BACKGROUND: To investigate the alterations of high-density lipoprotein (HDL) subclasses in endogenous hypertriglyceridemic subjects. METHODS: Apolipoprotein A-I contents of plasma HDL subclasses were quantitated by 2-dimensional gel electrophoresis in 236 normolipidemic subjects (including 146 males and 90 females) and 176 endogenous hypertriglyceridemic subjects (including 103 males and 73 females). RESULTS: Apolipoprotein A-I contents of small-sized pre-beta1-HDL and HDL3a were significantly higher (P < .01 and P < .01, respectively), but those of large-sized HDL2a and HDL2b were significantly lower (P < .01 and P < .01, respectively) in hypertriglyceridemic subjects versus normolipidemic subjects. Moreover, with the elevation of triglyceride levels, small-sized pre-beta1-HDL and HDL3a increased successively; however, large-sized HDL2a and HDL2b decreased successively. Males had significantly higher apolipoprotein A-I contents of small-sized pre-beta1-HDL and HDL3b (P < .05 and P < .05, respectively), but lower contents of large-sized HDL2b (P < .01) than females in both normolipidemic and hypertriglyceridemic subjects. CONCLUSIONS: The particle size of HDL shifted toward smaller size in hypertriglyceridemic subjects, especially in male subjects. Of note, the shift was more obvious with the elevation of triglyceride levels. The changes mentioned above indicate that HDL maturation might be abnormal and reverse cholesterol transport might be weakened.
BACKGROUND: To investigate the alterations of high-density lipoprotein (HDL) subclasses in endogenous hypertriglyceridemic subjects. METHODS:Apolipoprotein A-I contents of plasma HDL subclasses were quantitated by 2-dimensional gel electrophoresis in 236 normolipidemic subjects (including 146 males and 90 females) and 176 endogenous hypertriglyceridemic subjects (including 103 males and 73 females). RESULTS:Apolipoprotein A-I contents of small-sized pre-beta1-HDL and HDL3a were significantly higher (P < .01 and P < .01, respectively), but those of large-sized HDL2a and HDL2b were significantly lower (P < .01 and P < .01, respectively) in hypertriglyceridemic subjects versus normolipidemic subjects. Moreover, with the elevation of triglyceride levels, small-sized pre-beta1-HDL and HDL3a increased successively; however, large-sized HDL2a and HDL2b decreased successively. Males had significantly higher apolipoprotein A-I contents of small-sized pre-beta1-HDL and HDL3b (P < .05 and P < .05, respectively), but lower contents of large-sized HDL2b (P < .01) than females in both normolipidemic and hypertriglyceridemic subjects. CONCLUSIONS: The particle size of HDL shifted toward smaller size in hypertriglyceridemic subjects, especially in male subjects. Of note, the shift was more obvious with the elevation of triglyceride levels. The changes mentioned above indicate that HDL maturation might be abnormal and reverse cholesterol transport might be weakened.