title: Very low density lipoprotein metabolism and plasma adiponectin as predictors of high-density lipoprotein apolipoprotein A-I kinetics in obese and nonobese men.
abstract: BACKGROUND
  Hypercatabolism of high-density lipoprotein (HDL) apolipoprotein (apo) A-I results in low plasma apoA-I concentration. The mechanisms regulating apoA-I catabolism may relate to alterations in very low density lipoprotein (VLDL) metabolism and plasma adiponectin and serum amyloid A protein (SAA) concentrations.
  
  
  OBJECTIVE
  We examined the associations between the fractional catabolic rate (FCR) of HDL-apoA-I and VLDL kinetics, plasma adiponectin, and SAA concentrations.
  
  
  METHODS
  The kinetics of HDL-apoA-I and VLDL-apoB were measured in 50 obese and 37 nonobese men using stable isotopic techniques.
  
  
  RESULTS
  In the obese group, HDL-apoA-I FCR was positively correlated with insulin, homeostasis model of assessment for insulin resistance (HOMA-IR) score, triglycerides, VLDL-apoB, and VLDL-apoB production rate (PR). In the nonobese group, HDL-apoA-I FCR was positively correlated with triglycerides, apoC-III, VLDL-apoB, and VLDL-apoB PR and negatively correlated with plasma adiponectin. Plasma SAA was not associated with HDL-apoA-I FCR in either group. In multiple regression analyses, VLDL-apoB PR and HOMA-IR score, and VLDL-apoB PR and adiponectin were independently predictive of HDL-apoA-I FCR in the obese and nonobese groups, respectively. HDL-apoA-I FCR was positively and strongly associated with HDL-apoA-I PR in both groups.
  
  
  CONCLUSIONS
  Variation in VLDL-apoB production, and hence plasma triglyceride concentrations, exerts a major effect on the catabolism of HDL-apoA-I. Insulin resistance and adiponectin may also contribute to the variation in HDL-apoA-I catabolism in obese and nonobese subjects, respectively. We also hypothesize that apoA-I PR determines a steady-state, lowered plasma of apoA-I, which may reflect a compensatory response to a primary defect in the catabolism of HDL-apoA-I due to altered VLDL metabolism.
authors.affiliation: School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital, Perth, Western Australia 6847, Australia.
authors.forename: Dick C
authors.initials: DC
authors.lastname: Chan
authors.forename: P Hugh R
authors.initials: PH
authors.lastname: Barrett
authors.forename: Esther M M
authors.initials: EM
authors.lastname: Ooi
authors.forename: Juying
authors.initials: J
authors.lastname: Ji
authors.forename: Doris T
authors.initials: DT
authors.lastname: Chan
authors.forename: Gerald F
authors.initials: GF
authors.lastname: Watts
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D016632:Apolipoprotein A-I / Q000378:metabolism*; D001055:Apolipoproteins B / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008079:Lipoproteins, VLDL / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009765:Obesity / Q000378:metabolism*; D012044:Regression Analysis
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008075:Lipoproteins, HDL; D008079:Lipoproteins, VLDL