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Published on: October 12, 2017
Alterations of HDL subclasses in hyperlipidemia
1Department of Biochemistry and Apolipoprotein Research Unit, West China Medical Center, Sichuan University, Chengdu, 610041 Sichuan, People's Republic of China.
Insights
High-density lipoprotein (HDL) subclasses shift to smaller sizes in hyperlipidemic individuals, suggesting abnormal HDL maturation. This finding is crucial for understanding atherosclerosis development and lipid metabolism in these patients.
Area of Science:
- Lipid Metabolism
- Cardiovascular Research
- Atherosclerosis
Background:
- Different high-density lipoprotein (HDL) subclasses possess distinct metabolic functions.
- HDL influences atherogenesis, and alterations in HDL subclass distribution correlate with atherosclerosis incidence.
Purpose of the Study:
- To investigate the distribution of apolipoprotein (apo)A-I in HDL subclasses among hyperlipidemic subjects.
- To correlate HDL subclass characteristics with lipid profiles in hyperlipidemia.
Main Methods:
- Two-dimensional gel electrophoresis coupled with apoA-I immunodetection was used.
- Analysis was performed on plasma samples from hypercholesterolemic (HTC), hypertriglyceridemic (HTG), mixed hyperlipidemic (MHL), and normolipidemic individuals.
Main Results:
- Hyperlipidemic subjects showed increased apoA-I in smaller HDL subclasses (prebeta(1), prebeta(2), HDL(3c), HDL(3b), HDL(3a)) and decreased apoA-I in larger subclasses (HDL(2a), HDL(2b)).
- Plasma triglyceride levels positively correlated with smaller HDL subclasses and negatively with larger ones.
- HDL particle size shifted towards smaller sizes in hyperlipidemic individuals.
Conclusions:
- The observed shift in HDL particle size towards smaller sizes in hyperlipidemic subjects suggests potential abnormalities in HDL maturation.
- These findings highlight the altered HDL subclass profile in hyperlipidemia and its implications for atherosclerosis.
Background:
It is generally accepted that different high-density lipoprotein (HDL) subclasses have distinct but interrelated metabolic functions. HDL is known to directly influence the atherogenic process and changes in HDL subclasses distribution may be related to the incidence and prevalence of atherosclerosis.
Method:
The relative apolipoprotein (apo)A-I contents (% apoA-I) of plasma HDL subclasses were determined by two-dimensional gel electrophoresis coupled with immunodetection for apoA-I, in 39 hypercholesterolemic (HTC) subjects, 97 hypertriglyceridemic (HTG) subjects and 32 mixed hyperlipidemic (MHL) subjects, and 124 normolipidemic subjects.
Results:
The relative apoA-I contents of prebeta(1)-HDL, prebeta(2)-HDL, HDL(3c), HDL(3b) and HDL(3a) significantly increased while HDL(2a) and HDL(2b) significantly decreased in hyperlipidemic subjects. In HTC subjects of hyperlipidemia, the concentrations of prebeta(1)-HDL were significantly lower and HDL(2b) concentrations were significantly higher than in HTG and MHL subjects. In HTG subjects, the concentrations of HDL(3a) were significantly higher and the concentrations of HDL(2b) were lower than in HTC and MHL subjects. In total hyperlipidemic subjects, plasma triglyceride (TG) concentrations showed positive correlation with prebeta(1)-HDL, prebeta(2)-HDL, HDL(3b) and HDL(3a) and negative correlation with HDL(2a) and HDL(2b). The total cholesterol (TC) concentrations showed positive correlation with the relative apoA-I contents of prebeta(1)-HDL and HDL(3b), whereas the HDL-C concentrations showed negative correlation with the relative apoA-I contents of prebeta(1)-HDL and HDL(3a) and positive correlation with those of HDL(2a) and HDL(2b). The relative apoA-I contents of prebeta(1)-HDL, prebeta(2)-HDL, HDL(3b), and HDL(3a) were positively correlated whereas those of HDL(2a) and HDL(2b) were negatively correlated with TG/HDL-C ratio.
Conclusion:
The particle size of HDL in hyperlipidemic subjects shifted towards smaller sizes, which, in turn, indicates that the maturation of HDL may be abnormal in hyperlipidemic subjects.
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