Metabolic Disorders of Serum Lipoproteins in Endotoxin‐Poisoned Mice: The Role of High Density Lipoprotein (HDL) and Triglyceride‐Rich Lipoproteins

Sakaguchi, Shuhei

doi:10.1111/j.1348-0421.1982.tb00251.x

Cited by 33 publications

(27 citation statements)

References 46 publications

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“…A number of reports are now available which show that suppression of LPL activities in adipose tissue, heart or post-heparin plasma resulting in hypertriglyceridemia occurs in infections or endotoxemia (1,3,8,9,(12)(13)(14). However, changes in H-TGL under such conditions are not well established.…”

Section: Discussionmentioning

confidence: 99%

“…From these reports, differences might also be expected between the effect of endotoxin on either H-TGL or LPL activity. Sakaguchi (14) recently showed a slight increase in H-TGL activity after injection of endotoxin from Salmonella typhimurium in mice. Our data, however, show clearly that the activity of H-TGL as well as that of LPL was decreased in animals treated with endotoxin from E. coli.…”

Section: Discussionmentioning

confidence: 99%

“…Part of the mechanism of this impaired removal of plasma triglyceride has been shown to be a deficiency of lipoprotein lipase (LPL) in adipose tissue (8,9,(12)(13)(14). Despite the observations concerning LPL described above, only a little information is available about another important enzyme for triglyceride removal, hepatic triglyceride lipase (H-TGL).…”

mentioning

confidence: 99%

“…A variety of invasions such as bacterial, viral and protozoan infections or tumors cause several physiological and biochemical disorders in the mammalian host (4,5,(12)(13)(14)(15). These include responses such as fever, mobilization of phagocytes, and activation of the immune system.…”

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confidence: 99%

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Lipid Metabolism in Endotoxic Rats

Kawakami

Murase

Itakura

et al. 1986

Microbiology and Immunology

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Studies were conducted to investigate the effect of E. coli endotoxin administration on hepatic triglyceride lipase (H-TGL) activity in rats, since H-TGL activity is known to behave differently from lipoprotein lipase (LPL) activity in various situations. Plasma triglyceride and free fatty acid concentrations were markedly elevated in animals after injection of endotoxin. Cholesterol and phospholipids were also increased significantly. Lipoprotein analysis by ultracentrifugation showed that the most pronounced increase of lipoproteins was in the VLDL and IDL fractions. Triglyceride lipase activities in post-heparin plasma were markedly decreased. A selective assay for H-TGL activity using a specific antibody revealed that this enzyme as well as LPL is significantly decreased (26% of control) in endotoxic animals. Thus, the increase of VLDL and IDL appears to result from the decrease of both of LPL and H-TGL.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Lipid Metabolism in Endotoxic Rats

Kawakami

Murase

Itakura

et al. 1986

Microbiology and Immunology

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“…Sakaguchi (8) reported that serum ex-lipoprotein (HDL) in the electrophoretic patterns was reduced according to the dosage of endotoxin given 18 hr postintoxication, and that the fraction in mice injected with lead acetate plus endotoxin was markedly lower than that mice given in the endotoxin alone. Freudenberg et al (2) surmised that HDL represents a transport protein for LPS in plasma to organs of clearance or to other cellular targets, and that LPS interacts with plasma HDL, forming a complex with characteristic electrophoretic mobility.…”

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confidence: 99%

Effect of Endotoxin Administration in Trypan Blue Pretreated Mice

Abe¹,

Sakaguchi²,

Sakaguchi³

1983

Microbiology and Immunology

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In a previous paper (7) we reported that administration of endotoxin plus lead acetate to mice resulted in marked formation of lipid peroxide, and the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in the liver were lower than those in mice treated with endotoxin alone. It has been noted that a blockade of the reticuloendothelial system (RES) increases the sensitivity of animals to the lethal effect of endotoxin (12). However, because of its numerous biological effects on cell metabolism, lead acetate, an RES depressor, can be considered to be a specific blocker different from the other agents. The present study was carried out to observe the effect of endotoxin administration under RES depression by trypan blue.Male ddY mice (Shizuoka Experimental Animal Farm Co., Japan), 6 to 7 weeks old and weighing 22 to 25 g, were purchased and maintained in this laboratory for at least one week. Salmonella typhimurium endotoxin (Westphal preparation obtained from Difco, Detroit, MI, U.S.A.) was used throughout this study. This toxin was suspended in normal saline prior to use. A dose of 50 mg/kg or 200 mgjkg of 1.25% trypan blue (Wako Pure Chemical Industries Ltd., Osaka) was injected intravenously into mice 24 hr before endotoxin administration unless otherwise noted. Control mice were injected intraperitoneally with 0.2 ml of a 0.9% saline solution. Mice were fasted after endotoxin administration.Lipid peroxide in liver tissue homogenates (in 8.1 % sodium dodecyl sulfate[SDS] containing 20% acetate buffer, pH 3.5) was determined fluorometrically with thiobarbituric acid (TBA) by a modification (4) of Vagi's method (14). Isozymes of lactate dehydrogenase were estimated electrophoretically according to the method by which NADH is formed in the presence ofphenazine methosulfate and NBT is reduced to a strongly colored formazan using the "LDH Isozyme-Test Kit" (Wako Pure Chemical Industries Ltd., Osaka). Serum lipoprotein was separated by disk-gel electrophoresis in 3.75% polyacrylamide gel performed with a previously stained lipoprotein according to the method of Narayan et al (3). Table 1 shows the percentage of survival after endotoxin injection in trypan blue (TB)-pretreated mice. TB was injected intravenously into mice at doses of 50 mg/kg, 100 mg/kg, and 200 mg/kg. Twenty-four hours after TB injection, 18 mg/kg of endotoxin was administered intraperitoneally to the mice. TB (200 973

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Tumor necrosis factor up-regulates expression of low-density lipoprotein receptors on HepG2 cells

Liao

Florén

1993

Hepatology

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Tumor necrosis factor mediates most biological activities of endotoxin and also, in part, mediates endotoxin-induced disturbances in lipid metabolism. In this study, the effect of tumor necrosis factor on low-density lipoprotein receptor activity was investigated in cells of HepG2, a well-differentiated human hepatoma cell line. Pretreatment of the cells with tumor necrosis factor leads to enhanced binding, uptake and degradation of 125I-labeled low-density lipoprotein. This effect of tumor necrosis factor was dose and time dependent. Tumor necrosis factor-stimulated enhancement of low-density lipoprotein binding occurred at all stages of cell growth. However, addition of an excess of unlabeled low-density lipoprotein, to down-regulate low-density lipoprotein receptors before exposure to tumor necrosis factor of the cells, completely abolished the effects of tumor necrosis factor. Competition experiments using unlabeled low-density lipoprotein and blockage experiments with a monoclonal low-density lipoprotein receptor antibody showed that tumor necrosis factor-stimulated low-density lipoprotein binding takes place through stimulation of low-density lipoprotein receptors. Comparison of the kinetics of specific low-density lipoprotein binding in the unstimulated cells and in the tumor necrosis factor-stimulated cells indicated that tumor necrosis factor caused a 30% increase in maximum velocity with no significant change in Michaelis constant, suggesting that tumor necrosis factor increases the number of low-density lipoprotein receptors on the cells rather than changing binding affinity. Preincubation of the cells with cycloheximide or actinomycin D totally abolished the up-regulatory effect of tumor necrosis factor on low-density lipoprotein receptors. Tumor necrosis factor did not stimulate proliferation of HepG2 cells, as judged by cell protein determination or by [3H]thymidine incorporation. In conclusion, this study suggests that tumor necrosis factor up-regulates expression of low-density lipoprotein receptors on HepG2 cells by stimulation of de novo synthesis of receptors, independent of cell growth.

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Metabolic Disorders of Serum Lipoproteins in Endotoxin‐Poisoned Mice: The Role of High Density Lipoprotein (HDL) and Triglyceride‐Rich Lipoproteins

Cited by 33 publications

References 46 publications

Lipid Metabolism in Endotoxic Rats

Lipid Metabolism in Endotoxic Rats

Effect of Endotoxin Administration in Trypan Blue Pretreated Mice

Tumor necrosis factor up-regulates expression of low-density lipoprotein receptors on HepG2 cells

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