Scope: Reduced digestibility of foods containing oxidized proteins and the subsequent excessive accumulation of undigested components in the colon may cause changes in the intestinal flora composition. This study evaluates the characteristics of this change and the potential adverse effects on organisms. Methods and results: Pork is cooked using sous-vide or at high temperature and pressure (HTP), then freeze-dried, resulting in different levels of oxidized damage. Mice are fed diets containing low-(LOP), medium-(MOP), or high-oxidative damage pork (HOP) for 12 weeks. HOP intake increases mice body weight, induces inflammatory response, and causes oxidative stress, as indicated by the accumulation of oxidative products. Increased serum LPS levels and downregulation of tight junction-related genes in the mucosa suggest mucosal barrier damage. Alterations in the cecal microbiota include reduced relative abundance of the mucin-degrading bacteria Akkermansia, beneficial bacteria Lactobacillus and Bifidobacterium, and H 2 S-producing bacteria Desulfovibrio and increased relative abundance of the pro-inflammatory bacteria Escherichia-Shigella and pathobiont Mucispirillum.
This study aims to investigate the health effects of long-term dietary oxidized tyrosine (O-Tyr) and its main product (dityrosine) administration on mice metabolism. Mice received daily intragastric administration of either O-Tyr (320 μg/kg body weight), dityrosine (Dityr, 320 μg/kg body weight), or saline for consecutive 6 weeks. Urine and plasma samples were analyzed by NMR-based metabolomics strategies. Body weight, clinical chemistry, oxidative damage indexes, and histopathological data were obtained as complementary information. O-Tyr and Dityr exposure changed many systemic metabolic processes, including reduced choline bioavailability, led to fat accumulation in liver, induced hepatic injury, and renal dysfunction, resulted in changes in gut microbiota functions, elevated risk factor for cardiovascular disease, altered amino acid metabolism, induced oxidative stress responses, and inhibited energy metabolism. These findings implied that it is absolutely essential to reduce the generation of oxidation protein products in food system through improving modern food processing methods.
The findings suggested that decreased insulin secretion triggered by OTPs may be mediated by oxidative stress and mitochondrial damage in pancreatic β cells.
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