Molecular mechanisms of insulin-and exercise-induced glucose uptake

众所周知，过量的盐摄入会导致血压升高，高血压往往与胰岛素抵抗并存。然而，盐摄入量对胰岛素抵抗发展的贡献仍不清楚。本文对三种盐敏感大鼠模型(高盐喂养的SpragueDawley大鼠、Dahl盐敏感大鼠和慢性血管紧张素II(AII)注射大鼠)的胰岛素抵抗进行了综述。三种模型共有的一个值得注意的观察是，尽管它们存在胰岛素抵抗，但从IR和IRS激活到PI 3-Kinase Akt激活的早期胰岛素信号步骤明显增强。提示盐敏感型高血压胰岛素抵抗的分子机制是独一无二的。其他已知的导致胰岛素抵抗的因素--例如肥胖--实际上抑制了早期的胰岛素信号，但对于与高盐摄入相关的胰岛素抵抗，受损的一步必须位于胰岛素信号通路的下游。更重要的是，氧化应激增加似乎是MI和高盐诱导的胰岛素抵抗的关键因素。

It is well known that excessive salt intake induces elevation of blood pressure and that hypertension often coexists with insulin resistance. The contribution made by salt intake to the development of insulin resistance remains unclear, however. In this minireview, the insulin resistance seen in three salt-sensitive rat models (the high-salt-fed Sprague-Dawley rat, the Dahl salt sensitive rat and the chronically angiotensin II (AII)-infused rat) are presented. One notable observation common to all three models was that, despite their insulin-resistance, the early insulin signaling steps leading from activation of IR and IRSs to activation of PI 3-kinase Akt were apparently enhanced. This suggests that the molecular mechanism underlying the insulin resistance related to the salt-sensitive hypertension is unique. Other factors known to cause insulin resistance -e.g., obesity -actually suppress early insulin signaling, but for insulin resistance related to high salt intake, the impaired step must be further downstream in the insulin signaling pathway. What's more, increased oxidative stress appears to be crucially involved in both MI-and high-salt-induced insulin resistance.