[Lipid fraction content of puncture biopsy material from the liver of patients with diabetes mellitus and obesity]. / Sudurzhanie na lipidnite fraktsii v punktsionnobiopsichen material ot cheren drob na bolni sus zakharen diabet i zatlustiavane.

The quantity of the main lipid classes in hepatic tissue has been determined via thin layer chromatography on silica gel, the tissue obtained by blind hepatic biopsy in 20 patients with diabetes mellitus and obesity and in a control group of 5 patients with no hepatic disease. A considerable increase of lipid in liver was established in the patients with diabetes mellitus and obesity-the fraction of neutral lipids mainly. The fatty infiltration of liver in diabetics was accompanied by a considerable increase of triglyceride concentration--3,78 g/100 g wet body mass as compared with the controls--0,95 g/100 g wet body mass. Increased concentration of esters and cholesterol (80%) was established in the liver of the patients with diabetes and obesity as well as increased fraction of free fatty acids (230%). The concentrations of total phospholipids and free cholesterol in liver in both groups of patients proved to be rather close. The fatty infiltration of liver of diabetics with obesity was accompanied by marked increase of percentage content of triglycerides--from 17.3% in the control group to 42.1% from the total lipids in the patients with diabetes and obesity. Reverse alterations were established for the fraction of total phospholipids. Pronounced increase of the coefficient triglycerides/total phospholipids was established in case of diabetes and obesity.

[Effect of ethanol on the biosynthesis of major components of triacylglycerols and phospholipids in the rat liver]. / Vliianie étanola na biosintez osnovnykh komponentov triatsilglitseridov i fosfolipidov v pecheni krys.

Content of triacylglycerols was increased in rat liver tissue after administration of ethanol. Independent studies of biosynthesis of fatty acid and glycerol components of glycerolipids exhibited that 3H-leucine was mainly consumed in synthesis of glycerol moiety of phospholipids and triacylglycerols, whereas 14C-acetate was utilized in synthesis of fatty acids. Ethanol activated most distinctly the synthesis of glycerol moiety as compared with the synthesis of triacylglycerol fatty acids. In rat liver tissue ethanol caused an accumulation of unsaturated and monoenic fatty acids, while the ratio of arachidonic acid in phospholipids was decreased. Synthesis of triacylglycerol fatty acids was activated in presence of ethanol with simultaneous decrease in the rate of the label incorporation into linoleic and arachidonic acids; synthesis of fatty acids was stimulated de novo but the following elongation and desaturation of linoleic acid was inhibited. Ethanol activated more effectively esterification of fatty acids with formation of triacylglycerols as compared with phospholipids. Incorporation of the label into glycerol molecule occurred in response to activation of glycero-glyconeogenesis by ethanol. Acetyl-CoA, derived from 14C-acetate, was mainly used in synthesis of triacylglycerols, diacylglycerols, free cholesterol and its esters. Acetyl-CoA, produced from 3H-leucine, was mostly common involved in synthesis of monoacylglycerols and phospholipids.

[The effect of glucose and cycloheximide on glycerolipid biosynthesis in the rat liver]. / Deistvie gliukozy i tsiklogeksimida na biosintez glitserolipidov v pecheni krys.

Glucose and cycloheximide activated biosynthesis of phospholipids and, especially, of triacylglycerols involving 14C-acetate in rat liver tissue in vivo. Starvation did not affect the glycerolipid biosynthesis but decreased markedly the cholesterol production. In liver tissue of starved rats cycloheximide activated synthesis of glycerolipids and inhibited the cholesterol synthesis. Administration of glucose into the animals under conditions of their satiation augmented the fatty acid synthesis; the activating effect of cycloheximide was more distinct as compared with glucose. In satiated animals the most part of the label was incorporated into glycerolipid fatty acids after glucose and cycloheximide administration. Starvation inhibited synthesis of fatty acids with simultaneous activation of the glycerolipid glycerol production; cycloheximide activated still further the glyceroneogenesis. Both glucose and cycloheximide activated biosynthesis of palmitic and oleic acids of glycerolipids and inhibited the arachidonic acid synthesis. Similarity in the effect of glucose and cycloheximide on the glycerolipid biosynthesis might occur due to stimulation of glyceroneogenesis and to augmented production of alpha-glycerophosphate, which in turn increased the fatty acid esterification.

[Effect of adrenocorticotropic hormone on the biosynthesis of glycerolipid components in the rat liver]. / Deistvie adrenokortikotropnogo gormona na biosintez sostavnykh komponentov glitserolipidov v pecheni krys.

Single administration of ACTH led to stimulation of synthesis of saturated and monoenic fatty acids in liver tissue as well as to their esterification with formation of triacyl glycerols. The hormone inhibited elongation and desaturation of fatty acids and decreased the formation of polyenic fatty acids in liver tissue. Cycloheximide alone or simultaneously with ACTH activated synthesis of unsaturated and monoenic fatty acids and stimulated the glycerophosphate shunt of triacyl glycerols synthesis. The tropic hormone activated glyceroneogenesis contributing to an increase in concentration of both alpha-glycerophosphate and long-chain fatty acids in hepatocytes; either ACTH or cycloheximide stimulated the triacyl glycerols synthesis via induction of the key enzymes by excess of the substrates. Consumption of acetyl-CoA, derived from labeled leucine, for biosynthesis of individual lipids was regulated by other mechanisms distinct from those involved in consumption of acetyl-CoA pool, derived from labelled acetate.

[Effects of cortisol on lipid and lipoprotein synthesis in rat hepatocytes]. / Deistvie kortizola na biosintez lipidov i lipoproteidov v gepatotsitakh krys.

Under in vivo conditions cortisol induces moderate hyperlipidemia followed by an increase in the phospholipid and triglyceride concentrations in the blood and a decrease of cholesterol; similar changes were observed in the liver. At all time intervals studied cortisol inhibits the phospholipid and cholesterol syntheses and decreases the specific radioactivities of the lipids in the mitochondrial fraction. The hormone has an inhibiting effect on the fatty acid synthesis at early postinjection stages. The phospholipid synthesis is increased after adrenalectomy and is then inhibited after injection of the hormone. A single injection of ACTH or cortisol causes suppression of phospholipid and cholesterol syntheses and a decrease in their specific radioactivities in the mitochondria. A similar effect is observed under stress conditions. In addition, the hormone inhibits the synthesis of lipoprotein apoproteins of very low and high densities. After 5 hours following the hormone injection the lipoprotein apoprotein synthesis in the liver is activated; the activation of apoprotein synthesis is also observed after adrenalectomy. However, the injection of the hormone to adrenalectomized rats decreases the apoprotein synthesis. It was shown that in blood serum cortisol affects the conversions of very low density lipoproteins into low density lipoproteins, thus providing for hyperlipidemia.

[Cortisol, adrenocorticotropic hormone and apolipoprotein synthesis in rat hepatocytes]. / Kortizol, adrenokortikotropnyi gormon i biosintez apolipoproteinov v gepatotsitakh krys.

The influence of cortisol (5 mg/kg body wt administered daily for 5 and 10 days) on biosynthesis of apoproteins of lipoproteins of very low density in the liver and on the synthesis of apolipoproteins of very low, low, and high density (VLDL, LDL, and HDL apoproteins, respectively) in the blood serum of adrenalectomized animals, and after replacement cortisol therapy was studied. Cortisol treatment during these periods resulted in the VLDL apoproteins biosynthesis inhibition in the rat liver. The synthesis of apolipoproteins was increased by adrenalectomy; this effect was eliminated after replacement cortisol treatment. The apoprotein synthesis was stimulated within 5 hours by single injection of cortisol or ACTH. Study of the blood serum apolipoproteins specific radioactivity indicated metabolic change of lipoproteins, such as disturbed conversion from VLDL to LDL. Single and prolonged cortisol administration led to the opposite results. The authors believe that the metabolic disturbances of lipoproteins in the blood play a more important role in the pathogenesis of cortisol-induced hyperlipidemia than lipoprotein syntesis stimulation in the liver.

[Effect of a single ethanol injection on lipid and lipoprotein synthesis in rat liver]. / Vliianie odnokratnogo vvedeniia etanola na sintez lipidov i lipoproteidov v pecheni.

A single ethanol injection results in the increase of mono-, di- and tri-glicerides synthesis in rat liver, and also of the synthesis of apoprotein of very low density lipoproteins, their formation and secretion. Different uptake of pools of 14C-acetyl CoA, synthesized from injected 14C-acetate, and 3H-acetyl CoA, synthesized through metabolic pathways of 3H-leucine, indicates the compartmentalization of acetyl CoA in the synthesis of saturated and unsaturated fatty acids. 3H-acetyl CoA is more intensively used in the synthesis of unsaturated fatty acids than 14C-acetyl CoA synthesized from acetate. Ethanol increases the uptake of acetyl CoA, synthesized from acetate, for the synthesis of all the lipids, probably, for the expense of the increased synthesis of endogenous acetate in metabolic transformation of ethanol.