Sniderman A D, Cianflone K
McGill Unit for the Prevention of Cardiovascular Disease, Royal Victoria Hospital, Montreal, Quebec, Canada.
Ann Med. 1994 Dec;26(6):388-93.
The adipsin-ASP pathway provides a mechanism by which the adipocyte is able to regulate its rate of de novo triglyceride synthesis and reesterification. The adipocyte can synthesize and secrete the three proteins necessary for the formation of the effector molecule, acylation stimulating protein (ASP). ASP increases membrane transport of glucose and the activity of diacylglycerol acyltransferase and by virtue of both of these effects markedly increases the rate of triglyceride synthesis. Awareness of the pathway will allow, we believe, a new understanding of the regulation of triglyceride removal from plasma. Accordingly, the concept of microenvironmental metabolic regulation of triglyceride hydrolysis at the endothelial surface and triglyceride synthesis within the adipocyte will be presented. In addition, the pathogenetic sequence by which dysfunction of this pathway can lead to dyslipoproteinaemia will be reviewed. Emphasis, however, will be placed on the role this pathway may play in the pathogenesis of obesity and the adaptation to negative caloric balance in the obese.
脂肪酶-ASP途径提供了一种机制,通过该机制脂肪细胞能够调节其从头合成甘油三酯和再酯化的速率。脂肪细胞可以合成并分泌形成效应分子酰化刺激蛋白(ASP)所需的三种蛋白质。ASP增加葡萄糖的膜转运以及二酰甘油酰基转移酶的活性,并且由于这两种作用,显著提高甘油三酯的合成速率。我们相信,了解该途径将有助于对从血浆中清除甘油三酯的调节有新的认识。因此,将介绍在内皮表面甘油三酯水解和脂肪细胞内甘油三酯合成的微环境代谢调节概念。此外,还将回顾该途径功能障碍导致血脂蛋白异常血症的发病机制顺序。然而,重点将放在该途径在肥胖症发病机制中可能发挥的作用以及肥胖者对负热量平衡的适应上。