ArticleJournal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)2025
A selenomethionine deficient, high-fructose diet does not lead to cardiometabolic disorder in the selenocysteine lyase knockout mice.
Article in Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
background/purposeHigh-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 (H
methodsIn 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/
conclusionWe 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.
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