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Hormones responsible for the metabolic adaptation to brief fasting

負(fù)責(zé)代謝適應(yīng)短暫禁食的激素

說(shuō)人話就是，你短期絕食，代謝肯定要適應(yīng)這種變化對(duì)吧，那是什么激素讓代謝產(chǎn)生了這種適應(yīng)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，這一切都是為了提高脂解的速度，不是嗎。脂肪組織中的脂解速率由細(xì)胞內(nèi)cAMP的含量決定，cAMP對(duì)胰島素和去甲腎上腺素都有反應(yīng)。

說(shuō)白了就系camp干的好事，介個(gè)camp能對(duì)胰島素et去甲腎腺素有反應(yīng)，camp系一種腺苷，環(huán)磷酸腺苷，這玩意也是一種信使。。這玩意系atp脫了2個(gè)磷脂縮合的。。主要作用就系營(yíng)養(yǎng)心肌，換言之 這玩意越多，脂代謝越快

second messenger systems involved in activation of hormone-sensitive lipase

參與激素敏感脂肪酶激活的第二信使系統(tǒng)

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.

這種適應(yīng)的主要荷爾蒙因素是胰島素，或者更確切地說(shuō)，它的缺乏。由于缺乏正常的葡萄糖峰值（考慮到缺乏進(jìn)食），胰島素水平下降。胰島素是脂解的主要抑制劑，因?yàn)槠浼?xì)胞內(nèi)結(jié)構(gòu)域的酪氨酸激酶活性激活磷酸二酯酶，使細(xì)胞內(nèi)cAMP水平保持在較低水平。隨著胰島素水平的下降，背景交感神經(jīng)活性變得沒(méi)有對(duì)抗，激素敏感的脂肪酶開始分解其甘油三酯儲(chǔ)存，向血液中釋放美味的脂肪酸。

因?yàn)榘ゐI，自然血糖低，自然胰島素下降。胰島素高→脂肪消耗慢。胰島素高→脂肪解就快。camp低→脂肪酶就活躍了，甘油三酯就開始變成脂肪酸了。這些脂肪酸開始參與三羧酸循環(huán)

(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，該途徑中有三種脂肪酶，因?yàn)楦视蜕嫌腥齻€(gè)脂肪酸分子。只有第一種脂肪酶對(duì)激素敏感。）

介個(gè)有中學(xué)化學(xué)or生物基礎(chǔ)的應(yīng)該偶知道吧。。甘油三酯三個(gè)鍵，第一個(gè)鍵和后面兩個(gè)鍵連接的官能團(tuán)并不一樣，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，去甲腎上腺素增加了脂解速率（通過(guò)影響無(wú)聊而孤獨(dú)的β-3受體，它似乎在脂解之外沒(méi)有太多功能），而胰島素降低了脂解的速率。在經(jīng)常浸泡在去甲腎上腺素和胰島素輸注中的ICU患者中，哪種影響占主導(dǎo)地位？很難說(shuō)。與危重癥相關(guān)的兒茶酚胺過(guò)量肯定會(huì)導(dǎo)致脂解，即使在沒(méi)有外源性兒茶酚胺的情況下也是如此。

換言之β-3受體只會(huì)影響脂肪解，木有其他功能的樣子。。去甲腎上腺素這玩意是收camp影響的，camp低了，導(dǎo)致去甲腎上腺素高了，然后就增加了脂肪解

兒茶酚胺高了→脂肪gg快，胰島素高了→脂肪gg慢，去甲腎上腺素高了→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)

禁食時(shí)的蛋白水解和脂解沒(méi)有得到研究，但很明顯，胰島素缺乏也會(huì)激活蛋白水解途徑（因?yàn)殪o脈注射少量葡萄糖似乎會(huì)抑制蛋白水解）

這其實(shí)很好理解，胰島素少了→蛋白分解快。葡萄糖多了→蛋白水解慢 很合理的說(shuō)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?

這就引出了一個(gè)有趣的問(wèn)題。沒(méi)有人會(huì)躺在那里，在重癥監(jiān)護(hù)室的頭幾天安靜地挨餓。這些病人怎么了？

這個(gè)其實(shí)好解釋吧。。病人都快gg了。。體內(nèi)各種信號(hào)系統(tǒng) 通道系統(tǒng)都亂了唄。。

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.

他們?nèi)匀话ゐI。

但是，如果每天輸送150克（600千卡）左右的簡(jiǎn)單碳水化合物（即3升5%葡萄糖，或約600毫升Jevity），蛋白水解途徑就會(huì)被切斷。脂解仍在繼續(xù)，但外源性葡萄糖會(huì)導(dǎo)致足夠的胰島素釋放，從而中止生酮。

換言之，血糖對(duì)于蛋白水解 et 脂肪水解雖然都有抑制作用。然而一個(gè)是直接的，一個(gè)是間接的。前者直接影響，然而原理我我還沒(méi)研究。后者則是間接影響，通過(guò)血糖→胰島素→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.

簡(jiǎn)而言之，給患者喂食哪怕是少量的碳水化合物也可以防止酮癥和蛋白質(zhì)分解代謝。

偷偷地，通過(guò)將胰島素作為胰島素-葡萄糖輸注的一部分來(lái)給藥，可以達(dá)到同樣的效果。按照方案速率（80ml/小時(shí)），24小時(shí)內(nèi)只能產(chǎn)生1920ml的5%葡萄糖，這還差100克（或400千卡）；但外源性胰島素?zé)o論如何都會(huì)切斷生酮和蛋白水解。

這個(gè)很好理解啦，血糖 et 胰島素是線性正相關(guān)，那你往患者體內(nèi)注入哪個(gè)其實(shí)意思都差不多的說(shuō)喵。。