The study of different processing techniques, such as sprouting, cooking and fermentation, can help to develop new products for human health. In this work, raw, cooked and fermented seeds and germinated seeds of Chenopodium quinoa Willd. var. Tunkahuan and Amaranthus caudatus L. var. Alegrìa were compared for the content of antioxidant molecules, total antioxidant capacity and mineral elements. Fermentation was induced spontaneously, with the yeast Saccharomyces cerevisiae, with the bacterium Lactobacillus plantarum and with both microorganisms, for 24 and 48 h. The increase in antioxidant molecules and antioxidant activity was induced by germination, by 24 h of spontaneous fermentation (polyphenols and flavonoids) and by 24 h of L. plantarum fermentation (total antioxidant activity) for both species. Germinated seeds of the two plants showed higher values in respect to seeds of macroelements and microelements. No genotoxic but rather protective effects were determined for seed and germinated seed extracts using the D7 strain of S. cerevisiae, a good tool for the evaluation of protection from oxidative damage induced by radical oxygen species (ROS) in cells and tissues. Therefore, the two varieties could be very suitable for their use in human diet and in supplements, especially as germinated seeds or as fermented foods.

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.