High-density lipoprotein (HDL) particles without apolipoprotein A-II (Lp A-l) may be more anti-atherogenic than HDL with apo A-II (Lp A-I-AII) and Lp A-I is reported selectively to be reduced in cases of intra-abdominal obesity. We explored the mechanisms of this reduction by studying the turnover of Lp A-I and Lp A-I A-II in postmenopausal women well characterized for total body, regional and sub-regional adiposity by body mass index (BMI), truncal girth ratio, and abdominal magnetic resonance imaging (MRI), respectively. We tested for possible cause-effect relationships by measuring inter-correlations among these variables. Intra-abdominal fat area correlated strongly and positively with the fractional catabolic rate (FCR) of Lp A-I (r = 0.98, P = 0.003). Intra-abdominal fat only showed a non-significant trend toward correlation with the FCR of Lp A-I A-II (r = 0.84, P = 0.07), and had no correlation with the production or transport rate (TR) of either Lp A-I or Lp A-I A-II (r = 0.48 and 0.02. respectively, P > 0.1). Subjects were studied both with and without estrogen replacement, allowing exploration of a possible interaction of adiposity with estrogen effects on HDL turnover. Response of HDL turnover to estrogen did not correlate with adiposity, except for tt parameter of' waist to hip ratio (WHR), which predicted the increase in LP A-I TR with estrogen (r = 0.84, P = 0.04). We conclude that intra-abdominal fat may lower HDL levels by increasing the FCR of Lp A-I, suggesting a mechanism by which central adiposity may be proatherogenic. Published by Elsevier Science Ireland Ltd.