Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona, Spain.
J Mol Endocrinol. 2010 Jul;45(1):33-43. doi: 10.1677/JME-09-0160. Epub 2010 Apr 16.
Antioxidant-based treatments are emerging as an interesting approach to possibly counteract obesity fat accumulation complications, since this is accompanied by an increased systemic oxidative stress. The aim of this study was to analyze specific metabolic effects of vitamin C (VC) on epididymal primary rat adipocytes. Cells were isolated and incubated for 72 h in culture medium, in the absence or presence of 1.6 nM insulin, within a range of VC concentrations (5-1000 microM). Glucose- and lipid-related variables as well as the secretion/expression patterns of several obesity-related genes were assessed. It was observed that VC dose dependently inhibited glucose uptake and lactate production, and also reduced glycerol release in both control and insulin-treated cells. Also, VC caused a dramatic concentration-dependent fall in leptin secretion especially in insulin-stimulated cells. In addition, VC (200 microM) induced Cdkn1a and Casp8, partially inhibited Irs3, and together with insulin drastically reduced Gpdh (listed as Gpd1 in the MGI database) gene expressions. Finally, VC and insulin down-regulatory effects were observed on extracellular and intracellular reactive oxygen species production respectively. In summary, this experimental assay describes a specific effect of VC in isolated rat adipocytes on glucose and fat metabolism, and on the secretion/expression of important obesity-related proteins.
抗氧化剂治疗方法作为一种可能对抗肥胖脂肪积累并发症的有趣方法正在出现,因为这伴随着全身性氧化应激的增加。本研究的目的是分析维生素 C (VC) 对附睾原代大鼠脂肪细胞的特定代谢影响。细胞在培养物中分离并孵育 72 小时,在无或存在 1.6 nM 胰岛素的情况下,在 VC 浓度范围内(5-1000 microM)。评估葡萄糖和脂质相关变量以及几种肥胖相关基因的分泌/表达模式。结果表明,VC 呈剂量依赖性抑制葡萄糖摄取和乳酸产生,并降低对照和胰岛素处理细胞中的甘油释放。此外,VC 特别在胰岛素刺激的细胞中引起瘦素分泌的显著浓度依赖性下降。此外,VC(200 microM)诱导 Cdkn1a 和 Casp8,部分抑制 Irs3,并与胰岛素一起大大降低 Gpdh(在 MGI 数据库中列为 Gpd1)基因的表达。最后,观察到 VC 和胰岛素对细胞外和细胞内活性氧物质产生分别具有下调作用。总之,这项实验描述了 VC 在分离的大鼠脂肪细胞中对葡萄糖和脂肪代谢以及重要肥胖相关蛋白的分泌/表达的特定作用。