Green Pea (Pisum sativum L.) Hull Polyphenol Extract Alleviates NAFLD through VB6/TLR4/NF-κB and PPAR Pathways.

Green pea hull is a processing byproduct of green pea and rich in polyphenols. Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic disease characterized by accumulation of lipids in the liver for which there are no effective treatment strategies. Here, a mouse model of NAFLD induced by a DSS+high-fat diet (HFD) was established to investigate the effect of green pea hull polyphenol extract (EGPH). The results show that EGPH relief of NAFLD was a combined effect, including reducing hepatic fat accumulation, improving antioxidant activity and blood lipid metabolism, and maintaining glucose homeostasis. Increased intestinal permeability aggravated NAFLD. Combined metabolomics and transcriptomic analysis showed that vitamin B6 is the key target substance for EGPH to alleviate NAFLD, and it may be the intestinal flora metabolite. After EGPH intervention, the level of vitamin B6 in mice was significantly increased, and more than 60% in the blood enters the liver, which activated or inhibited PPAR and TLR4/NF-κB signaling pathways to relieve NAFLD. Our research could be a win-win for expanding the use of green pea hull and the search for NAFLD prophylactic drugs.

Multi-omics reveals that green pea (Pisum sativum L.) hull supplementation ameliorates non-alcoholic fatty liver disease via the SHMT2/glycine/mTOR/PPAR-γ signaling pathway.

Diets rich in various active ingredients may be an effective intervention strategy for non-alcoholic fatty liver disease (NAFLD). The green pea hull (GPH) is a processing by-product of green peas rich in dietary fiber and polyphenols. Here, a mouse model of NAFLD induced by DSS + high-fat diet (HFD) was established to explore the intervention effect of the GPH. The results showed that dietary supplements with the GPH can inhibit obesity and reduce lipid accumulation in the mouse liver to prevent liver fibrosis. GPH intervention can improve liver antioxidant capacity, reduce blood lipid deposition and maintain glucose homeostasis. DSS-induced disruption of the intestinal barrier aggravates NAFLD, which may be caused by the influx of large amounts of LPS. A multi-omics approach combining metabolomics and transcriptomic analysis indicated that glycine was the key target and its content was decreased in the liver after GPH intervention, and that dietary supplements with the GPH can relieve NAFLD via the SHMT2/glycine/mTOR/PPAR-γ signaling pathway, which was further supported by liver-associated protein expression. In conclusion, our study demonstrated that dietary GPH can significantly ameliorate NAFLD, and the future development of related food products can enhance the economic value of the GPH.