【十翻】p2【渣自翻】参与激素敏感脂肪酶激活的第二信使系统second messenger system

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Hormones responsible for the metabolic adaptation to brief fasting

负责代谢适应短暂禁食的激素

说人话就是，你短期绝食，代谢肯定要适应这种变化对吧，那是什么激素让代谢产生了这种适应呢

Well, its all about increasing the rate of lipolysis, is it not. And the rate of lipolysis in fatty tissues is governed by the intracellular content of cAMP, which responds to both insulin and noradrenaline.

好吧，这一切都是为了提高脂解的速度，不是吗。脂肪组织中的脂解速率由细胞内cAMP的含量决定，cAMP对胰岛素和去甲肾上腺素都有反应。

说白了就系camp干的好事，介个camp能对胰岛素et去甲肾腺素有反应，camp系一种腺苷，环磷酸腺苷，这玩意也是一种信使。。这玩意系atp脱了2个磷脂缩合的。。主要作用就系营养心肌，换言之 这玩意越多，脂代谢越快

second messenger systems involved in activation of hormone-sensitive lipase

参与激素敏感脂肪酶激活的第二信使系统

激素-敏感 ？敏感性激素把？

The major hormonal player in this adaptation is insulin, or rather, its lack. With the absence of regular glucose peaks (given the lack of eating) insulin levels drop. Insulin is the primary inhibitor of lipolysis, because the tyrosine kinase activity of its intracellular domain activates a phosphodiesterase, which keeps intracellular cAMP levels low. As insulin levels drop, the background sympathetic activity becomes unopposed, and the hormone sensitive lipase begins to dismantle their triglyceride stores, releasing delicious fatty acids into the bloodstream.

这种适应的主要荷尔蒙因素是胰岛素，或者更确切地说，它的缺乏。由于缺乏正常的葡萄糖峰值（考虑到缺乏进食），胰岛素水平下降。胰岛素是脂解的主要抑制剂，因为其细胞内结构域的酪氨酸激酶活性激活磷酸二酯酶，使细胞内cAMP水平保持在较低水平。随着胰岛素水平的下降，背景交感神经活性变得没有对抗，激素敏感的脂肪酶开始分解其甘油三酯储存，向血液中释放美味的脂肪酸。

因为挨饿，自然血糖低，自然胰岛素下降。胰岛素高→脂肪消耗慢。胰岛素高→脂肪解就快。camp低→脂肪酶就活跃了，甘油三酯就开始变成脂肪酸了。这些脂肪酸开始参与三羧酸循环

(Yes, there are three lipases in the pathway, because there are three fatty acid molecules attached to the glycerol. Only the first lipase is hormone-sensitive.)

（是的，该途径中有三种脂肪酶，因为甘油上有三个脂肪酸分子。只有第一种脂肪酶对激素敏感。）

介个有中学化学or生物基础的应该偶知道吧。。甘油三酯三个键，第一个键和后面两个键连接的官能团并不一样，很合理。。

So, noradrenaline increases the rate of lipolysis (by affecting the bored and lonely beta-3 receptor, which doesn't seem to have much of a function outside of lipolysis), and insulin decreases the rate of lipolysis. Which effect is dominant in ICU patients who are frequently marinading in infusions of both noradrenaline and insulin? Hard to say. The catecholamine excess associated with critical illness definitely causes lipolysis, even in absence of exogenous catecholamines.

因此，去甲肾上腺素增加了脂解速率（通过影响无聊而孤独的β-3受体，它似乎在脂解之外没有太多功能），而胰岛素降低了脂解的速率。在经常浸泡在去甲肾上腺素和胰岛素输注中的ICU患者中，哪种影响占主导地位？很难说。与危重症相关的儿茶酚胺过量肯定会导致脂解，即使在没有外源性儿茶酚胺的情况下也是如此。

换言之β-3受体只会影响脂肪解，木有其他功能的样子。。去甲肾上腺素这玩意是收camp影响的，camp低了，导致去甲肾上腺素高了，然后就增加了脂肪解

儿茶酚胺高了→脂肪gg快，胰岛素高了→脂肪gg慢，去甲肾上腺素高了→脂肪gg快

Proteolysis in fasting is not studied as well as lipolysis, but it is clear that an insulin deficit also activates proteolytic pathways (because the administration of small amounts of intravenous dextrose seems to inhibit proteolysis)

禁食时的蛋白水解和脂解没有得到研究，但很明显，胰岛素缺乏也会激活蛋白水解途径（因为静脉注射少量葡萄糖似乎会抑制蛋白水解）

这其实很好理解，胰岛素少了→蛋白分解快。葡萄糖多了→蛋白水解慢 很合理的说poi

Which brings up an interesting question. Nobody ever just lies there and starves quietly for their first few days in the ICU. What happens to these patients?

这就引出了一个有趣的问题。没有人会躺在那里，在重症监护室的头几天安静地挨饿。这些病人怎么了？

这个其实好解释吧。。病人都快gg了。。体内各种信号系统 通道系统都乱了呗。。

They still starve.

But, if 150g (600kcal) or so of simple carbohydrate is delivered every day (which is 3 litres of 5% dextrose, or around 600ml of Jevity), the proteolytic pathway is switched off. Lipolysis continues, but the exogenous glucose results in enough insulin release to abort the ketogenesis.

他们仍然挨饿。

但是，如果每天输送150克（600千卡）左右的简单碳水化合物（即3升5%葡萄糖，或约600毫升Jevity），蛋白水解途径就会被切断。脂解仍在继续，但外源性葡萄糖会导致足够的胰岛素释放，从而中止生酮。

换言之，血糖对于蛋白水解 et 脂肪水解虽然都有抑制作用。然而一个是直接的，一个是间接的。前者直接影响，然而原理我我还没研究。后者则是间接影响，通过血糖→胰岛素→脂肪水解

In short, feeding your patient even a tiny amount of carbohydrate will prevent ketosis and protein catabolism.

Sneakily, one can achieve the same effect by administering insulin as a part of an insulin-dextrose infusion. At protocol rate (80ml/hr) one ends up giving only 1920ml of 5% dextrose in 24 hours, which is just short of 100g (or 400kCal); but the exogenous insulin switches off the ketogenesis and proteolysis anyway.

简而言之，给患者喂食哪怕是少量的碳水化合物也可以防止酮症和蛋白质分解代谢。

偷偷地，通过将胰岛素作为胰岛素-葡萄糖输注的一部分来给药，可以达到同样的效果。按照方案速率（80ml/小时），24小时内只能产生1920ml的5%葡萄糖，这还差100克（或400千卡）；但外源性胰岛素无论如何都会切断生酮和蛋白水解。

这个很好理解啦，血糖 et 胰岛素是线性正相关，那你往患者体内注入哪个其实意思都差不多的说喵。。