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The effect of heparin on the proportion of cholesterol esters, lecithin/lysolecithin ratio, and lecithin: cholesterol acyltransferase (LCAT) activity was studied in twelve patients with cholestasis. A good correlation was observed between a decreased LCAT activity and the proportion of cholesterol esters, and no consistent variation was noted after heparin. The lecithin/lysolecithin ratio was increased in 7 patients and became normal after heparin in 6 cases. The clearance of lipoprotein-X after heparin seems to be not related to LCAT activity. These results demonstrate that heparin does not modify the LCAT activity, and suggest that heparin induces an increase of phospholipase activity in some patients with cholestasis.

Lecithin: Cholesterol acyltransferase (LCAT) activity was measured in serum and liver tissue from patients with parenchymal liver disease. Serum LCAT activity was within normal limits and it was probably related to the absence of clinical and laboratory evidence of a decompensated liver function. Liver tissue LCAT activity is about tenfold lower than that in serum. The relative proportion of cholesterol esters in liver tissue was much higher that could be expected according the low tissue LCAT activity. This findings suggest that LCAT is a "plasma specific" enzyme and that cholesterol esters in parenchyma may be considered as a storage form of cholesterol esterified in plasma pool.

Serum lipoprotein-X was investigated in 12 patients with cholestasis in basal conditions and 20 minutes after intravenous heparin. In all cases, lipoprotein-X was positive in the first sample and became negative after heparin. A decrease in triglycerides was observed in all patients after heparin with an increase in free fatty acids and mobilization of prebetalipoproteins, and a transformation of lecithin into lysoleithin in 4 cases after heparin. These facts suggest that heparin plays an important role in the mobilization of serum lipoprotein-X.

The triglyceride decrease and free fatty acid increase by lipoproteinlipase post-heparin effect does not modify the Lecithin:Cholesterol Acyltransferase activity in vitro, using homologous substrate, in normal subjects. These findings agree with the unmodified proportion of esterified cholesterol and relative proportion of phospholipids on thin layer chromatographic fractioning after heparin. The conclusion is reached that heparin has no action on Lecithin:Cholesterol Acyltransferase activity in normal subjects.

Serum concentration of apoprotein A, high density lipoprotein (HDL)-cholesterol and HDL-phospholipids has been studied in thirteen consecutive episodes of diabetic ketoacidosis. In three patients with type I diabetes mellitus HDL2 and HDL3 subfractions were also measured. Patients with type I diabetes showed greatly decreased HDL-cholesterol concentration on admission which increased into the normal range after insulin treatment, while HDL-phospholipids decreased during treatment and apoprotein A remained almost unmodified. In three patients with type I diabetes a virtual absence of HDL2-cholesterol subfraction was observed, which rose to normal values during recovery. Conversely, in type II diabetes mellitus HDL-cholesterol was slightly reduced on admission, and tended to decrease during recovery. These findings imply the existence of abnormalities in the qualitative composition of HDL, and indicate that HDL-cholesterol can fluctuate much more rapidly than previously thought.

A method for determining Lecithin: Cholesterol Acyltransferase (LCAT) activity is presented. Trace amounts of labelled cholesterol are added to innactivated homologous substrate from a pool of normal serum. LCAT activity is determined measuring the cholesterol esterification, and is expressed as micrograms of cholesterol esters formed per milliliter plasma per hour. LCAT time-course, reproducibility, activity after serum storage at 4 degrees C, and normal values from 20 healthy subjects are studied.

It is generally accepted that the bile acids are responsible for pathologies as a result of deficiency or by toxic action. Quantitative deficiency is difficult to evaluate but the normal pool of bile acids is generally considered to be between 2 and4 grams. Daily loss and replacement by synthesis is thought to be between 500 and 700 mg. There is experimental evidence to demonstrate the toxic action of certain bile acids on metabolic structures and processes. There is no doubt that alterations in the metabolism of bile acids give rise to certain pathologic aspects in some diseases of the gastrointestinal tract or the hepatobiliary system. There are other conditions, on the other hand, in which the study of these acids may reveal significant physiopathologic implications. The first group includes terminal ileopathy, blind loop syndrome, gastric ulcer, gastritis, cholestasis, cirrhosis of the liver, and cholelithiasis. In the second group are such diverse conditions as acute pancreatitis, cancer of the colon, endocrine disturbances, some hyperlipidemias, and others. Much of the present day understanding of the physiopathology of the bile acids will probably have to be revised in the nex few years, in view of the rapid advances being made in this field.

Serum high-density lipoprotein cholesterol (HDL-C) has been determined in 85 patients with peripheral vascular disease (PVD) and in 72 healthy control subjects. HDL-C levels were significantly decreased in patients with PVD. Considering other vascular risk factors as diabetes mellitus, smoking and hypertension, there were no differences in HDL-C levels. Twenty-three patients received heparin as treatment, this subgroup showed a HDL-C levels higher than patients who were not under heparin therapy. The possible clinical implications of these facts are discussed.

Bile acids play a fundamental role in the degradation and absorption of intestinal lipids. The primary ones are cholic acid and chenodeoxycholic acid which are synthesized from cholesterol in the liver and conjugate with taurine and glycine amino acids. The secondary bile acids are derived from the primary ones by the enzyme action of intestinal bacteria through a process of deconjugation and dehydroxylation. Their detergent property is based on the molecular configuration of these compounds, which present a hydrophilic and a hydrotion of these compounds, which present a hydrophilic and a hydrophobic surface. The different enzymes in the liver cells that intervene in the process of synthesis of bile acids are now known. A basic element in their physiology is the enterohepatic circulation, enabling the organism to take maximum advantage of these compounds. The dynamics of the cycle are maintained and regulated by the system of uptake and secretion of the cells, cholecystokinin, intestinal peristalsis, active transport across the ileal membrane, and by portal venous flow. Much of our knowledge about the biogenesis and functions of the bile acids has been acquired quite recently. Research over the past three decades has contributed to a great advance in our understanding of their physiology.