Liver Triglyceride Accumulation Research Articles

Peroxidation of liver lipids in the pathogenesis of the ethanol-induced fatty liver.

Administration of an acutely intoxicating dose of ethanol produced significant increases in the concentration of liver triglyceride and enhanced the peroxidation of liver lipids in rats. Adipose triglyceride and lipid peroxide concentrations were unaltered. Coenzyme Q(4), an effective antioxidant, significantly inhibited accumulation of liver triglyceride following ethanol intoxication and prevented the peroxidation of liver lipids. These results, which demonstrate the selective ability of ethanol to induce peroxidation of liver lipids, together with the effectiveness of antioxidants, support the previously proposed hypothesis that peroxidation of liver lipids following ethanol intoxication is a factor in the pathogenesis of ethanol-induced liver injury.

Peroxidation of Liver Lipids in the Pathogenesis of the Ethanol-Induced Fatty Liver

Administration of an acutely intoxicating dose of ethanol produced significant increases in the concentration of liver triglyceride and enhanced the peroxidation of liver lipids in rats. Adipose triglyceride and lipid peroxide concentrations were unaltered. Coenzyme Q 4 , an effective antioxidant, significantly inhibited accumulation of liver triglyceride following ethanol intoxication and prevented the peroxidation of liver lipids. These results, which demonstrate the selective ability of ethanol to induce peroxidation of liver lipids, together with the effectiveness of antioxidants, support the previously proposed hypothesis that peroxidation of liver lipids following ethanol intoxication is a factor in the pathogenesis of ethanol-induced liver injury.

Fatty acid synthesis during early linoleic acid deficiency in the mouse

The capacity of liver to synthesize long-chain fatty acids is greatly enhanced during early linoleate deficiency in mice. The enzymes catalyzing the synthesis of fatty acids from acetate or malonyl CoA were measured directly in soluble fractions isolated from liver. The period of dietary restriction of linoleate is also accompanied by a rapid fall in the relative linoleate content of the liver; by marked changes in the composition of the fatty acids in liver; and by an accumulation of liver triglyceride.

Effect of 3, 5 dimethylpyrazole on blood free fatty acids and glucose

3, 5 Dimethylpyrazole lowers plasma free fatty acids in fed and fasted rats as well as in rats exposed to cold, submitted to adrenalectomy or treated with noradrenaline, ACTH or chlorpromazine. The accumulation of liver triglycerides following cold exposure, ethanol administration or ACTH treatment is also inhibited by 3, 5 dimethylpyrazole. In contrast with the marked effect on lipid metabolism, 3, 5 dimethylpyrazole did not exhibit any major effect on normal level of blood glucose or on hyperglycemia induced by glucose load or chlorpromazine treatment.

Liver Lipid Accumulation in Isoleucine-deficient Rats

Rats made acutely deficient in isoleucine by force-feeding a diet completely devoid of isoleucine, had higher concentrations of liver triglycerides than control rats. When liver slices from fed, but deficient rats were incubated with acetate-2-C14, total incorporation of the label into the fatty acids of triglycerides was nearly 4 times higher than in the triglycerides of control livers. Fatty acid analyses of the triglycerides of deficient rat livers revealed higher proportions of palmitic, stearic and oleic acids and lower proportions of linoleic and arachidonic acids than were in control livers. Lipoprotein synthesis appeared not to be impaired by the deficiency, since there were no differences in serum cholesterol, phospholipid, and lipoprotein concentrations in the 2 groups. Some impairment in the removal of liver triglyceride in deficient rats was suggested, however, because more linoleic acid accumulated in these animals than in the controls. The results indicated, therefore, that increased fatty acid synthesis in the liver may have been an important factor contributing to the excessive accumulation of liver triglyceride in isoleucine-deficient rats.

The influence of phenoxybenzamine and isopropylmethoxamine (BW 61-43) on some cardiovascular, metabolic, and histopathologic effects of norepinephrine infusions in dogs

The effects of intravenous norepinephrine infusion (0.5 mg/kg in two hours) in conscious dogs can be classified according to the influence of pretreatment with phenoxybenzamine (2 or 5 mg/kg intravenously one hour before norepinephrine) or isopropylmethoxamine (BW 61-43) (8 mg/kg intravenously 20 to 30 minutes before infusion). Effects blocked or reduced by phenoxybenzamine, but not by BW 61-43, include the rise in arterial pressure, electrocardiographic changes, accumulation of pericardial fluid rich in lactic dehydrogenase, the rise in hematocrit, presence of inclusion bodies in liver cells, and necrosis of the adrenal cortex. Effects blocked by BW 61-43, but not by phenoxybenzamine, include the rises in plasma FFA and glucose and the accumulation of triglycerides in liver. Both phenoxybenzamine and BW 61-43 block, at least partially, the accumulation of triglycerides in heart. Neither phenoxybenzamine nor BW 61-43 prevents the norepinephrine-induced depletion of glycogen in liver.

Triglyceride alterations in normal and reticuloendothelial stimulated rats following carbon tetrachloride

AbstractThe administration of a single dose of carbon tetrachloride to normal rats was associated with a significant increase in liver triglyceride concentration and a pronounced reduction in plasma triglycerides. The evaluation of hepatic activity indicated that the removal of bromsulphalein from plasma was significantly impaired while phagocytic function remained unaltered. Animals with pronounced hyperplasia and hyperfunction of the reticulo‐endothelial system induced by zymosan were less susceptible to carbon tetrachloride, manifesting a smaller degree of liver triglyceride accumulation and maintenance of a normal plasma triglyceride level. The possible significance of these findings are discussed.