| Literature DB >> 24374344 |
Balázs Legeza1, Zoltán Balázs1, Alex Odermatt2.
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.Entities:
Keywords: 11β-HSD; 11β-hydroxysteroid dehydrogenase; 11β-hydroxysteroid dehydrogensae; ATGL; Adipocyte; C/EBPα; CCAT/enhancer-binding protein α; DMEM; Dulbecco’s modified Eagles medium; ER; F6P; FBS; FFA; Fructose; GLUT5; Glucocorticoid; H6PDH; HPRT; HSL; Lipolysis; Metabolic syndrome; Metabolism; PPARγ; TLC; adipocyte triglyceride lipase; endoplasmic reticulum; fetal bovine serum; free fatty acids; fructose-6-phosphate; glucose transporter 5; hexose-6-phosphate dehydrogenase; hormone sensitive lipase; hypoxanthine-guanine phosphoribosyltransferase; peroxisome proliferator-activated receptor γ; thin layer chromatography
Mesh：
Substances：
Year: 2013 PMID： 24374344 DOI： 10.1016/j.febslet.2013.12.014
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124