创伤应激后的脂肪代谢

Fat metabolism following traumatic stress

创伤后脂肪代谢的特点是消化吸收障碍、肝脏摄取减少、脂肪动员、肝脏输出、肝外组织摄取、脂肪氧化产能、甘油三酯水解-再酯化循环增加等，这些变化机制与交感神经兴奋、胰岛素抵抗和炎症反应有关，使脂肪取代葡萄糖成为主要能源物质。补充葡萄糖可以抑制脂肪氧化但不能抑制脂肪水解和再酯化，补充长链脂肪乳能预防必需脂肪酸缺乏，补充胆固醇能促进脂肪乳吸收和利用。通过干预脂肪代谢，有望改善创伤的预后。

Lipids metabolism can change after traumas such as operation or injury. The process is comprised of accelerated hydrolysis of triglyceride in adipose tissue, accelerated absorption of fatty acids by extra-hepatic tissue, improved lipid oxidation rate, and augmented re-esterification of fatty acids in liver and adipose tissue. Mechanisms of lipid mobilization include sympathetic stimulation, insulin resistance, and inflammation. However, lipid absorption by liver and intestine is .inhibited after trauma. Through post-trauma nutritional support, glucose administration improves re-esterification of fatty acids and inhibits lipid oxidation without affecting lipolysis. Fat emulsion infusion inhibits both absorption and secretion of triglyceride in liver. Therefore, clinicians should avoid over-alimentation of glucose and fat to prevent lipid overload, particularly in liver. Intervention of post-trau- matic lipid metabolism improves the outcomes： administration of long-chain triglycerides can prevent exhaustion of essential fatty acids, and administration of cholesterol can improve absorption and oxidation of fat emulsion.