title: Response of plasma ASP to a prolonged fast.
abstract: OBJECTIVE
  To determine the changes in the plasma level of acylation stimulating protein (ASP) during a one month total fast in female subjects with marked obesity.
  
  
  METHODS
  Patients with marked obesity underwent a month total fast, before, during (2 weeks), and at the end of which, a variety of relevant metabolic parameters were measured.
  
  
  METHODS
  A metabolic unit of a teaching hospital.
  
  
  METHODS
  10 women with marked obesity were studied and the results compared with those in 16 age-matched controls.
  
  
  METHODS
  Plasma ASP, lipoprotein lipids, apoB, free fatty acid, and ketone levels.
  
  
  RESULTS
  At baseline, fasting levels of ASP in the obese group were double that in control subjects (116 +/- 26 vs 53 +/- 30 nM P < 0.001). During the fast, ASP levels dropped progressively and were within the normal range at the end of the study (63 +/- 16 vs 53 +/- 30 nM pNS). In addition, there was a strong correlation between the plasma ASP at baseline before beginning the fast and the 4 week drop in ASP. That is, those subjects who had the highest starting ASP also had the largest 4 week drop in ASP (r2 = 0.644, P < 0.005). Of interest, as plasma ASP levels dropped, plasma free fatty acid and ketone levels rose and when all timepoints were considered, there was a significant inverse relation between plasma ASP and plasma free fatty acid (r2 = 0.295, P < 0.0002).
  
  
  CONCLUSIONS
  The pattern of responses during the fast is that of increasing mobilization of fatty acids from adipose tissue coincident with decreased activity of the pathway responsible for the storage of adipocyte triglyceride mass. The data are consistent, therefore, with the role proposed for ASP as a major determinant of the rate of triglyceride synthesis in human adipocytes and thus a potentially important factor in the pathophysiology of obesity.
authors.affiliation: McGill Unit for the Prevention of Cardiovascular Disease, Royal Victoria Hospital, Montreal, Canada.
authors.forename: K
authors.initials: K
authors.lastname: Cianflone
authors.forename: D
authors.initials: D
authors.lastname: Kalant
authors.forename: E B
authors.initials: EB
authors.lastname: Marliss
authors.forename: R
authors.initials: R
authors.lastname: Gougeon
authors.forename: A D
authors.initials: AD
authors.lastname: Sniderman
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001055:Apolipoproteins B / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D015926:Complement C3a / Q000031:analogs & derivatives*; D005215:Fasting / Q000097:blood*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D013997:Time Factors; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D001055:Apolipoproteins B; D001798:Blood Proteins; D005230:Fatty Acids, Nonesterified; D014280:Triglycerides; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; D002784:Cholesterol