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  3. Canola Oil Ameliorates Obesity by Suppressing Lipogenesis and Reprogramming the Gut Microbiota in Mice via the AMPK Pathway

Canola Oil Ameliorates Obesity by Suppressing Lipogenesis and Reprogramming the Gut Microbiota in Mice via the AMPK Pathway

  • Nutrients. 2024 Oct 4;16(19):3379. doi: 10.3390/nu16193379.
Jing Gao 1 2 3,  Li Ma 1 2 3,  Jie Yin 4,  Tiejun Li 5,  Yulong Yin 3 4 5,  Yongzhong Chen 1 2 3
Affiliations

Affiliations

  • 1 Research Institute of Oil Tea Camellia, Hunan Academy of Forestry, Shao Shan South Road, No. 658, Changsha 410004, China.
  • 2 National Engineering Research Center for Oil Tea Camellia, Changsha 410004, China.
  • 3 Yuelushan Laboratory, Changsha 410004, China.
  • 4 College of Animal Science and Technology, Hunan Co-Innovation Center of Animal Production Safety, Hunan Agricultural University, Changsha 410127, China.
  • 5 Key Laboratory of Agro-Ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Hunan Provincial Key Laboratory of Animal Nutritional Physiology and Metabolic Process, Chinese Academy of Sciences, Changsha 410125, China.
PMID: 39408346 DOI: 10.3390/nu16193379
Abstract

Background: 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.

Methods: 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.

Results: 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 Akkermansia, Dubosiella, and Alistipes 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.

Conclusions: 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 Alistipes via the AMPK signaling pathway.

Keywords

AMPK signaling pathway; acetic acid; canola oil; gut microbiota; lipid metabolism; obesity.

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