title: Critical review of acylation-stimulating protein physiology in humans and rodents.
abstract: 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.
authors.affiliation: McGill University, Cardiology, H7.30, Royal Victoria Hospital, 687 Pine Ave West, Montreal, Quebec, Canada H3A 1A1. katherine.cianflone@mcgill.ca
authors.forename: Katherine
authors.initials: K
authors.lastname: Cianflone
authors.forename: Zhunan
authors.initials: Z
authors.lastname: Xia
authors.forename: Lan Ying
authors.initials: LY
authors.lastname: Chen
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001798:Blood Proteins / Q000172:deficiency / Q000502:physiology*; D001835:Body Weight; D002318:Cardiovascular Diseases / Q000378:metabolism; D003176:Complement C3 / Q000378:metabolism / Q000502:physiology; D015926:Complement C3a / Q000031:analogs & derivatives*; D011415:Complement Factor B / Q000378:metabolism / Q000502:physiology; D011416:Complement Factor D; D003920:Diabetes Mellitus / Q000378:metabolism; D006801:Humans; D006949:Hyperlipidemias / Q000378:metabolism; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D009765:Obesity / Q000378:metabolism; D019518:Postprandial Period; D051381:Rats; D012697:Serine Endopeptidases / Q000378:metabolism / Q000502:physiology; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D001798:Blood Proteins; D003176:Complement C3; D020738:Leptin; D014280:Triglycerides; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; D012697:Serine Endopeptidases; C493488:CFD protein, human; D011416:Complement Factor D; C493491:complement factor D, mouse; D011415:Complement Factor B