N‐ϒ‐(l‐Glutamyl)‐l‐Selenomethionine Inhibits Fat Storage via the Stearoyl‐CoA Desaturases FAT‐6 and FAT‐7 and the Selenoprotein TRXR‐1 in Caenorhabditis elegans

Scope Selenium is an important nutrient for human health. The influence of dietary selenium on lipid metabolism remains largely unknown. N‐γ‐(l‐glutamyl)‐l‐selenomethionine (Glu‐SeMet) on inhibition of fat accumulation and its underlying mechanisms in the nematode Caenorhabditis elegans are investigated. Methods and results Triacylglyceride quantification and post‐fixed Nile red staining methods are conducted to evaluate fat accumulation in wild‐type N2 worms in normal or high‐glucose diet. Glu‐SeMet (0.01 µm) treatment effectively reduces fat storage in wild‐type N2 C. elegans in both a normal and high‐glucose diet. Further evidence shows that Glu‐SeMet (0.01 µm) decreases the ratio of oleic acid/stearic acid (C18:1Δ9/C18:0) using gas chromatography–mass spectrometry analysis. The mRNA levels of fatty acid stearoyl‐CoA desaturases, FAT‐6 and FAT‐7, and the mediator‐15 (MDT‐15) are downregulated while the wild‐type N2 worms are co‐treated with high glucose and Glu‐SeMet (0.01 µm). The effect of reduced fat accumulation is absent in fat‐6, fat‐7, and trxr‐1 mutant worms under high glucose and Glu‐SeMet (0.01 µm) co‐treatment. Conclusions This study demonstrates that Glu‐SeMet inhibiting fat accumulation may be associated with FAT‐6 and FAT‐7 and the selenoprotein TRXR‐1 in C. elegans. This study implies a potential for Glu‐SeMet as a new treatment for obesity or its complications. Organic selenium Glu‐SeMet inhibits fat storage via the stearoyl‐CoA desaturases FAT‐6 and FAT‐7, and the selenoprotein TRXR‐1 in C. elegans. This study implies a potential for Glu‐SeMet as a new treatment for obesity or its complications.