Selenium Improves Inflammation and Glucose Metabolism during 3T3-L1 Adipocyte Differentiation

This study investigated the impact of selenium in ameliorating abnormalities of glucose metabolism and inflammatory responses during the differentiation of preadipocytes into adipocytes. Sodium selenite (SS), a water-soluble form of selenium, effectively suppressed the expression of RAR-related orphan receptor gamma (ROR γ), a key regulator of lipid and glucose metabolism, which is upregulated during adipocyte differentiation, at both the protein and gene levels. SS treatment significantly enhanced the protein expression of insulin receptor substrate-1 (IRS-1) and glucose transporter type 4 (GLUT4), critical components of the insulin signaling pathway. Furthermore, SS effectively suppressed the expression of the gluconeogenesis regulatory genes glucose 6 phosphatase (G6pase) and phosphoenolpyruvate carboxykinase (PEPCK), which are abnormally upregulated during adipocyte differentiation. In addition, the SS treatment markedly reduced the production of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), which contribute to insulin resistance and chronic inflammation, during the differentiation. These findings indicate that selenium plays a beneficial role in improving glucose metabolism dysregulation and inflammatory responses driven by inflammatory cytokines. Moreover, these results suggest that selenium could be used not only for the prevention and improvement of insulin resistance and chronic inflammatory conditions but also as functional evaluation data for selenium-enriched foods, including tea.