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，并且高血压常常与胰岛素抵抗共存。然而，盐的摄入对胰岛素抵抗的影响尚不清楚。本文介绍了三种盐敏感大鼠模型（高盐喂养Sprague-Dawley大鼠、Dahl盐敏感大鼠和慢性血管紧张素II （AII）输注大鼠）的胰岛素抵抗情况。所有三种模型的一个值得注意的共同观察结果是，尽管它们具有胰岛素抵抗，但从IR和IRSs激活到PI 3-激酶Akt激活的早期胰岛素信号传导步骤明显增强。这表明与盐敏感性高血压相关的胰岛素抵抗的分子机制是独特的。其他已知的导致胰岛素抵抗的因素，如肥胖，实际上抑制了早期胰岛素信号，但对于高盐摄入相关的胰岛素抵抗，受损的步骤必须在胰岛素信号通路的下游。更重要的是，氧化应激的增加似乎在高盐和高盐诱导的胰岛素抵抗中都起着至关重要的作用。

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.