ENDUR-ACIN® effect on HDL cholesterol is mediated by plasma cholesterol esterification, study shows
Highlights
- ENDUR-ACIN® improves blood lipids in men with and without CHD
- Effective dosage is 1,500 to 2,000 mg/day for 4 months
- Increases in HDL cholesterol and apo-AI levels higher in men with CHD
- Changes in HDL cholesterol mediated by plasma cholesterol esterification
Summary
The aim of this preliminary open-label study was to examine the effect of ENDUR-ACIN® treatment on cholesterol esterification in the plasma of men with moderate hypercholesterolemia.
The study involved 44 men had coronary heart disease (CHD) and 25 men without CHD, aged 35-52 years, with total cholesterol levels above 225 mg/dl after a 2-month lipid-lowering diet. The men were treated with ENDUR-ACIN® (1,500-2,000 mg/day) for 4 months. There were no between-group differences in lipid and apolipoprotein levels at baseline, except high-density lipoprotein (HDL) cholesterol, which was significantly lower in men with CHD (43 mg/dl) compared to men without CHD (49 mg/dl).
Results indicate that ENDUR-ACIN® treatment had a beneficial effect on blood lipids and lipoproteins in both men with and without CHD (see Table 1). A treatment-mediated increase in lecithin-cholesterol acyltransferase (LCAT) activity was reported with an increase in the fractional esterification rate in the men with CHD (mean change 2.6% to 4.2%) and, to a lesser extent, in the men without CHD (from 2.5% to 3.9%). Molar esterification rates also rose in both groups.
Table 1. Blood Lipid Changes with ENDUR-ACIN® Treatment Based on Disease State | ||
Parameter | Men with CHD | Men without CHD |
Total Cholesterol | -10% | -15% |
LDL Cholesterol | -16 | -19 |
HDL Cholesterol | +19 | +10 |
Triglycerides | -14 | -29 |
Apo-A-I | +16 | +10 |
Apo-B | -20 | -25 |
CHD indicates coronary heart disease; LDL, low-density lipoprotein, HDL, high-density lipoprotein, Apo-B, apolipoprotein B, Apo-A-I, apolipoprotein A-I. |
These findings indicate that an ENDUR-ACIN®-mediated change in HDL cholesterol is accompanied by an HDL-mediated increase in plasma cholesterol esterification, which may be a protective factor against coronary atherosclerosis.