Copyright © 2014 by the Endocrine Society. Context: Low plasma high-density lipoprotein (HDL) cholesterol is a major abnormality in abdominal obesity. This relatesdueto acceleratedHDLcatabolism, but the underlyingmechanismrequires 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. Objectives: 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. Design: Wecarried 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: Weshow 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, weshowanassociationbetweenliver fatandapoA-IFCRthat ismostlymediated byVLDL1-TG production. These data indicate that, inabdominalobesity, dysfunctionalVLDL1metabolism is an important modulator of HDL apoA-I catabolism.