Silicon-enriched functional meat enhances colonic barrier function by regulating tight junction protein expression, oxidative stress, and inflammation responses in a diabetic dyslipidemia model†

Western diets are linked to metabolic disorders such as Type 2 diabetes mellitus (T2DM) and diabetic dyslipidemia, which involve hyperglycemia, insulin resistance, high plasma cholesterol levels and altered lipoprotein profiles. The T2DM progression also involves glucolipotoxicity, wherein elevated glucose and fatty acid levels induce oxidative stress and inflammation. Excessive intake of saturated fats and/or cholesterol can trigger dysbiosis, which weakens the colonic barrier, increases its permeability, and promotes chronic low-grade inflammation, thereby accelerating the progression of T2DM. Silicon, an essential trace element, has demonstrated antidiabetic, hypolipidemic, antioxidant and anti-inflammatory properties, suggesting its potential as a nutritional adjuvant in therapeutic management of T2DM and the maintenance of gut health. In this study, 24 male Wistar rats were divided into three groups: (1) an early-stage T2DM group (ED) fed a control meat incorporated into a high saturated-fat diet; (2) a late-stage T2DM group (LD) fed a control meat incorporated into a high-saturated fat and high cholesterol diet combined with streptozotocin and nicotinamide injection; and (3) a late-stage T2DM group fed a silicon enriched meat (LD-Si). Microbiota composition, lipoperoxidation and concentrations of fat, cholesterol, oxysterols and short-chain fatty acids and silicon were assayed in feces. The colonic tissue morphology, barrier integrity, antioxidant capacity and inflammatory markers were measured to evaluate the impact of silicon on colonic health and intestinal barrier function. Silicon enriched meat (Si-RM) consumption increased faecal fat and cholesterol excretion and reduced toxic luminal environments by modulating oxysterols. Si-RM consumption also enhanced colonic barrier integrity, increasing tight junction proteins and goblet cells, and exhibited antioxidant effects via the pNrf2 pathway and superoxide dismutase activity. Furthermore, silicon reduced the pro-inflammatory cytokines TNFα and IL-6, likely through inhibition of the TLR4/NFκB pathway. The results suggest that silicon's ability to enhance intestinal barrier integrity, reduce oxidative stress, and prevent inflammation could slow down T2DM progression, making it a promising nutritional adjuvant for managing the disease.