New method for isolating and quantifying intermediate and beta-very-low-density lipoprotein cholesterol

We describe a new method, useful to clinical laboratories, for assessing intermediate density (IDL) or beta-very-low-density (beta-VLDL) lipoprotein cholesterol. The technique involves selective precipitation properties of the qualitative Wieland and Seidel post-electrophoretic method that immobilizes IDL and beta-VLDL in the beta-zone of an agarose slide (Clin Chem 1973;19:1139-41). In our method, we separate low-density lipoprotein (LDL) in a second electrophoretic step, in which LDL moves toward the anode, and then quantify the cholesterol of the above lipoproteins remaining in the precipitate band at the beta-zone. Replicate within-run precision (CV) of 15 aliquots of a sera pool was 10.1%. The correlation with sequential ultracentrifugation of 30 samples was r = 0.96 (P less than 0.001). Serum reference values for 30 normal individuals are 57 +/- 7.0 mg/L. Seven phenotype III hyperlipoproteinemic patients had the highest concentrations of IDL or beta-VLDL cholesterol in serum, 1620 +/- 346 mg/L.     

Cholesterol determination in high-density lipoproteins separated by three different methods.

We describe a simplified method for measuring high-density lipoprotein cholesterol in serum after very-low- and low-density lipoproteins have been precipitated from the specimen with sodium phosphotungstate and Mg2+. Values so obtained correlate well with values obtained with the heparin-Mn2+ precipitation technique (r = 0.95, CV less than 5% in 66% of the subjects studied and between 5 and 10% in the remaining ones) or by ultracentrifugal separation (r = 0.82, CV less than 5% in 80% of the subjects studied and between 5 and 10% in the remaining ones). Our precipitation technique is more appropriate for routine clinical laboratory use.     

Comparison of two micromethods for determination of lipoprotein cholesterol in plasma.

We compared the results obtained by a micromethod for the determination of plasma lipoprotein cholesterol, in which electrophoresis is used to separate the lipoprotein fractions (beta-, pre-beta-, and alpha-lipoproteins), with those determinations with ultracentrifugation (low-density, very-low-density, and high-density lipoproteins). Precision of determination (coefficient of variation, CV, %) was the same for beta- and low-density lipoproteins (1.6%), and for pre-beta- and very-low-density lipoproteins (3.7%); however, determination of alpha-lipoprotein cholesterol was more precise (1.4%) than that of high-density lipoprotein cholesterol (3.1%). Analytical recovery of lipoprotein cholesterol was the same for both methods (98--100%) and the results were closely correlated (r = 0.943). The procedure has been used to determine the cholesterol content of plasma lipoprotein fractions of apparently healthy adults (both sexes). Lipoprotein cholesterol concentrations in our population sample compare well with those reported for other groups of similar age, in particular Stanford long-distance runners.     

Decreases in apolipoprotein(a) after renal transplantation: implications for lipoprotein(a) metabolism.

Serum concentrations of apolipoprotein(a) [apo(a)], the unique glycoprotein of lipoprotein(a), are increased in patients with end-stage renal failure. We prospectively studied serum apo(a) and other lipoproteins in 20 consecutive patients, ages 46 +/- 11 years, before and for six months after successful renal transplantation. All patients received cyclosporine, and no patient was treated for hyperlipidemia. The mean creatinine clearance increased from 7.5 mL/min before transplant surgery to 40.9 mL/min six months afterwards (P less than 0.001). Apo(a) decreased from a median of 403 units/L before transplantation to 184 units/L at one week (P less than 0.001) and was 170 units/L (P less than 0.001) at six months. For the assay used, 1 unit of apo(a) is equivalent to 1 mg of lipoprotein(a). In contrast, from baseline to six months, increases were found for low-density lipoprotein (LDL) cholesterol (P = 0.03), high-density lipoprotein cholesterol (P = 0.06), apo B (P = 0.07), and apo A-I (P = 0.01). The decrease in apo(a) in individual patients was significantly correlated with the increase in creatinine clearance (r = -0.48, P less than 0.001). The single patient who developed nephrotic syndrome after renal transplantation had marked increases in apo(a) (693-1595 units/L), apo B, and LDL cholesterol, which paralleled the degree of proteinuria. These findings suggest that abnormal renal function affects the regulation of lipoprotein(a) metabolism.     

Dual-precipitation method evaluated for determination of high-density lipoprotein (HDL), HDL2, and HDL3 cholesterol concentrations

We evaluated a dual-precipitation method for determining cholesterol in high-density lipoprotein (HDL) and its subfractions HDL2 and HDL3. After total HDL was isolated by precipitation of very-low-density (VLDL) and low-density (LDL) lipoproteins with polyethylene glycol (Mr 8000), HDL2 was isolated from total HDL by precipitation with dextran sulfate (Mr 15,000), leaving HDL3 in the supernate. Concentration of total HDL cholesterol after precipitation of VLDL and LDL with PEG showed significant proportional and constant biases of -3.8% and 0.04 mmol/L, respectively, when compared with a phosphotungstic acid-based comparison method, although results by the two methods were correlated highly (r = 0.99, P less than 0.001). HDL2 and HDL3 cholesterol concentrations measured with the present technique were not different from those obtained by density-gradient ultracentrifugation or by combined precipitation-ultracentrifugation.     

Beta-lipoprotein cholesterol quantitation with polycations.

We compared direct determination of beta-lipoprotein cholesterol after selective extraction of very-low-density and high-density lipoproteins from serum with poly(ethyleneimine) and a cation-exchange resin with the classical quantitation after lipoprotein fractionation with the ultracentrifuge. At beta-lipoprotein cholesterol concentrations between 1.50 and 5.00 g/liter the correlation is linear (r = 0.95). The precision for the extraction procedure is as good (CV 2.4-2.8%) as for the quantitation by ultracentrifugation (CV 3.2-6.0%). From solutions of isolated lipoproteins, very-low-density lipoproteins are 93% extracted and high-density lipoproteins 60%, but low-density-lipoproteins only 5%. The molecular mechanism of the extraction is supposed to be due to both hydrophobic interaction of long-chain fatty acid residues and ionic interaction of phospholipids located at the surface of very low-density and high-density lipoproteins and the lipophilic polycation.     

Comparison of ultracentrifugation and a precipitation method for high-density lipoprotein cholesterol quantitation in insulin-dependent diabetic patients

We compared sodium phosphotungstic acid and magnesium chloride precipitation method for high-density lipoprotein (HDL) cholesterol quantitation with the ultracentrifugation method in 64 insulin-dependent diabetic patients with plasma triglyceride less than 3 mmol/l. The cholesterol content of HDL after precipitation of very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) was 86% +/- 3% of the cholesterol content of HDL (q greater than 1.063) determined after ultracentrifugation at q = 1.063 (1.33 +/- 0.05 mmol/l vs 1.55 +/- 0.06 mmol/l; p less than 0.001). HDL cholesterol determined after precipitation closely correlated to HDL cholesterol determined after ultracentrifugation (r = 0.97; p less than 0.001). The absolute difference between the HDL cholesterol values obtained by the two methods was correlated to HDL cholesterol (ultracentrifugation) (r = 0.75; p less than 0.001), but it was not correlated to VLDL cholesterol, LDL cholesterol, triglyceride, HbA1c, blood glucose or serum albumin. LDL cholesterol calculated by use of Friedewald's formula was 108% +/- 4% of the cholesterol content of LDL (q = 1.019 to 1.063), determined after ultracentrifugation, but the calculated and the ultracentrifugally determined LDL cholesterol values were closely correlated (r = 0.98; p less than 0.001). These results suggest that during sodium phosphotungstic acid and magnesium chloride precipitation of plasma from diabetic patients, a constant fraction of HDL cholesterol is co-precipitated, resulting in a systematic difference in HDL cholesterol quantitation when compared with the ultracentrifugation method.     

Five methods for determining low-density lipoprotein cholesterol compared

We evaluated three precipitation methods for determination of low-density lipoprotein cholesterol in serum and an indirect method involving the Friedewald formula (Clin Chem 18: 499-502, 1972) by comparison with results by ultracentrifugation. The results of all methods for 83 sera, including 59 hyperlipidemic type IIA, IIB, and IV sera agreed very well, at least for concentrations of serum triglycerides below 8 mmol/L. The accuracy of the Friedewald formula was confirmed in 285 other sera, including 66 sera with triglycerides content between 4.52 and 8.0 mmol/L. For type III sera, the precipitation methods produced similar values to those obtained with the Friedewald formula, all being much higher than the ultracentrifugation values. Density-gradient ultracentrifugation showed that the very-low-density lipoprotein remnants in type III sera almost completely coprecipitated with the low-density lipoproteins. The precipitation methods are not only accurate but also very precise (CV less than 5%); they can therefore be used in clinical laboratories to measure atherogenic low-density lipoproteins plus the remnants of very-low-density lipoproteins. However, when serum triglycerides and high-density lipoprotein cholesterol also are determined, the Friedewald formula is a reliable alternative.     

Lipoprotein cholesterol concentrations in the plasma of human subjects as measured in the fed and fasted states

Lipoprotein cholesterol concentrations in plasma are routinely estimated by using the Friedewald formula, whereby very-low-density lipoprotein cholesterol (VLDL-C) is estimated to be one-fifth the plasma triglyceride concentration. Ordinarily, this formula is applied only to plasma sampled from patients in the fasted state. To determine whether lipoprotein cholesterol measurements are altered substantially in plasma sampled from nonfasting subjects, we obtained postprandial blood samples from 22 healthy subjects (nine men, 13 women, ages 22-79 years) fed a fat-rich meal (1 g fat per kilogram body wt.). The plasma triglyceride concentration increased postprandially in all subjects (233 +/- 16% of baseline at 3 h). The mean cholesterol concentration in plasma was essentially unchanged. High-density lipoprotein cholesterol (HDL-C) was significantly decreased (94 +/- 2% at 3 h, P less than 0.001). VLDL-C and low-density lipoprotein cholesterol (LDL-C), estimated by the Friedewald formula, were compared with measurements obtained by modified Lipid Research Clinics (LRC) methodology. As measured by either method, VLDL-C increased and LDL-C decreased significantly after the fat-rich meal. These postprandial changes were significantly greater (P less than 0.01) when estimated by the Friedewald formula than by LRC methodology. We conclude that (a) lipoprotein cholesterol concentrations measured in the fed subject differ significantly from those measured in the fasted subject, and (b) plasma must be obtained after at least a 12-h fast if an individual's risk of coronary heart disease is to be accurately assessed.     

Automated enzymatic standardized lipid analyses for plasma and lipoprotein fractions

Excellent normal ranges for plasma lipid and lipoprotein cholesterol levels have been developed by the Lipid Research Clinics program, standardized by the Centers for Disease Control (CDC). However these values were generated by methods not currently in use in most clinical chemistry laboratories. Automated enzymatic methods for cholesterol, triglycerides and free glycerol determinations, as well as a dextran sulfate-Mg2+ procedure for separation of high density lipoproteins (HDL) with standardization are described. Similar methods for the measurement of unesterified cholesterol and phospholipids are also given. Serum pools for total cholesterol with values ranging from 1220-3490 mg/l produced coefficients of variation (CV) less than or equal to 2.85%; reference values for low total cholesterol samples in a range of 280-727 mg/l gave CV of 4.35% or less; HDL cholesterol reference values of 265-640 mg/l yielded CV less than or equal to 3.70%; and values for triglycerides between 0.74 and 3.05 mmol/l gave CV of 4.22% or less through three to eight testing cycles (9-24 mth). These data indicate that long term CDC standardization of total cholesterol, triglycerides, and HDL cholesterol can be obtained with automated enzymatic methods utilizing commercially available reagents.     

The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high-density lipoproteins

The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low-density and high-density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very-low- plus low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P less than 0.02), and an effect of treatment duration was observed. The changes in high-density lipoprotein total cholesterol (P less than 0.02), free cholesterol (P less than 0.001), triacylglycerol (P less than 0.05) and the free cholesterol/cholesteryl ester molar ratio in high-density lipoproteins (P less than 0.01) were inversely-related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high-density lipoprotein lipids observed in hypothyroidism.     

Plasma lipid transfer protein as a determinant of the atherogenicity of monkey plasma lipoproteins.

This study was undertaken to determine potential tissue sources of plasma cholesteryl ester transfer protein (CETP), and to assess the influence of CETP on lipoprotein concentrations and atherosclerosis. In a group of 28 cynomolgus monkeys fed high fat, high cholesterol diets, plasma CETP concentration was strongly correlated with the abundance of CETP mRNA in liver and in adipose tissue, and with the output of CETP in liver perfusates. Plasma CETP concentration showed a strong inverse correlation with HDL cholesterol concentrations (r = -0.62, P less than 0.001) and a positive correlation with LDL cholesterol concentration (r = 0.54, P less than 0.005) and molecular weight (r = 0.57, P less than 0.001). The extent of coronary artery atherosclerosis was positively correlated with LDL cholesterol concentration and molecular weight, and with plasma CETP concentration. Thus, in monkeys fed an atherogenic diet, individual variation in CETP mRNA abundance in liver and adipose tissue probably plays a major role in the determination of plasma CETP levels. In plasma, CETP influences the distribution of cholesteryl esters between LDL and HDL, and CETP concentration appears to be a key determinant of the relative atherogenicity of the plasma lipoproteins.     

Quantification of lipoprotein cholesterol in serum from children with different lipoprotein profiles: heparin-calcium precipitation and ultracentrifugation compared

We compared the serum lipoprotein cholesterol concentrations in subgroups of children (n = 360), ages 5-17 years, as measured by the heparin-Ca2+ and preparative ultracentrifugation methods. Children were grouped from the total population on the basis of their previous results for serum beta- and pre-beta-lipoprotein cholesterol (Group I: low beta- and low pre-beta-; Group II: high beta- and low pre-beta; Group III: high beta- and high pre-beta-; Group IV: low beta- and high pre-beta-). The values for very-low-density (VLDL) cholesterol by ultracentrifugation method were 44, 53, 15, and 10 mg/L greater than the values for pre-beta-lipoprotein cholesterol by the heparin-Ca2+ method in Groups I, II, III, and IV, respectively; the differences were not significant in Group IV. The values of low-density (LDL) cholesterol were 64, 137, 144, and 73 mg/L less than the values for beta-lipoprotein cholesterol in Groups I, II, III, and IV, respectively (p less than 0.005). On the other hand, high-density (HDL) cholesterol concentrations in the respective four groups were 10, 37, 93, and 52 mg/L greater than alpha-lipoprotein cholesterol concentrations; the differences were significant for Groups II, III, and IV (p less than 0.005). Overall, the values for LDL-cholesterol correlated highly with beta-lipoprotein cholesterol (r = 0.94), whereas correlations for VLDL- and HDL-cholesterol values with pre-beta-lipoprotein cholesterol (r = 0.76) and alpha-lipoprotein cholesterol (r = 0.77) were somewhat lower. The differences between these two methods may result from their different operational definitions for measuring serum lipoproteins and the possibility that without appropriate corrections the values obtained by preparative ultracentrifugation do not serve as reference values.     

Polyacrylamide gel electrophoresis in quantification of high-density lipoprotein cholesterol

We evaluated a method for quantifying high-density lipoprotein cholesterol in plasma, based on electrophoretic migration of the prestained (with Sudan Black III) sample through a discontinuous polyacrylamide++ gel and densitometric integration of the stain associated with each class of lipoprotein. With this method, operations can be carried out on all types of lipoproteins over a broad range of concentrations. Overloading with very-low and low-density lipoproteins did not affect reliability within a wide range of HDL concentrations (0.45 to 16.60 mmol/L). Results for 22 individual plasma samples from normal and dyslipemic subjects correlated well with those by ultracentrifugal analysis (r=0.96; Student's t= 0.90, p > 0.30). We conclude that this method is reliable, sensitive, and accurate, It may be used for simultaneously typing dyslipoproteinemias and assaying HDL cholesterol.     

Type 1 (insulin-dependent) versus Type 2 (non-insulin-dependent) diabetes mellitus: characterization of serum lipoprotein alterations

Serum lipoprotein lipids and apolipoproteins A-I, B, and E were investigated in Type 1 (insulin-dependent) diabetics, Type 2 (non-insulin-dependent) diabetics, and two control groups, twenty subjects each. Lipoproteins were separated and analysed by common methods, apolipoproteins were measured by endpoint immunonephelometry. Compared with controls, Type 2 diabetics had increased serum apolipoprotein E levels (0.116 +/- 0.020 vs. 0.079 +/- 0.014 g 1-1, P less than 0.01) together with an increased content of cholesteryl ester-enriched very low-density lipoproteins. Furthermore, Type 2 diabetics had higher apolipoprotein B concentrations (1.06 +/- 0.21 vs. 0.85 +/- 0.21 g l-1 P less than 0.01), but lower high-density lipoprotein cholesterol concentrations than the controls. Conversely, Type 1 diabetics had elevated serum apolipoprotein A-I values vs. controls and Type 2 diabetics (1.70 +/- 0.33 vs. 1.49 +/- 0.22 and 1.43 +/- 0.21 g 1-1, P less than 0.01). It is concluded that Type 2 diabetics, like other groups at risk for atherosclerotic diseases, are characterized by an increased concentration of partly catabolized very low-density lipoproteins. Sufficiently insulinized Type 1 diabetics have, on the other hand, an increased number of high-density lipoprotein particles.     

Mathematical evaluation of methods for estimation of the concentration of the major lipid components of human serum lipoproteins.

The concentration of total cholesterol and triglycerides in the three major lipoprotein classes of human serum was measured in 136 men, randomly selected from an industrial population, by a quantitative method of lipoprotein electrophoresis on agarose gel and of fractions separated by preparative ultracentrifugation. Correlation coefficients for the two estimates were 0.98 for triglycerides in very low-density lipoproteins, 0.93 for total cholesterol in low-density lipoproteins, and 0.75 for total cholesterol in high-density lipoproteins. Data obtained form the analyses of the ultracentrifugal fractions were used to develop regression equations that predict the concentrations of total cholesterol and triglycerides in the lipoprotein classes from their concentrations in whole serum. These equations take into account the inverse curvilinear relationship between total cholesterol in high-density lipoproteins and serum tiriglyceride concentration. When applied to a separate sample of 530 men, the predicted values for triglycerides in very low-density lipoproteins and total cholesterol in low-density lipoproteins correlated as well with ultracentrifugal values as did the electrophoretic estimates. However, for total cholesterol in high-density lipoproteins, the electrophoretic method was superior. Similar regression equations were developed from ultracentrifugal lipoprotein analyses in 158 women from the same industrial population. Although the concentration of total cholesterol in the low-density lipoproteins estimated by both electrophoresis and the regression equations agreed closely in most cases with the ultracentrifugal values, errors exceeded 10% with sufficient frequency to limit the value of the estimates for this purpose. In both men and women, the ratio of total cholesterol to triglycerides in high-density lipoproteins was a hyperbolic function of serum triglyceride concentration, suggesting that cholesteryl esters in the core of this lipoprotein are progressively replaced by triglycerides as the concentration of triglycerides in very low-density lipoproteins increases. This altered composition of nonpolar lipids accounts, at least in part, for the reduction of cholesterol in high-density lipoproteins in hyperlipemic individuals.     

化学沉淀法测定小而密低密度脂蛋白方法的建立

目的利用化学沉淀原理建立小而密低密度脂蛋白(sdLDL)快速、简便的检测方法。方法通过比较不同种类及不同浓度沉淀剂对血清样本中脂蛋白的分离效果,确定最终沉淀剂,并对化学沉淀法测定血清sdLDL-C的精密度、线性范围和回收率进行分析。结果最终选择140 U/mL肝素-90 mmol/L Mg2+作为沉淀剂测定血清sdLDL胆固醇(sdLDL-C)含量。化学沉淀法测定sdLDL-C在0.14~1.44 mmol/L范围内线性关系良好,回归方程为Y=1.025X-0.197,r=0.988;对高、低2组不同sdLDL-C浓度的样本批内变异系数(CV)分别为2.83%、3.19%,批间CV分别为5.49%、6.13%;回收率为83.81%。结论 sdLDL化学沉淀法具有样本用量少、操作简便、成本低廉等优点,更适合常规实验室检测血清sdLDL-C含量。     

Impact of postprandial lipaemia on low-density lipoprotein (LDL) size and oxidized LDL in patients with coronary artery disease

BACKGROUND: Remnant lipoprotein particles (RLPs) and oxidative stress are components of postprandial state. We investigated the concentrations of triglyceride-rich lipoproteins (TRLs), RLPs, low-density lipoprotein (LDL) size, and oxidized LDL (oxLDL) during alimentary lipaemia, and evaluated whether changes among these variables could be associated with the severity and extent of coronary artery disease (CAD). MATERIALS AND METHODS: Eighty men and 27 women with clinically suspected CAD underwent quantitative coronary angiography (QCA). TRLs were isolated by density gradient ultracentrifugation before and 6 h after an oral fat load. RLPs were measured by an immunoseparation method, oxLDL by ELISA, and LDL size by gradient gel electrophoresis. RESULTS: Triglycerides, apolipoprotein (apo) B-48, and apoB-100 concentration in Swedberg flotation units (Sf) > 400 and in Sf 12-400 fractions were markedly increased at 6 h. Postprandial cholesterol content of RLPs (RLP-C) correlated with respective triglycerides in Sf > 400 (r = 0.737) and Sf 12-400 (r = 0.857), apoB-48 in Sf > 400 (r = 0.710) and Sf 12-400 (r = 0.664), apoB-100 in Sf > 400 (r = 0.812) and Sf 12-400 (r = 0.533). RLP-C correlated with oxLDL both in fasting and in fed state (r = 0.482 and r = 0.543, respectively) and inversely with LDL size (r = -0.459 and r = -0.442, respectively). (P < 0.001 for all). OxLDL was elevated postprandially (P < 0.001). In multivariate analysis, oxLDL was a determinant of severity and extent of CAD. CONCLUSION: Postprandial state is associated with oxidative stress. The magnitude of oxLDL increases during alimentary lipaemia and is associated with coronary atherosclerosis.     

The role of lipids in the pathogenesis of glomerulosclerosis in the rat following subtotal nephrectomy

Similarities between atherosclerosis and glomerulosclerosis suggest that hyperlipidaemia may contribute to glomerular injury. Dietary supplementation with 4% cholesterol + 1% cholic acid was administered to rats 4 weeks after 1 1/3 nephrectomy and continued for 7 weeks. There was a significant increase in serum cholesterol (peak = 11.52 +/- 1.09 mmol l-1 vs. 4.73 +/- 0.31 on control diet, P less than 0.001) and triglyceride concentrations (peak = 2.31 +/- 0.27 mmol l-1 vs. 1.41 +/- 0.29, P less than 0.05) and a marked increase in beta-migrating lipoproteins. The severity of hypercholesterolaemia was significantly correlated with proteinuria (control diet: r = 0.600, cholesterol diet: r = 0.672, P less than 0.0001) as was hypertriglyceridaemia (control diet: r = 0.544, cholesterol diet: r = 0.678, P less than 0.0001). The percentage of glomeruli containing lipid deposits was increased from 21% to 60% (P less than 0.05). The kidney total cholesterol content was increased from 29.2 +/- 0.8 to 47.7 +/- 3.3 mumols g-1 dry weight (P less than 0.0001), with esterified cholesterol increasing from 7.5 +/- 0.4% to 14.5 +/- 2.1% of total (P less than 0.01). Serum cholesterol concentration was significantly correlated with both glomerular lipid deposition (rs = 0.7195, P less than 0.0001) and tissue total cholesterol content (rs = 0.6053, P less than 0.001). Lipid vacuolation was prominent in the paramesangium and within mesangial cells. Despite these changes hypertension, uraemia, proteinuria and glomerulosclerosis were not significantly increased on the cholesterol diet. Cholesterol deposition in the glomeruli occurs secondary to hyperlipidaemia in rats following subtotal nephrectomy but over 7 weeks no exacerbation of glomerulosclerosis is detectable.     

Neuron-specific enolase concentrations in serum and cerebrospinal fluid in patients with no previous history of neurological disorder

Valdemarsson, S., Hedner, P. &; Nilsson-Ehle, P. Treatment of hyperthyroidism: effects on hepatic lipase, lipoprotein lipase, LCAT and plasma lipoproteins.

The activities of hepatic lipase and of lipoprotein lipase, the elimination rate of exogenous triglyceride and the cholesterol esterification rate were determined and related to plasma lipoprotein concentrations in 16 patients before and after treatment for hyperthyroidism.

The activity of hepatic lipase was significantly higher (65%) before than after treatment, while the activity of lipoprotein lipase and the elimination rate of exogenous triglyceride remained unchanged. The endogenous cholesterol esterifying ability decreased after treatment, whereas no change occurred in the fractional cholesterol esterification rate measured with normal plasma as substrate. The concentrations of LDL-cholesterol and HDL-cholesterol increased significantly after treatment.

The decrease in hepatic lipase activities was correlated to the decrease in S-T₃ concentrations (r = 0.77, P < 0.001) and to the increase in HDL-cholesterol concentrations (r = 0.51, P < 0.05). The activities of lipoprotein lipase were positively correlated to the concentrations of HDL-cholesterol both before (r = 0.54, P < 0.05) and after (r = 0.59, P < 0.05) treatment.

These results support the view that hepatic lipase and lipoprotein lipase are both important determinants of plasma HDL concentrations and suggest that-an increased hepatic lipase activity contributes to the lower HDL levels in hyperthyroid patients.