Studies on the plasma lipid profiles, and LCAT and CETP activities according to hyperlipoproteinemia phenotypes (HLP)

Atherosclerosis. 2001 Dec;159(2):381-9. doi: 10.1016/s0021-9150(01)00513-5.

Abstract

Hyperlipoproteinemia phenotypes (HLP), one of genetic disorders with an estimated prevalence of 0.5-2% in the general population, is responsible for 10% of premature CHD. After first screening with the high cholesterol (>6.47 mM/l) and triglyceride (TG) (>2.6 mM/l) levels without medication, subjects were typed for HLP classification. Differential metabolic effects of HLP types on plasma lipid profiles and the reverse cholesterol transport system (RCT) were studied in 196 HLP types (91.2%) and 19 non-HLP (8.8%). A total of 45% of subjects had primary HLP and the others had NIDDM (10.7%), hypertension (9.3%) and other chronic diseases. Type IV HLP (58.6%) was most predominant and Types IIa, IIb, III and V comprised 16.7, 12.1, 2.3 and 1.4% of the HLP. Type I was not found. Plasma lipids excluding apo A-I and Lp(a) were significantly different among HLP compared to non-HLP (P<0.001). Since Type V and III impact the clearance of TG-riched lipoproteins, TG and VLDL-C levels were higher in V and III. TG and LDL-C were higher in Type II than those in the others because of defect of LDL receptors. LCAT activity, lower in Type III and Type IV and highest in Type V, was highly associated with plasma free cholesterol levels and the ratio of apoB/apoA and LDL/HDL. CETP activity was highest in Type V due to high VLDL-C and TG and low HDL-C. The ratio of LCAT/CETP was not different among HLP types but was significantly lower in HLP than in non-HLP. CETP increased 2-3 times as well as LCAT decreased among HLP patients compared to non-HLP. We conclude non-HLP subjects with high cholesterol and TG levels do not always mean high risk of CHD and the intervention effects of HLP types would lead to impose the risk of CHD by the impact of RCT.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Analysis of Variance
  • Carrier Proteins / blood*
  • Carrier Proteins / genetics
  • Cholesterol Ester Transfer Proteins
  • Female
  • Glycoproteins*
  • Humans
  • Hyperlipoproteinemias / blood
  • Hyperlipoproteinemias / genetics*
  • Lipids / blood*
  • Male
  • Middle Aged
  • Phosphatidylcholine-Sterol O-Acyltransferase / blood*
  • Phosphatidylcholine-Sterol O-Acyltransferase / genetics
  • Polymorphism, Genetic
  • Probability
  • Prospective Studies
  • Reference Values
  • Sensitivity and Specificity

Substances

  • CETP protein, human
  • Carrier Proteins
  • Cholesterol Ester Transfer Proteins
  • Glycoproteins
  • Lipids
  • Phosphatidylcholine-Sterol O-Acyltransferase