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Mol Nutr Food Res ; 63(4): e1800784, 2019 02.
Article in English | MEDLINE | ID: mdl-30467983

ABSTRACT

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.


Subject(s)
Caenorhabditis elegans Proteins/metabolism , Caenorhabditis elegans/drug effects , Selenomethionine/analogs & derivatives , Selenomethionine/pharmacology , Thioredoxin Reductase 1/metabolism , Animals , Caenorhabditis elegans/metabolism , Caenorhabditis elegans Proteins/genetics , Diet/adverse effects , Fatty Acids/analysis , Fatty Acids/metabolism , Glucose/adverse effects , Lipid Metabolism/drug effects , Lipid Metabolism/genetics , Mutation , Stearoyl-CoA Desaturase/genetics , Stearoyl-CoA Desaturase/metabolism , Thioredoxin Reductase 1/genetics , Triglycerides/metabolism
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