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果糖促进 3T3-L1 脂肪细胞的分化,并加速脂代谢。

Fructose promotes the differentiation of 3T3-L1 adipocytes and accelerates lipid metabolism.

机构信息

Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.

Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.

出版信息

FEBS Lett. 2014 Jan 31;588(3):490-6. doi: 10.1016/j.febslet.2013.12.014. Epub 2013 Dec 24.

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.

摘要

过量的果糖摄入和升高的糖皮质激素会导致代谢综合征。我们发现,仅用果糖作为碳水化合物来源,就足以使 3T3-L1 成纤维细胞分化为脂肪细胞。在含有果糖的培养基中培养细胞,会导致 11β-羟类固醇脱氢酶 1(11β-HSD1)的表达和活性增加。用转染的 HEK-293 细胞进行的实验表明,与葡萄糖相比,果糖在细胞内质网(ER)中更有效地生成 NADPH。在果糖存在的情况下分化的脂肪细胞显示出 FABP4 表达、C/EBPα 与 C/EBPβ 比值和脂肪分解增加。因此,过量的果糖可能通过增强 11β-HSD1 活性和增加脂肪细胞中的脂肪分解来引起不良的代谢效应。

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