Transcriptomics reveals the anti-obesity mechanism of Lactobacillus plantarum fermented barley extract

• Published in: Food research international 2022-07, Vol.157, p.111285-111285, Article 111285
• Main Authors: Gu, Yaoguang, Bai, Juan, Zhang, Jiayan, Zhao, Yansheng, Pan, Ruirong, Dong, Ying, Cui, Henglin, Xiao, Xiang
• Format: Article
• Language: English
• Subjects: adipocytes; adipose tissue; AMP-activated protein kinase; AMPK; Barley; blood glucose; energy; fatty acids; fermentation; food research; genome; High fat diet; lactic acid; Lactobacillus plantarum; mitochondria; nutritive value; obesity; PGC1α; phosphorylation; transcriptomics; transmission electron microscopes; weight gain
• ISSN: 0963-9969; 1873-7145
• DOI: 10.1016/j.foodres.2022.111285

[Display omitted] •Supplementation of fermented barley extract inhibited fatty acid synthesis in high fat diet rats.•Fermented barley extracts enhanced fatty acid oxidation via activating AMPK pathway.•Protein isolated from fermented barley extract is responsible for maintaining mitochondrial integrity and proliferation. Fermentation by lactic acid bacteria can improve the nutritional value and biological function of cereal. Our previous studies have confirmed that Lactobacillus plantarum fermented barley extract (LFBE) can alleviate obesity caused by high-fat diet (HFD) in rats, while the precise mechanism remains unclear. Herein, we explored the effect of LFBE on the adipose tissue in obese rats and its mechanism via transcriptomics technology. Results showed that administration of LFBE in obese rats for 8 weeks significantly alleviated weight gain, reduced fasting blood glucose, and inhibited lipid accumulation. Transmission electron microscope (TEM) observation of adipose tissue found that LFBE held the ability to maintain mitochondria integrity and functionality. Transcriptomics analysis revealed that LFBE increased the expressions of mitochondrial β-oxidized-related genes, while inhibiting the expressions of fatty acid synthesis-related genes. Furthermore, KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis and western blotting studies confirmed that LFBE mainly enhanced the energy consumption of adipocytes through the phosphorylation of AMP-Activated Protein Kinase (AMPK) and the mitochondrial proliferation pathway regulated by peroxisome proliferative activated receptor, gamma, coactivator 1 alpha (PGC1α). Taken together, these findings indicated that LFBE could ameliorate HFD-induced obesity by activating AMPK/PGC1α axis regulated signaling pathways.