[Determination of lecithin-cholesterol acyltransferase. Studies on the precipitation of beta-lipoproteins by dextran sulphate (author's transl)]. / Dosage de la lécithine-cholestérol acyltransferase. Intérêt de la précipitation des beta-lipoprotéines par le sulfate de dextrane.

Uncertainties in assays of lecithin-cholesterol acyltransferase (LCAT) are generally related to the degree of isotopic equilibrium obtained by rapid exchange of unesterified cholesterol between the different lipoproteins. A new method is presented based on the precipitation of serum beta-lipoprotein with sulfated polysaccharides prior to the LCAT determination. In the absence of Beta-lipoproteins, more than 7 per cent of serum free cholesterol is esterified in the first hour and the reaction rate is linear for about 2 h. LCAT activities with normal serum expressed as cholesterol esterified per microliter mol/1/h are lower than the values reported by others. The reason for this discrepancy is that free cholesterol specific activity in total serum does not reflect the true specific activity of LCAT cholesterol substrate.

A rapid method for lecithin:cholesterol acyltransferase estimation in human serum.

All the described procedures for lecithin:cholesterol acyltransferase (LCAT) determination in the plasma have raised criticisms: Lack of sensitivity for methods using colorimetric determination of unesterified cholesterol or phosphatidyl-choline in plasma before and after incubation at 37 degrees C. Incomplete isotopic equilibrium of the free cholesterol substrate between the different lipoproteins in radioassay procedures. Gas-liquid chromatography methods cannot be used when LCAT activity is low. A new method, easier, more sensitive and accurate has been developed in our laboratory:plasma samples are delipoproteinized by coprecipitation with Intralipid, dextran sulphate, and calcium chloride. Cholesterol esterification is assayed by a short incubation (30 min) of 100 microliter delipoproteinized plasma and a 30 microliter of 3H-cholesterol-labelled substrate. About 15% of cholesterol is esterified in these conditions in 30 min (35 +/- 7 micromole/h/l). The LCAT reaction is linear for about one hour.

[Practical value of the selective precipitation of LDL, LDL-phospholipids and the molar ratio of cholesterol to LDL-phospholipids in lecithin-cholesterol-acyltransferase deficiency]. / Intérêt pratique de la précipitation sélective des LDL, LDL-phospholipides et rapport molaire cholestérol sur phospholipides des LDL (LDL-RMCP) dans les déficiences en lécithine-cholestérol-acyl-transférase.

There is a high morbidity from hepato-biliary disease in France. These diseases are often accompanied by a reduction in serum lecithin-cholesterol-acyl-transferase activity, which is difficult and costly to diagnose in the laboratory. Thanks to a simple and inexpensive method of selective precipitation of light lipoproteins, we have been able to establish the practical value of the determination of the LDL-phospholipids and the molar cholesterol ratio on the phospholipids in the LDL (MCPR) in familial or secondary deficiencies of Lecithin-Cholesterol-Acyl-Transferase. These conditions are characterized by a high proportion of serum phospholipids transported by the LDL (more than 60%) and by the marked reduction in the cholesterol ratio of the phospholipids in the LDL. The authors propose a classification for the commonest causes of lecithin-cholesterol-acyl-transferase deficiency.

[Value of LDL-cholesterol determination in hyperlipoproteinemias]. / Intérêt de la détermination du LDL-cholestérol dans les hyperlipoprotéinémies.

Serum LDL-cholesterol concentrations were measured after precipitation in various forms of dyslipidaemia. LDL-cholesterol values were increased in hypercholesterolaemia and decreased in hypertriglyceridaemia. The LDL-cholesterol/total cholesterol ratio decreased with the presence of triglycerides. These data have prompted the authors to propose a classification of dyslipidaemia into hyper-and hypoLDLaemia. Such a classification would be helpful in the prevention, diagnosis and therapeutic surveillance of these diseases.

Reduction of plasma lecithin--cholesterol acyltransferase activity by acute magnesium deficiency in the rat.

Weanling Wistar rats were pair-fed for 8 days control and magnesium-deficient diets. Acute magnesium deficiency increased plasma triglycerides and free cholesterol levels and decreased esterified cholesterol levels. The plasma activity of lecithin--cholesterol acyltransferase was markedly diminished in fasting magnesium-deficient rats (54% reduction) and plasma high density lipoprotein (HDL) free cholesterol was significantly increased in the HDL fraction. The results of this study showing that dietary magnesium affects the activity of the enzyme involved in the esterification of free cholesterol to cholesterol ester provide a possible basis for the reduced plasma cholesterol esterification and hyperlipidemia associated with acute magnesium deficiency.

[Low-density lipoprotein cholesterol levels in hypercholesterolemic rabbits with or without carbon monoxide poisoning]. / Teneur en cholestérol des lipoprotéines légères chez le lapin hypercholestérolémique intoxiqué ou non par l'oxyde de carbone.

Low-density lipoproteins isolated by a selective precipitation procedure have been investigated in cholesterol-fed rabbits exposed or not to carbon monoxide. The main findings are a higher increase of their cholesterol content and cholesterol to phospholipid molar ratio without a modification in lecithin-cholesterol-acyltransferase activity in intoxicated animals. Thus, the aggravating effect of carbon monoxide exposure on the atherogenic properties of these lipoproteins could accelerate the development of atherosclerosis in cholesterol-fed rabbits.

[The effects of Triton WR 1339 on the secretion of bile lipids in the rat]. / Effets du Triton WR 1339 sur la sécrétion des lipides bilaires chez le rat

Rats bearing a biliary fistula received i.v. a solution of Triton WR 1339. Bile and plasma lipid composition was studied every 2 hrs and compared to that of control rats injected with saline. Two hours after Triton injection a sharp decrease in the bile secretion of lecithins (-- 93%), cholesterol (-- 50%) and bile salts (-- 50%) was observed together with a fall in bile flow (-- 20%). Eight hours after Triton administration the biliary output of lecithins, cholesterol and bile salts was lowered to --73%, --50% and --34% respectively compared to control animals. At that time an accumulation of L.C.A.T. substrates (lecithins and cholesterol) was observed in the plasma of Triton group. These modifications of biliary lipids after inhibition of L.C.A.T. activity by Triton W 1339 could be the result of a decreased production of plasma lysolecithins and cholesterol esters suggesting that both lipids could be important precursors for the synthesis of bile constituents. Furthermore this support the view that the production by the liver of plasma and bile lipids follows two distinct pathways.