Cianflone Katherine, Xia Zhunan, Chen Lan Ying
McGill University, Cardiology, H7.30, Royal Victoria Hospital, 687 Pine Ave West, Montreal, Quebec, Canada H3A 1A1.
Biochim Biophys Acta. 2003 Jan 31;1609(2):127-43. doi: 10.1016/s0005-2736(02)00686-7.
In the last few years, there has been increasing interest in the physiological role of acylation-stimulating protein (ASP). Recent studies in rats and mice, in particular in C3 (-/-) mice that are ASP deficient, have advanced our understanding of the role of ASP. Of note, the background strain of the mice influences the phenotype of delayed postprandial triglyceride clearance in ASP-deficient mice. Administration of ASP in all types of lean and obese mice studied to date, however, enhances postprandial triglyceride clearance. On the other hand, regardless of the background strain, ASP-deficient mice demonstrate reduced body weight, reduced leptin and reduced adipose tissue mass, suggesting that ASP deficiency results in protection against development of obesity. In humans, a number of studies have examined the relationship between ASP, obesity, diabetes and dyslipidemia as well as the influence of diet, exercise and pharmacological therapy. While many of these studies have small subject numbers, interesting observations may help us to better understand the parameters that may influence ASP production and ASP action. The aim of the present review is to provide a comprehensive overview of the recent literature on ASP, with particular emphasis on those studies carried out in rodents and humans.
在过去几年中,人们对酰化刺激蛋白(ASP)的生理作用越来越感兴趣。最近在大鼠和小鼠身上开展的研究,特别是在缺乏ASP的C3(-/-)小鼠身上进行的研究,加深了我们对ASP作用的理解。值得注意的是,小鼠的背景品系会影响ASP缺陷小鼠餐后甘油三酯清除延迟的表型。然而,在迄今为止研究的所有类型的瘦小鼠和肥胖小鼠中,给予ASP均可增强餐后甘油三酯的清除。另一方面,无论背景品系如何,ASP缺陷小鼠的体重、瘦素水平和脂肪组织量均降低,这表明ASP缺乏可预防肥胖的发生。在人类中,许多研究探讨了ASP、肥胖、糖尿病和血脂异常之间的关系,以及饮食、运动和药物治疗的影响。虽然其中许多研究的受试者数量较少,但有趣的观察结果可能有助于我们更好地理解可能影响ASP产生和ASP作用的参数。本综述的目的是全面概述近期关于ASP的文献,特别强调在啮齿动物和人类中开展的那些研究。