Department of Nutrition, University of Massachusetts, Amherst, Massachusetts 01003, USA.
Nutr Rev. 2011 Mar;69(3):155-61. doi: 10.1111/j.1753-4887.2011.00377.x.
Insulin resistance and type 2 diabetes have been treated with the PPARγ agonists thiazolidinediones, or TZDs, since the 1990s. One mechanism by which these drugs may work is through PPARγ-mediated upregulation of adiponectin, an endogenous adipokine that has been shown to increase insulin sensitivity. Interestingly, α- and γ-tocopherol, two vitamin E vitamers, have structural similarities to the TZDs and have also been linked to enhanced insulin sensitivity. A recent study identified a novel function of α- and γ-tocopherol in 3T3-L1 preadipocytes: upregulation of an endogenous ligand involved in activating PPARγ. This study also found that tocopherols dramatically enhanced adiponectin expression and that this effect was mediated through a PPARγ-dependent process. These findings illustrate a possible mechanistic link between vitamin E and insulin sensitivity.
自 20 世纪 90 年代以来，过氧化物酶体增殖物激活受体γ（PPARγ）激动剂噻唑烷二酮类药物（TZDs）一直被用于治疗胰岛素抵抗和 2 型糖尿病。这些药物可能的作用机制之一是通过 PPARγ 介导的脂联素（一种内源性脂肪因子）的上调，脂联素已被证明可以增加胰岛素敏感性。有趣的是，α-和γ-生育酚，两种维生素 E 的同分异构体，与 TZDs 具有结构相似性，并且也与增强胰岛素敏感性有关。最近的一项研究确定了 α-和γ-生育酚在 3T3-L1 前脂肪细胞中的一个新功能：上调一种内源性配体，该配体参与激活 PPARγ。这项研究还发现，生育酚可显著增强脂联素的表达，而这种作用是通过 PPARγ 依赖的过程介导的。这些发现说明了维生素 E 和胰岛素敏感性之间可能存在一种机制联系。
