Vornoli Andrea, Souid Aymen, Lazzari Barbara, Turri Federica, Pizzi Flavia, Bramanti Emilia, Campanella Beatrice, Trouki Cheherazade, Raffaelli Andrea, Wójcik Marta, Della Croce Clara Maria, Giorgetti Lucia, Longo Vincenzo, Capra Emanuele, Pozzo Luisa
Institute of Agricultural Biology and Biotechnology, National Research Council, Via Moruzzi 1, 56124 Pisa, Italy.
Institute of Agricultural Biology and Biotechnology, National Research Council, Via Corti 12, 20133 Milan, Italy.
Molecules. 2024 Dec 17;29(24):5954. doi: 10.3390/molecules29245954.
Beer and its components show potential for reducing hepatic steatosis in rodent models through multiple mechanisms. This study aimed to evaluate beer's anti-steatotic effects in a high-fat diet (HFD)-induced mouse model of Metabolic dysfunction-Associated Liver Disease (MASLD) and to explore the underlying mechanisms. In the HFD group, steatosis was confirmed by altered blood parameters, weight gain, elevated liver lipid content, and histological changes. These markers were normalized in the HFD+beer group, reaching levels similar to the control (CTR) group. Protein carbonylation and lipid peroxidation levels were consistent across all groups, suggesting that the model represents an early stage of MASLD without oxidative stress. Transcriptomic and CpG methylation analyses revealed clear distinctions between the CTR and HFD groups. RNA sequencing identified 162 differentially expressed genes (DEGs) between the CTR and HFD groups, primarily related to inflammation and lipid regulation. Beer consumption modified the health of the HFD mice, affecting inflammation but not lipid homeostasis (CTR vs. HFD+beer, DEGs = 43). The CpG methylation analysis indicated that beer lowered methylation, impacting genes linked to lipid accumulation and inflammation. A cecal metabolite analysis suggested that beer improved short-chain fatty acid metabolism (SCFA). In summary, a moderate beer intake may mitigate MASLD by modulating lipid metabolism and SCFA pathways, likely through polyphenol activity.
啤酒及其成分通过多种机制在啮齿动物模型中显示出减轻肝脂肪变性的潜力。本研究旨在评估啤酒在高脂饮食（HFD）诱导的代谢功能障碍相关肝病（MASLD）小鼠模型中的抗脂肪变性作用，并探索其潜在机制。在HFD组中，通过血液参数改变、体重增加、肝脏脂质含量升高和组织学变化证实了脂肪变性。这些指标在HFD+啤酒组中恢复正常，达到与对照组（CTR）相似的水平。所有组的蛋白质羰基化和脂质过氧化水平一致，表明该模型代表了无氧化应激的MASLD早期阶段。转录组学和CpG甲基化分析揭示了CTR组和HFD组之间的明显差异。RNA测序确定了CTR组和HFD组之间162个差异表达基因（DEG），主要与炎症和脂质调节有关。饮用啤酒改善了HFD小鼠的健康状况，影响炎症但不影响脂质稳态（CTR组与HFD+啤酒组相比，DEG = 43）。CpG甲基化分析表明，啤酒降低了甲基化，影响了与脂质积累和炎症相关的基因。盲肠代谢物分析表明，啤酒改善了短链脂肪酸代谢（SCFA）。总之，适度饮用啤酒可能通过调节脂质代谢和SCFA途径减轻MASLD，可能是通过多酚活性实现的。
