期刊
CELL METABOLISM
卷 14, 期 1, 页码 104-115出版社
CELL PRESS
DOI: 10.1016/j.cmet.2011.05.009
关键词
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资金
- Hong Kong Research Grant Council [4653/08M, 466110, HKU 2/07C, HKU4/CRF10]
- CUHK
- CUHK Li Ka Shing Institute of Health Sciences
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.
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