Keiji Mimura

Selective urinary excretion of phosphatidyl ethanolamine in patients with chronic glomerular diseases

Urinary phospholipids and lipoproteins in chronic glomerular diseases were analyzed. The subjects used were 26 patients consisting of 14 with chronic glomerulonephritis and 12 with nephrotic syndrome. Nine healthy normals served as controls. Phospholipids were isolated by one-dimensional thin-layer chromatography (TLC) using an internal standard for quantification and partially by two-dimensional TLC and, furthermore, quantified by two different methods to ascertain the kinds of phospholipids. Urinary lipoproteins were isolated by density gradient ultracentrifugation and analyzed by electrophoresis. The urinary excretion of phosphatidyl ethanolamine (PE) was recognized exclusively in the patient group and that of phosphatidyl serine (PS) in most cases with nephrotic syndrome. The daily urinary PE excretion rate was closely correlated to the urinary albumin excretion rate. However, phosphatidyl choline (PC) and sphingomyelin (SPH), which are main phospholipids in serum and red blood cell membranes, in most cases were hardly detected in urine. These observations were confirmed by two-dimensional TLC using valuable spot tests for identification of phospholipids and also by the two different quantification methods. In density gradient ultracentrifugation, urinary lipoproteins did not form such peaks as seen in the profiles of serum lipoproteins. The presence of urinary lipoproteins in two nephrotic patients has been shown, but although the method used was not very sensitive, it was suggested that lipoproteins were hardly excreted into urine as the lipoprotein deficient fraction (LPDF) (d greater than 1.21 g/ml), in which albumin is predominant. PE was found mainly in LPDF of urine, although the amount of PE in urinary lipoproteins was very limited.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of platelet-activating factor on lipoprotein lipase and blood lipids.

We investigated the effect of platelet-activating factor (PAF) and of the PAF specific antagonist CV-6209 on plasma lipid metabolism, and particularly on post-heparin plasma lipolytic activity in male Wistar rats. Lipoprotein lipase (LPL) activity was enhanced by intravenous injection of PAF before intravenous injection of heparin when the PAF dose was low (0.2 μg/kg). PAF activated hepatic triacylglycerol lipase (HTGL) activity dose-dependently. Plasma triacylglycerols (TG) significantly decreased with the activation of LPL and/or HTGL. Plasma total cholesterol (TC) and phospholipid (PL) levels decreased at a low dose of PAF (0.2 μg/kg), but increased when higher doses were used. The PAF antagonist CV-6209 partially reversed the PAF induced effects on HTGL, TC and PL.