Adiponectin Is Required for PPAR gamma-Mediated Improvement of Endothelial Function in Diabetic Mice
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AbstractRosiglitazone 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.
All Author(s) ListWong WT, Tian XY, Xu AM, Yu J, Lau CW, Hoo RLC, Wang Y, Lee VWY, Lam KSL, Vanhoutte PM, Huang Y
Journal nameCell Metabolism
Detailed descriptionTo ORKTS: duplication
Volume Number14
Issue Number1
Pages104 - 115
LanguagesEnglish-United Kingdom
Web of Science Subject CategoriesCell Biology; CELL BIOLOGY; Endocrinology & Metabolism; ENDOCRINOLOGY & METABOLISM

Last updated on 2020-13-09 at 02:51