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首页> 外文期刊>Cell metabolism >Adiponectin is required for PPARgamma-mediated improvement of endothelial function in diabetic mice.
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Adiponectin is required for PPARgamma-mediated improvement of endothelial function in diabetic mice.

机译：脂联素是糖尿病小鼠中PPARγ介导的内皮功能改善所必需的。

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摘要

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.
机译：罗格列酮是通常用于治疗糖尿病的PPARγ激动剂。除了提高胰岛素敏感性外，罗格列酮还通过一种尚不为人所知的机制恢复了正常的血管功能。在这里，我们显示脂联素是必需的，以介导PPARgamma对糖尿病小鼠血管内皮的作用。在db / db和饮食诱导的肥胖小鼠中，罗格列酮对PPARγ的激活可恢复主动脉的内皮依赖性舒张，而缺乏脂联素或经抗脂联素抗体治疗的糖尿病小鼠则无反应。罗格列酮刺激脂联素从脂肪外植体中释放，罗格列酮治疗小鼠的皮下脂肪移植在未经治疗的db / db受体中概括了血管舒张。从机理上讲，脂联素激活了主动脉中的AMPK / eNOS和cAMP / PKA信号通路，从而增加了NO的生物利用度并降低了氧化应激。综上所述，这些结果表明，脂肪细胞衍生的脂联素是PPARγ介导的糖尿病内皮功能改善所必需的。因此，脂肪组织代表了治疗糖尿病性血管病的有希望的靶标。

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