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Structural characterization of a α-d-glucan from Ginkgo biloba seeds and its protective effects on non-alcoholic fatty liver disease in mice. | LitMetric

Structural characterization of a α-d-glucan from Ginkgo biloba seeds and its protective effects on non-alcoholic fatty liver disease in mice.

Carbohydr Polym

State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi 214122, China; School of Food Science and Technology, Jiangnan University, Wuxi 214122, China. Electronic address:

Published: February 2025

AI Article Synopsis

  • Nonalcoholic fatty liver disease (NAFLD) is a major global health concern, but Ginkgo biloba seeds may offer a solution through their polysaccharides, specifically GBSP-2.
  • GBSP-2 has been shown to alleviate NAFLD in mice by reducing liver fat, inflammation, oxidative stress, and improving metabolism, while also positively altering gut microbiota.
  • The mechanism involves the activation of the AMPK/ACC signaling pathway, which reduces lipid synthesis and contributes to the protective effects on liver health.

Article Abstract

Nonalcoholic fatty liver disease (NAFLD) poses a great global challenge to public health, yet it holds promise for amelioration through plant-derived polysaccharide. Ginkgo biloba seeds have long been used as medicine and food, which has potential benefits for various chronic diseases. However, the protective role of Ginkgo biloba seed polysaccharide against NAFLD remains unclear. In this study, we isolated and purified polysaccharide (GBSP-2) from Ginkgo biloba seeds. GBSP-2 is composed of α-d-glucopyranose residues, which are interconnected with α-d-glucopyranose units linked by (1→4) bonds, (1→4,6) bonds and (1→3,4) bonds, the ratio distribution is 15:1:1. By studying a mouse model, we investigated the effect of GBSP-2 (100 or 200 mg/kg) on high-fat-diet-induced NAFLD. We demonstrated that GBSP-2 significantly alleviated NAFLD, as evidenced by reduced hepatic steatosis, decreased inflammation, improved oxidative stress and ameliorative glucolipid metabolic disorders. Furthermore, GBSP-2 mitigated gut microbiota disturbance of NAFLD mice and markedly increased the abundance of Akkermansia, Romboutsia, Lactobacillus and Bacteroides. Mechanistically, GBSP-2 could activate AMPK/ACC signaling pathway to inhibit lipid synthesis by generating 3,4-dihydroxyphenylpropionic acid (DHPPA). Overall, these findings suggest that GBSP-2 plays a multi-channel and multi-target role in improving NAFLD through the gut-liver axis.

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Source
http://dx.doi.org/10.1016/j.carbpol.2024.123022DOI Listing

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