吃得太甜，堪比喝酒！贾伟/郑晓皎团队Cell子刊：高糖饮食诱导肠道细菌生成乙醛，毒害肝脏

Core Viewpoint - The study highlights the urgent need for innovative treatment strategies to prevent the progression from Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) to Metabolic Dysfunction-Associated Steatotic Hepatitis (MASH), which can lead to irreversible liver damage [2][3]. Group 1: Research Findings - The research published by a team from Shanghai Jiao Tong University indicates that a high-sugar diet leads to the production of endogenous acetaldehyde by gut microbiota, which damages the liver and accelerates the progression from MASLD to MASH without alcohol consumption [2][7]. - Approximately 30.69% of the global population is affected by MASLD, with about 16.02% progressing to MASH, and these numbers are expected to rise with increasing obesity rates [5]. - The study identifies that excessive dietary fructose accelerates the progression from MASLD to MASH through the mediation of endogenous acetaldehyde generated by gut microbiota [7][9]. Group 2: Mechanism and Treatment Strategy - The research team discovered that acetaldehyde produced by gut microbiota enters the liver via the portal vein, upregulating MMP7 expression and activating hepatic stellate cells (HSC), promoting fibrosis in mouse and cell models [7]. - To combat this pathogenic pathway, the team isolated a probiotic strain, Ligilactobacillus salivarius CTMT1, capable of clearing acetaldehyde, and engineered a strain with enhanced acetaldehyde degradation capabilities [7]. - The engineered probiotics effectively reduced liver fibrosis and inflammation in preclinical models, suggesting a promising therapeutic strategy targeting gut microbiota-mediated aldehyde metabolism to prevent MASH [9].