title: Interrelationships between the kinetics of VLDL subspecies and HDL catabolism in abdominal obesity: a multicenter tracer kinetic study.
abstract: BACKGROUND
  Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relates due to accelerated HDL catabolism, but the underlying mechanism requires further elucidation. The relationships between HDL catabolism and other variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL1, VLDL2) kinetics, liver fat, or visceral adiposity, remain to be investigated.
  
  
  OBJECTIVE
  Our aim was to study the associations between HDL apolipoprotein (apo)-A-I fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and estimates of liver and visceral and sc fat.
  
  
  METHODS
  We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity.
  
  
  RESULTS
  In a multivariate analysis, among the morphological and biological parameters that may predict apoA-I FCR, liver fat (β = .400, P = .003), and VLDL1-apoB (β = .307, P = .020) were independently associated with apoA-I FCR. In a multivariate analysis, among the kinetic parameters, VLDL1-triglycerides (TGs) indirect FCR (β = -.357, P = .001), VLDL1-TG production rate (β = 0.213, P = .048), and apoA-II FCR (β = .667, P < .0001) were independently associated with apoA-I FCR. After adjustment for VLDL1-TG production rate, liver fat was no more correlated with apoA-I FCR. No association between apoA-I FCR and visceral fat was observed.
  
  
  CONCLUSIONS
  We show that VLDL1 is an important independent determinant of apoA-I FCR and more precisely that apoA-I FCR is independently associated with both catabolism and the production of VLDL1-TG. In addition, we show an association between liver fat and apoA-I FCR that is mostly mediated by VLDL1-TG production. These data indicate that, in abdominal obesity, dysfunctional VLDL1 metabolism is an important modulator of HDL apoA-I catabolism.
authors: Departments of Endocrinology-Diabetology (B.V., I.R.) and Medical Biology (L.D.), University Hospital, and INSERM CRI 866 (B.V., L.D.), 21000 Dijon, France; Departments of Molecular and Clinical Medicine (M.A., J.B.) and Mathematical Sciences (M.A.), University of Gothenburg, S-405 30 Gothenburg, Sweden; Faculty of Engineering, Computing, and Mathematics (H.B.), University of Western Australia, Perth, Western Australia 6872, Australia; Lipid Disorders Clinic (H.B., G.F.W., D.C.), Metabolic Research Centre, Department of Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia 6847, Australia; and Heart and Lung Centre (S.S., N.M., M.-R.T.), Helsinki University Central Hospital and Research Programs' Unit, Department of Diabetes and Obesity, University of Helsinki, and Department of Medicine (N.M., J.K.), Helsinki University Central Hospital, 00290 Helsinki, Finland.
authors: Bruno
authors: B
authors: Vergès
authors: Martin
authors: M
authors: Adiels
authors: Jan
authors: J
authors: Boren
authors: Peter Hugh
authors: PH
authors: Barrett
authors: Gerald F
authors: GF
authors: Watts
authors: Dick
authors: D
authors: Chan
authors: Laurence
authors: L
authors: Duvillard
authors: Sanni
authors: S
authors: Söderlund
authors: Niina
authors: N
authors: Matikainen
authors: Juhani
authors: J
authors: Kahri
authors: Isabelle
authors: I
authors: Robin
authors: Marja-Riitta
authors: MR
authors: Taskinen
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D001053:Apolipoproteins / Q000378:metabolism*; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008079:Lipoproteins, VLDL / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D056128:Obesity, Abdominal / Q000378:metabolism*
chemical_list: D001053:Apolipoproteins; D008075:Lipoproteins, HDL; D008079:Lipoproteins, VLDL