Adiponectin Is Required for PPAR gamma-Mediated Improvement of Endothelial Function in Diabetic Mice
Publication in refereed journal


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摘要Rosiglitazone is a PPAR gamma agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPAR gamma effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPAR gamma activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPAR gamma-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy.
著者Wong WT, Tian XY, Xu AM, Yu J, Lau CW, Hoo RLC, Wang Y, Lee VWY, Lam KSL, Vanhoutte PM, Huang Y
期刊名稱Cell Metabolism
詳細描述To ORKTS: duplication
出版年份2011
月份7
日期6
卷號14
期次1
出版社CELL PRESS
頁次104 - 115
國際標準期刊號1550-4131
語言英式英語
Web of Science 學科類別Cell Biology; CELL BIOLOGY; Endocrinology & Metabolism; ENDOCRINOLOGY & METABOLISM

上次更新時間 2021-17-01 於 00:57