Hadji Lilas, Berger Emmanuelle, Soula Hédi, Vidal Hubert, Géloën Alain
Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France.
Université de Lyon, CARMEN INSERM U1060, INSA-Lyon, F-69621, Villeurbanne, France; IXXI Complex Systems Institute, F-69007, Lyon, France; EPI BEAGLE INRIA F-69621, Villeurbanne, France.
PLoS One. 2014 Aug 29;9(8):e106214. doi: 10.1371/journal.pone.0106214. eCollection 2014.
Adipocyte size and body fat distribution are strongly linked to the metabolic complications of obesity. The aim of the present study was to test the plasticity of white adipose tissue in response to insulin deprivation and replacement. We have characterized the changes of adipose cell size repartition and gene expressions in type 1 diabetes Sprague-Dawley rats and type 1 diabetic supplemented with insulin.
Using streptozotocin (STZ)-induced diabetes, we induced rapid changes in rat adipose tissue weights to study the changes in the distribution of adipose cell sizes in retroperitoneal (rWAT), epididymal (eWAT) and subcutaneous adipose tissues (scWAT). Adipose tissue weights of type 1 diabetic rats were then rapidly restored by insulin supplementation. Cell size distributions were analyzed using multisizer IV (Beckman Coulter). Cell size changes were correlated to transcriptional regulation of genes coding for proteins involved in lipid and glucose metabolisms and adipocytokines.
The initial body weight of the rats was 465±5.2 g. Insulin privation was stopped when rats lost 100 g which induced reductions in fat mass of 68% for rWAT, 42% for eWAT and 59% for scWAT corresponding to decreased mode cell diameters by 31.1%, 20%, 25.3%, respectively. The most affected size distribution by insulin deprivation was observed in rWAT. The bimodal distribution of adipose cell sizes disappeared in response to insulin deprivation in rWAT and scWAT. The most important observation is that cell size distribution returned close to control values in response to insulin treatment. mRNAs coding for adiponectin, leptin and apelin were more stimulated in scWAT compared to other depots in diabetic plus insulin group.
Fat depots have specific responses to insulin deprivation and supplementation. The results show that insulin is a major determinant of bimodal cell repartition in adipose tissues.
脂肪细胞大小和体脂分布与肥胖的代谢并发症密切相关。本研究的目的是测试白色脂肪组织对胰岛素剥夺和补充的可塑性。我们已经对1型糖尿病斯普拉格-道利大鼠以及补充胰岛素的1型糖尿病大鼠的脂肪细胞大小重新分布和基因表达变化进行了表征。
使用链脲佐菌素(STZ)诱导的糖尿病,我们诱导大鼠脂肪组织重量快速变化,以研究腹膜后(rWAT)、附睾(eWAT)和皮下脂肪组织(scWAT)中脂肪细胞大小分布的变化。然后通过补充胰岛素使1型糖尿病大鼠的脂肪组织重量迅速恢复。使用多通道粒度分析仪IV(贝克曼库尔特公司)分析细胞大小分布。细胞大小变化与参与脂质和葡萄糖代谢以及脂肪细胞因子的蛋白质编码基因的转录调控相关。
大鼠的初始体重为465±5.2克。当大鼠体重减轻100克时停止胰岛素剥夺,这导致rWAT的脂肪量减少68%,eWAT减少42%,scWAT减少59%,相应地,模式细胞直径分别减少31.1%、20%、25.3%。胰岛素剥夺对rWAT的大小分布影响最大。rWAT和scWAT中脂肪细胞大小的双峰分布在胰岛素剥夺后消失。最重要的观察结果是,胰岛素治疗后细胞大小分布恢复到接近对照值。与糖尿病加胰岛素组的其他脂肪库相比,scWAT中脂联素、瘦素和apelin的编码mRNA受到的刺激更大。
脂肪库对胰岛素剥夺和补充有特定反应。结果表明胰岛素是脂肪组织中双峰细胞重新分布的主要决定因素。