Two patterns of LDL metabolism in normotriglyceridemic patients with hypoalphalipoproteinemia.

Abstract

The objective of this study was to determine whether normotriglyceridemic patients with low levels of high density lipoprotein (HDL) cholesterol have concomitant defects in the metabolism of low density lipoproteins (LDLs). To address this question, measurements of turnover rates of apolipoprotein A-I (apo A-I) and LDL apolipoprotein B (apo B) were made in 36 middle-aged men with low HDL cholesterol (<40 mg/dL), normal triglyceride (<2S0 mg/dL), and normal total cholesterol (<90th percentile) levels. Similar measurements were made in eight hypertriglyceridemic men having low HDL levels. For control, turnover rates of LDL apo B were measured in 24 healthy, normolipidemic men, and apo A-I kinetics were determined in 20 other healthy men with normal HDL cholesterol levels. In all patients with low HDL levels, fractional catabolic rates (FCRs) for apo A-I were increased compared with control subjects; in contrast, input rates for apo A-I in low-HDL patients were similar to control. Hypertriglyceridemic patients had significantly higher FCRs for LDL (0.463±0.040 pool/day, [mean±SEM]) than control subjects (0.328±0.008 pool/day, p<0.001). In normolipidemic patients having low HDL, a bimodal pattern of LDL-apo B kinetics was observed. For 23 low-HDL patients, FCRs for LDL apo B averaged 0.450±0.017 pool/day and were significantly higher than control values. Additionally, in these patients, levels of very low density lipoprotein plus intermediate density lipoprotein (VLDL+IDL) cholesterol and VLDL+IDL apo B were higher than in control subjects (54±3 versus 32±3 mg/dL and 25±2 versus 18±1 mg/dL, respectively). The remaining 13 low-HDL patients had lower and essentially normal FCRs for LDL (0.300±0.009 pool/day); these patients also had relatively low levels of cholesterol and apo B in VLDL+IDL. Thus, two patterns of LDL kinetics were present in normotriglyceridemic patients with low HDL levels. One pattern was indistinguishable from that typically present in patients with hypertriglyceridemia, whereas the other was similar to normal control subjects. These two patterns of LDL-apo B kinetics may reflect different mechanisms for the causation of low HDL cholesterol concentrations. 1993;13:579-589) KEY WORDS • hypoalphalipoproteinemia • low HDL • LDL-apo B kinetics • apo A-I kinetics S erum levels of high density lipoprotein (HDL) cholesterol are correlated inversely with rates of coronary heart disease (CHD). 1 -3 The mechanisms underlying this inverse relation unfortunately are not well understood. According to one hypothesis, a low HDL level per se promotes coronary atherosclerosis; it could do this by failure to remove excess cholesterol from arterial wall cells 4 ' 5 or by failure to prevent oxidation 6 or self-aggregation 7 of low density lipoprotein (LDL). Another possibility is that a low HDL level reflects increased concentrations of other atherogenic lipoproteins, {Arteriosclerosis and Thrombosis

Different emergence phenology of European grapevine moth (Lobesia botrana, Lepidoptera: Tortricidae) on six varieties of grapes

“…The bimodality of the emergence pattern was tested using a bimodality coefficient (b) defined as: where S represents the skewness (asymmetry) of the distribution, K represents the kurtosis (peakedness) of the distribution, and n represents the sample size. A b -value greater than 0.55 indicates a bimodal distribution (Vega & Grundy, 1993) and S and K values of 0 indicate a normal distribution. Deviation from a normal distribution was tested by comparing skewness ( S <0: left-tailed, S >0: right-tailed) and kurtosis ( K <0: platykurtic, K >0: leptokurtic) to the theoretical value from Student's t -test for infinite degrees of freedom with an α risk of 5% ( t 0,05; ∞ =1,96) as: where s S =√[6 n ( n −1)/( n −2)( n +1)( n +3)] and s K =√ [24 n ( n −1) 2 /( n −3)( n −2)( n +3)( n +5)].…”

Effect of lifibrol on the metabolism of low density lipoproteins and cholesterol

“…For the turnover studies, patients had blood drawn under sterile conditions to isolate autologous LDL as detailed previously [15]. Briefly, LDL‐apo B was radiolabelled with 125 I using the iodine monochloride method [15].…”

“…For the turnover studies, patients had blood drawn under sterile conditions to isolate autologous LDL as detailed previously [15]. Briefly, LDL‐apo B was radiolabelled with 125 I using the iodine monochloride method [15]. The tracers were dialysed to remove unbound radioactive iodine; they were filtered through a pyrogen‐free millipore filter and mixed with unlabelled lipoprotein and sterile human serum albumin.…”

Hypercholesterolemia and dyslipidemia

“…As many as 36% of men with premature CAD have been reported to express this trait, which is a broad spectrum of overlapping disorders [75,79,80]. • One genetic cause is a polymorphism in the region between the apolipoprotein A-I and apolipoprotein C-III genes that results in abnormally low HDL values [81]. In these cases, elevated triglyceride level or elevated LDL-C level is not common, and isolated low HDL level is the main contributor to premature CAD.…”