Increased Hepatic Fibrogenesis in the Cholesterol-Fed Mouse

Lee, S. P.

doi:10.1042/cs0610253

Cited by 8 publications

(2 citation statements)

References 10 publications

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“…The ICG excretion rate decreased significantly with moderate steatosis. Thickening of the sinusoidal wall with membranous formation and proliferation of collagen fibres with 'intrasinusoidal block' decreases the diffusion of protein-bound substances such as ICG into the extravascular space [32,33]. Impairment of ICG excretion could also be explained by reduced transport across the biliary canalicular membrane which is energy-dependent and would be influenced by a reduction in hepatic adenosine triphosphate content [34], secondary to the reduction of regional blood volume and decrease of regional oxygenation [27].…”

Section: Discussionmentioning

confidence: 99%

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Seifalian¹,

El-Desoky²,

Davidson³

2001

Eur Surg Res

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Transplantation of a fatty liver is associated with a higher incidence of primary non-function of the graft. Indocyanine green (ICG) has been used for assessing hepatic dysfunction but not for quantifying liver steatosis. New Zealand white rabbits were fed a normal diet (group A) or a high-cholesterol (2%) diet for 4, 8, and 12 weeks in groups B, C, and D, respectively. Laparotomy was performed for liver exposure. Hepatic artery, portal vein, and total blood flow, hepatic microcirculation, portal pressure, liver function parameters, and blood cholesterol levels were measured. The hepatic ICG concentration was measured using near-infrared spectroscopy, and its uptake and excretion rates were calculated. The severity of steatosis was assessed from liver biopsy specimens by a semiquantitative grading system. Cholesterol feeding resulted in mild steatosis after 4 weeks and in moderate steatosis after 8 and 12 weeks. Mild steatosis was associated with insignificant changes in haemodynamic parameters, liver function, and ICG handling as compared with controls. Moderate steatosis caused a significant reduction in portal and total hepatic blood flow and microcirculation with a significant increase in hepatic artery flow and portal pressure. These haemodynamic changes were associated with a significant alteration in liver function tests. With moderate steatosis, ICG uptake and excretion were significantly reduced. The ICG uptake rate significantly correlated with total blood flow and microcirculation. The ICG excretion rate significantly correlated with the changes in bilirubin, liver enzymes, and albumin. Direct ICG quantification by near-infrared spectroscopy could be used to assess the severity of hepatic steatosis by reflecting impaired parenchymal perfusion and liver dysfunction.

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Section: Discussionmentioning

confidence: 99%

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Seifalian¹,

El-Desoky²,

Davidson³

2001

Eur Surg Res

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“…The most profound effect in this respect was a marked accumulation of cholesterol and triglycérides in the liver which also has been observed in other species such as rats (Morin et al, 1962;Rönnemaa, 1976;Hulbron et al, 1982;Martins and Dhopeswharkar, 1982;Beynen et al, 1984), guinea pigs (Beck and Drevon, 1980), rabbits (Lee and Ho, 1972;Gupta et al, 1976) and mice (Lee, 1981;Reihner and Stahlberg, 1996). The extremely high concentrations of cholesterol and triglycérides in VLDL might be the consequence of a very high rate of lipid secretion from liver into blood.…”

Section: Discussionmentioning

confidence: 80%

The effect of a combined dietary treatment with cholesterol and cholic acid on the lipid metabolism of geese at low or high choline concentrations

Eder

1999

Archiv für Tierernaehrung

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A previous study demonstrated that a dietary treatment of young geese with cholesterol and cholic acid raises lipid concentrations in the liver. The present study was carried out to investigate whether such a lipid accumulation caused by those hyperlipidemic compounds can be intensified by low dietary choline concentrations. Therefore, 38 eight-week old geese were divided into four groups of 9 or 10 animals each and received a basal diet poor in choline which consisted predominately of maize and soy protein isolate over a period of 8 weeks. Treatment factors were supplementation of diets with cholesterol and cholic acid (0 vs. 5 g of cholesterol and cholic acid each per kg) and supplementation of choline chloride (0 vs. 1.5 g/kg). Final body weights as well as carcass weights were neither influenced significantly by dietary treatment with cholesterol and cholic acid nor by low dietary choline concentrations. However, feeding diets supplemented with cholesterol and cholic acid markedly increased liver weights (two-fold), hepatic triglyceride (3.7-fold) and cholesterol (12-fold) concentrations and percentages of monounsaturated fatty acids at the expense of saturated and polyunsaturated fatty acids in the liver. In geese fed diets with cholesterol and cholic acid, insufficient choline supply did not intensify, but even slightly reduced hepatic lipid accumulation. Geese fed diets with cholesterol and cholic acid exhibited markedly increased levels of cholesterol, triglycerides and phospholipids in plasma and very low-density lipoproteins, regardless of the choline supply. Muscle tissue of geese fed diets supplemented with cholesterol and cholic acid exhibited also increased concentrations of triglycerides and cholesterol whereas the fatty acid composition of muscle lipids remained unchanged. Among geese without hyperlipidemic treatment, concentrations of triglycerides in plasma and very low-density lipoproteins as well as the concentrations of phosphatidylcholine in liver and muscle tissue were not reduced by low dietary choline concentrations. Therefore, it is suggested that those animals were able to synthesize endogenous sufficient choline.

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Cholesteryl ester storage disease: Pathologic changes in an affected fetus

et al. 1987

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The prenatal diagnosis of cholesteryl ester storage disease, a rare autosomal recessive disorder, was made by demonstration of deficient lysosomal acid lipase activity in cultured amniocytes from an at-risk fetus. The histochemical and ultrastructural changes in the affected fetus (at 17 gestational weeks) are described and compared to findings in liver and duodenal biopsy specimens from a 9-year-old homozygous female. Massive lysosomal cholesterol and lipid accumulation was demonstrated in fetal hepatocytes, adrenal cells and syncytiotrophoblasts. Of particular note was the observation of extensive necrosis in the fetal adrenal glands. Necrosis of the adrenals may precede the calcification observed in some patients with cholesteryl ester storage disease and in most patients with Wolman disease, an allelic variant due to lysosomal acid lipase deficiency. Fibrosis of the liver and lipid accumulation in macrophages in liver and duodenum, which were present in the 9-year-old homozygote, were not observed in the affected fetus, and therefore, may represent later manifestations of the disease.

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Increased Hepatic Fibrogenesis in the Cholesterol-Fed Mouse

Cited by 8 publications

References 10 publications

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

The effect of a combined dietary treatment with cholesterol and cholic acid on the lipid metabolism of geese at low or high choline concentrations

Cholesteryl ester storage disease: Pathologic changes in an affected fetus

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