The metabolism of high-density lipoprotein (HDL) is severely impaired in individuals with abdominal obesity. However, the specific metabolism of apolipoprotein (apo)-A-II, the second major apolipoprotein of HDL, remains poorly known. The relationships between HDL apoA-II catabolism and other metabolic variables that may be modified in abdominal obesity, such as very low-density lipoprotein (VLDL) subspecies (VLDL1, VLDL2) kinetics, remain to be investigated.
Our aim was to study the associations between apoA-II fractional catabolic rate (FCR) and the kinetics of VLDL subspecies and apoA-I.
We carried out a multicenter in vivo kinetic study using stable isotopes (deuterated leucine and glycerol) in 62 individuals with abdominal obesity.
In a univariate analysis, apoA-II FCR was positively correlated with body mass index, sc fat, liver fat, apoA-I FCR, apoA-I production rate (PR), apoA-II pool, apoA-II PR, VLDL1-triglyceride PR, VLDL2-triglyceride PR, VLDL2-triglyceride (TG) FCR, and VLDL2-apoB FCR and negatively with HDL cholesterol to apoA-I ratio. After adjustment for apoA-I FCR, a strong positive correlation between apoA-II FCR and VLDL1-TG indirect FCR was observed (r = 0.520, P < .0001). In a multivariate analysis, apoA-II FCR was independently and positively associated with apoA-I FCR (P < .0001) and VLDL1-TG indirect FCR (P < .0001). Both variables explained 59.7% of the variability in apoA-II FCR.
We show that, in abdominally obese individuals, apoA-II FCR is positively and independently associated with both apoA-I FCR and VLDL1-TG indirect FCR. These data suggest that, in a condition of delayed VLDL1 catabolism, such as abdominal obesity, retention of apoA-II in the VLDL1 pool may occur, with an effect on apoA-II catabolism. The consequences of this link between VLDL1 catabolism and apoA-II catabolism remain to be determined.
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