Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10870847 | FEBS Letters | 2014 | 7 Pages |
Abstract
Excessive fructose consumption and elevated glucocorticoids contribute to metabolic syndrome. We show that fructose as the only carbohydrate source is sufficient for the differentiation of 3T3-L1 fibroblasts into adipocytes. Differentiation of cells in fructose containing medium resulted in increased 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) expression and activity. Experiments with transfected HEK-293 cells suggested more efficient NADPH generation by fructose compared with glucose in the endoplasmic reticulum (ER). Adipocytes differentiated in the presence of fructose showed increased FABP4 expression, C/EBPα to C/EBPβ ratio and lipolysis. Thus, excessive fructose may cause adverse metabolic effects by enhancing 11β-HSD1 activity and increasing lipolysis in adipocytes.
Keywords
DMEMH6PDHF6P11β-HSDDulbecco’s modified eagles mediumHSLHprt11β-hydroxysteroid dehydrogenaseglucose transporter 5Glut5PPARγFBSTLCFFAC/EBPαAdipocyteAtglFree fatty acidsfetal bovine serumMetabolic syndromeendoplasmic reticulumFructosefructose-6-phosphateadipocyte triglyceride lipasehormone sensitive lipaseLipolysisMetabolismHexose-6-phosphate dehydrogenasehypoxanthine-guanine phosphoribosyltransferasethin layer chromatographyGlucocorticoidperoxisome proliferator-activated receptor γ
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Authors
Balázs Legeza, Zoltán Balázs, Alex Odermatt,