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- W1965015910 abstract "Rosiglitazone is a PPARγ 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 PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ 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 PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy." @default.
- W1965015910 created "2016-06-24" @default.
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- W1965015910 date "2011-07-01" @default.
- W1965015910 modified "2023-10-13" @default.
- W1965015910 title "Adiponectin Is Required for PPARγ-Mediated Improvement of Endothelial Function in Diabetic Mice" @default.
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- W1965015910 doi "https://doi.org/10.1016/j.cmet.2011.05.009" @default.
- W1965015910 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21723508" @default.
- W1965015910 hasPublicationYear "2011" @default.
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