Yvan-Charvet Laurent, Bobard Alexandre, Bossard Pascale, Massiéra Florence, Rousset Xavier, Ailhaud Gérard, Teboul Michèle, Ferré Pascal, Dagher Georges, Quignard-Boulangé Annie
INSERM, U671, Centre Biomédical des Cordeliers, 75270 Paris Cedex 06, France.
Arterioscler Thromb Vasc Biol. 2007 Jun;27(6):1340-5. doi: 10.1161/ATVBAHA.106.136382. Epub 2007 Mar 15.
This study examines the role of insulin and angiotensin II in high-density lipoprotein (HDL) metabolism by focusing on the regulation and function of scavenger receptor type-BI (SR-BI) in adipose tissue.
Insulin or angiotensin II injection in wild-type mice induced a decrease in circulating HDL and it was associated with the translocation of SR-BI from intracellular sites to the plasma membrane of adipose tissue. Refeeding upregulated adipose HDL selective cholesteryl esters uptake and SR-BI proteins through transcriptional and posttranscriptional mechanisms. This occurred along with a decrease in serum HDL and an increase in adipose cholesterol content. Similar results were obtained with transgenic mice overexpressing locally angiotensinogen in adipose tissue. In adipose 3T3-L1 cell line, HDL induced lipogenesis by increasing liver X receptor binding activity. This mechanism was dependent of insulin and angiotensin II.
Our results raise the possibility that adipose tissue SR-BI translocation might be a link between adipose tissue lipid storage and HDL clearance.
本研究通过关注脂肪组织中B类I型清道夫受体(SR-BI)的调节和功能,探讨胰岛素和血管紧张素II在高密度脂蛋白(HDL)代谢中的作用。
给野生型小鼠注射胰岛素或血管紧张素II可导致循环HDL水平降低,并与SR-BI从细胞内位点转运至脂肪组织质膜有关。再喂养通过转录和转录后机制上调脂肪HDL选择性胆固醇酯摄取和SR-BI蛋白。这伴随着血清HDL降低和脂肪胆固醇含量增加。在脂肪组织中局部过表达血管紧张素原的转基因小鼠也得到了类似结果。在脂肪3T3-L1细胞系中,HDL通过增加肝脏X受体结合活性诱导脂肪生成。该机制依赖于胰岛素和血管紧张素II。
我们的结果提示,脂肪组织SR-BI易位可能是脂肪组织脂质储存与HDL清除之间的一个联系。