Koki Takata

Serum lipids and lipoproteins in patients with gallstone (relationship between serum lipids and types of stones in roentgenograms and sectional views)

SummarySerum lipids and lipoproteins of gallstone patients were analyzed and compared with lithogenesity of bile and type of stones by roentgenographic and cross-sectional views.Incidences of hypercholesterolemia and triglyceridemia were higher in patients with radiolucent gallstones than with radiopaque stones. Furthermore, an incidence of hypertriglyceridemia was higher in patients with radiolucent solitary stones than with radiolucent multiple stones. The degrees of hyperlipidemia were moderate.Lipoprotein disc electrophoresis of sera of hyperlipidemic patients revealed type IIa, IIb or IV. More solitary and less multiple stones were seen in the hyperlipoproteinemic patients than normolipoproteinemic. Multiple stones with normolipoproteinemia were more accompanied by unsaturated bile (lithogenic index <1.0) than those with hyperlipoproteinemia and solitary stones with hyperlipoproteinemia or without.Solitary stones obtained surgically from normolipoproteinemic patients were pure cholesterol, combination or mixed stones, while multiple stones not including pure cholesterol and combination stones with pure cholesterol in the center. Solitary stones in hyperlipoproteinemic patients proved mostly either pure cholesterol or combination stones with pure cholesterol in the center, while multiple stones containing all types of stones inclusive of a small number of other miscellaneous stones except cholesterol stones. Collectively more mixed and other miscellaneous stones except cholesterol stones, and less pure cholesterol and combination stones with pure cholesterol in the center were shown in normolipidemic patients, and vice versa in hyperlipoproteinemic patients.These results suggested serum lipids and lipoproteins being closely related to the initial precipitation, aggregation of cholesterol crystals and development of cholesterol gallstones through lipid metabolism of the whole body.

Probucol Promotes Hepatic Uptake of High Density Lipoprotein in Rats

SummaryProbucol significantly reduced high density lipoprotein (HDL)-cholesterol and apolipoprotein AI in rats. Hepatic uptake of radiolabelled human HDL3 increased significantly in vivo and in the isolated perfused rat liver preparation. In vivo, uptake of HDL3 by the adrenal glands also increased significantly. Hepatic cholesterol content in probucol-treated rats tended to increase, whereas newly synthesised cholesterol decreased significantly. The results of the present study suggest that enhanced uptake of HDL is one of the mechanisms of lowering serum HDL with probucol treatment.

Changes in high density lipoproteins in patients with hepatobiliary diseases

SummaryLipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (<10 mg/dl).The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3 but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.