Liu Yuanxin, Liu Cuiping, Jiang Chao, Wang Su, Yang Qichao, Jiang Dan, Yuan Guoyue
Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China.
Public Laboratory Platform, First Affiliated Hospital of Najing Medical University, Nanjing 210029, China.
Biochem Biophys Res Commun. 2016 Mar 25;472(1):19-25. doi: 10.1016/j.bbrc.2016.01.143. Epub 2016 Jan 23.
Adiponectin, an adipose-specific protein hormone, is secreted from white adipose tissue and involved in glucose and lipid metabolism. It is assembled into low-molecular-weight trimer (LMW), middle-molecular-weight hexameric (MMW) and high-molecular-weight (HMW), among which HMW exhibits higher activity. In this study, we proved that C-reactive protein (CRP), an inflammatory marker, inhibited adiponectin expression, especially HMW in time-and dose-dependent manners. Furthermore, CRP decreased the HMW/total adiponectin ration and reduced adiponectin assembly by increasing ERp44, and decreasing Ero1-α and DsbA-L. CRP activated pAkt, the downstream of PI3K. Inhibition of PI3K or pAkt abolished the effect of CRP. Our study suggested that CRP decreased adiponectin expression and multimerization, while CRP-induced decline in adiponectin might be mediated through the PI3K/Akt pathway.
脂联素是一种脂肪特异性蛋白质激素，由白色脂肪组织分泌，参与葡萄糖和脂质代谢。它可组装成低分子量三聚体（LMW）、中分子量六聚体（MMW）和高分子量（HMW），其中HMW表现出更高的活性。在本研究中，我们证明炎症标志物C反应蛋白（CRP）以时间和剂量依赖性方式抑制脂联素表达，尤其是HMW。此外，CRP通过增加ERp44、降低Ero1-α和DsbA-L来降低HMW/总脂联素比值并减少脂联素组装。CRP激活PI3K的下游pAkt。抑制PI3K或pAkt可消除CRP的作用。我们的研究表明，CRP降低脂联素表达和多聚化，而CRP诱导的脂联素下降可能通过PI3K/Akt途径介导。
