LDL Peak Particle Diameter Research Articles

Complex segregation analysis of LDL peak particle diameter

A predominance of small low-density lipoprotein (LDL) particles, as determined by gradient gel electrophoresis (GGE), has been proposed to be a common genetic marker for risk of coronary heart disease. Previous analyses of the families in the Berkeley data set defined a dichotomous trait based on the LDL size distribution by GGE: subjects with a predominance of small LDL particles have LDL subclass "pattern B," while those with a predominance of large LDL particles have LDL subclass "pattern A." Using this definition, previous complex segregation analyses demonstrated a single major gene effect on pattern B with a dominant or additive mode of inheritance, and reduced penetrance in young males and premenopausal women. In the present analyses, a continuous variable denoted LDL peak particle diameter is used, reflecting the size (diameter in A) of the major LDL subclass, for comparison with the dichotomous LDL subclass pattern classification. After adjusting for age and gender, the results demonstrate a single major Mendelian gene effect, but the exact mode of inheritance could not be established. Thus, analysis of the continuous variable was not superior to that of the dichotomous classification in determining the mode of inheritance of the proposed single gene controlling LDL subclasses.

Changes in lipoprotein subfractions during diet-induced and exercise-induced weight loss in moderately overweight men.

We studied separately the effects of weight loss by calorie restriction (dieting) and by calorie expenditure (primarily, running) on lipoprotein subfraction concentrations in sedentary, moderately overweight men assigned at random into three groups as follows: exercise without calorie restriction (n = 46), calorie restriction without exercise (n = 42), and control (n = 42). Plasma lipoprotein mass concentrations were measured by analytic ultracentrifugation for flotation rates (F0(1.20), S0f) within high density lipoprotein (HDL) (F0(1.20) 0-9), low density lipoprotein (LDL) (S0f 0-12), intermediate density lipoprotein (IDL) (S0f 12-20), and very low density lipoprotein (VLDL) (S0f 20-400) particle distributions. Particle diameter and flotation rate of the most abundant LDL species were determined by nondenaturing polyacrylamide gradient gel electrophoresis and analytic ultracentrifugation, respectively. During the 1-year trial, the exercisers ran (mean +/- SD) 15.6 +/- 9.1 km/wk, and the dieters ate 340 +/- 71 fewer kilocalories per day than at baseline. Total body weight was reduced significantly more in dieters (-7.2 +/- 4.1 kg) and exercisers (-4.0 +/- 3.9 kg) than controls (0.6 +/- 3.7 kg). As compared with mean changes in controls, the exercisers and dieters significantly increased HDL2 mass (48.6% and 47.1%, respectively), decreased VLDL mass (-23.9% and -25.5%), and increased LDL peak particle diameter (2.4 and 3.2 A). When adjusted to an equivalent change in body mass index by analysis of covariance, 1) exercise-induced and diet-induced weight loss produced comparable mean changes in the mass of small LDL and VLDL, and in LDL peak particle diameter; 2) the exercisers versus control group difference in HDL2 was attributed to the exercisers' reduced body mass index; and 3) HDL2 increased significantly less in dieters than in exercisers. In dieters, low calorie intake might mitigate the effects of weight loss on HDL2.