠中的乙酸浓度显著增加。此外，我们注意到 Col 有助于肠道微生物群的重新编程。Col 处理 HFD 小鼠中的 、 和 的相对丰度增加。结果还表明，Col 显著提高了 HFD 小鼠中 AMP 激活蛋白激酶（AMPK）通路的磷酸化水平。
我们的研究结果表明，Col 改善了 HFD 小鼠的肥胖和抑制脂肪生成。潜在机制可能与肠道微生物群的重编程有关，特别是通过 AMPK 信号通路介导的乙酸增加表达。
