| First Author | Wong WT | Year | 2011 |
| Journal | Cell Metab | Volume | 14 |
| Issue | 1 | Pages | 104-15 |
| PubMed ID | 21723508 | Mgi Jnum | J:176078 |
| Mgi Id | MGI:5288287 | Doi | 10.1016/j.cmet.2011.05.009 |
| Citation | Wong WT, et al. (2011) Adiponectin is required for PPARgamma-mediated improvement of endothelial function in diabetic mice. Cell Metab 14(1):104-15 |
| abstractText | Rosiglitazone is a PPARgamma 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 PPARgamma effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARgamma 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 PPARgamma-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. |
