A selenomethionine deficient, high-fructose diet does not lead to cardiometabolic disorder in the selenocysteine lyase knockout mice

Abstract

Background/purpose

High-fructose consumption is a driver of cardiometabolic disorders and metabolic syndrome, and selenium (Se) deficiency further increases the risk of developing these diseases. Consuming high amounts of fructose induces insulin resistance and oxidative stress, and alters the cardiac lipidome. Se may reduce the detrimental impacts of fructose through its incorporation into selenoproteins like the glutathione peroxidases 1 and 4, (GPX1,4) and the thioredoxin reductase 1 (TXNRD1) whose primary function is to curb oxidative stress. When Se levels are limited, selenocysteine lyase (SCLY) decomposes selenocysteine (Sec) to hydrogen selenide (H₂Se), and loss of Scly results in metabolic syndrome in mice. However, it is unknown if SCLY is required to sustain the synthesis of critical antioxidant selenoproteins to prevent oxidative stress, cardiometabolic disorders, and metabolic syndrome caused by high-fructose consumption.

Methods

In this study, we analyzed cardiometabolic parameters, the cardiac lipidome, and the cardiac protein levels of GPX and TXNRD in male and female whole-body Scly knockout (Scly KO) mice fed a selenomethionine (SeMet) deficient, high-fructose diet.

Results/conclusion

We found that selenomethionine deficiency, coupled with high-fructose consumption does not lead to cardiometabolic disorder in the Scly KO mice, and suggests that there are compensatory mechanisms involving Se metabolism that are protective against fructose-induced cardiometabolic disorder.