Changes in lipoprotein binding and uptake by hepatocytes during rat liver regeneration

Trentalance, A.; Bruscalupi, Giovannella; Devirgiliis, Laura Conti; Leoni, Silvia; Mangiantini, M. T.; Rossini, L; Spagnuolo, S; Erickson, Sandra K.

doi:10.1007/bf01116000

Cited by 10 publications

(11 citation statements)

References 36 publications

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“…Partial liver resection resulted in a marked decrease in the concentration of VLDL lipid components, particularly triacylglycerol. These data are in agreement with those of Trentalance et al [10], who reported a decrease of plasma VLDL by approx. 50 % at 16 h after surgery.…”

Section: Discussionsupporting

confidence: 94%

“…In view of the discrepancies mentioned above (ref. [10] versus refs. [4,5]), we also measured lipid content and composition of the major lipoproteins (VLDL, LDL and HDL) as a function of post-surgery time.…”

Section: Introductionmentioning

confidence: 96%

“…There have been very few studies on the effects of PH on these key enzymes, except for an early report by Mangiapane et al [9], who showed that the activity of phosphatidate phosphohydrolase was increased in liver homogenates from sub-totally hepatectomized rats. Discrepant results have been published with respect to the effects of liver resection on lipoprotein secretion. Although several investigators showed that the secretion of lipoproteins was not inhibited after PH [4,5], Trentalance et al [10] recently reported that the plasma concentration of very-low-density lipoprotein (VLDL) was decreased at 16 h after surgery. Hitherto the effects of PH on the synthesis and secretion of triacylglycerol have been investigated in vivo by determining the incorporation of radioactive precursors into hepatic lipids and into components of VLDL secreted by the liver [4,5].…”

Section: Introductionmentioning

confidence: 99%

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Biosynthesis and secretion of triacylglycerol in rat liver after partial hepatectomy

Tijburg

Nyathi

Meijer

et al. 1991

Biochemical Journal

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Partially hepatectomized rats were used to investigate the mechanism of fatty-liver development in the regenerating rat liver. After partial hepatectomy the amount of hepatic triacylglycerol increased by almost 4-fold compared with sham-operated rats. The activities of both cytosolic and microsomal phosphatidate phosphohydrolase were enhanced at 12 h after surgery. The activity of diacylglycerol acyltransferase was increased at a later stage of regeneration. Analysis of plasma lipoproteins showed a significant decrease of lipids associated with very-low-density lipoproteins (VLDL). Relative to control, the rate of hepatic triacylglycerol synthesis from [3H]glycerol in vivo was stimulated at 22 h after partial liver resection. However, secretion of glycerol-labelled triacylglycerol in VLDL was the same in control and hepatectomized rats. In cultures of hepatocytes from hepatectomized donor rats, the concentration of triacylglycerol and the biosynthesis of this lipid from [3H]glycerol or from [3H]oleate were enhanced. The secretion of total triacylglycerol into the medium was not affected, resulting in a net accumulation of intracellular triacylglycerol. The rate of secretion of leucine-labelled apolipoproteins B and E associated with VLDL was similar in cell cultures from hepatectomized and sham-operated rats. The results of this study show that the enhancement of the biosynthesis of triacylglycerol in hepatectomized livers is not accompanied by an increase of the secretion of VLDL.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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Biosynthesis and secretion of triacylglycerol in rat liver after partial hepatectomy

Tijburg

Nyathi

Meijer

et al. 1991

Biochemical Journal

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“…Its expression was reported as significantly up-regulated in serum of patients diagnosed with DILI but not in those with non-alcoholic steatohepatitis [20,23]. Early work had shown transcriptional and posttranscriptional regulation of ApoE, ApoA1 and ApoA2 in liver tissue at various pathophysiological states [40] and changes in lipoprotein binding and uptake by hepatocytes during rat liver regeneration [41]. In a proteomic investigation of drug-induced steatosis a moderate but statistically significant up-regulation of ApoE was observed in rat liver, further documenting its prognostic value in predicting DILI.…”

Section: Discussionmentioning

confidence: 99%

Serum acute phase reactants hallmark healthy individuals at risk for acetaminophen-induced liver injury

et al. 2013

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BackgroundAcetaminophen (APAP) is a commonly used analgesic. However, its use is associated with drug-induced liver injury (DILI). It is a prominent cause of acute liver failure, with APAP hepatotoxicity far exceeding other causes of acute liver failure in the United States. In order to improve its safe use this study aimed to identify individuals at risk for DILI prior to drug treatment by searching for non-genetic serum markers in healthy subjects susceptible to APAP-induced liver injury (AILI).MethodsHealthy volunteers (n = 36) received either placebo or acetaminophen at the maximum daily dose of 4 g for 7 days. Blood samples were taken prior to and after APAP treatment. Serum proteomic profiling was done by 2D SDS-PAGE and matrix-assisted laser desorption/ionization-time of flight-mass spectrometry. Additionally, the proteins C-reactive protein, haptoglobin and hemopexin were studied by quantitative immunoassays.ResultsOne-third of study subjects presented more than four-fold increased alanine transaminase activity to evidence liver injury, while serum proteomics informed on 20 proteins as significantly regulated. These function primarily in acute phase and immune response. Pre-treatment associations included C-reactive protein, haptoglobin isoforms and retinol binding protein being up to six-fold higher in AILI susceptible individuals, whereas alpha1-antitrypsin, serum amyloid A, kininogen and transtyretin were regulated by nearly five-fold in AILI responders. When compared with published findings for steatohepatitis and cases of hepatocellular, cholestatic and mixed DILI, 10 proteins were identified as uniquely associated with risk for AILI, including plasminogen. Notably, this zymogen facilitates macrophage chemotactic migration and inflammatory response as reported for plasminogen-deficient mice shown to be resistant to APAP hepatotoxicity. Finally, analysis of a publicly available database of gene expression profiles of cultures of human hepatocytes treated with drugs labeled as no- (n = 8), low- (n = 45) or most-DILI-concern (n = 39) confirmed regulation of the identified biomarkers to demonstrate utility in predicting risk for liver injury.ConclusionsThe significant regulation of acute phase reactants points to an important link between AILI and the immune system. Monitoring of serum acute phase reactants prior to drug treatment may contribute to prevention and management of AILI, and may also be of utility for other drugs with known liver liabilities.

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“…Among the various metabolic processes that take place during hepatic regeneration some parameters of lipid metabolism have been reported : the rate of esterification of fatty acids from adipose tissue is higher, lipogenesis is increased [8], capacity to take up circulating lipoproteins is reduced, and lecithin cholesterol acyltransferase (LCAT) activity is low. Liver regeneration is also associated with a reduction in plasma levels of very-lowdensity lipoprotein (VLDL) and an increase in the levels of lowdensity lipoprotein (LDL) [9]. In order for the liver to be able to regain its complete functionality and regenerate its mass, contributions of metabolic precursors from other tissues are required.…”

Section: Introductionmentioning

confidence: 99%

Hepatic regeneration induces changes in lipoprotein lipase activity in several tissues and its re-expression in the liver

Sabugal

Robert

Julve

et al. 1996

Biochemical Journal

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We examined the expression of lipoprotein lipase (LPL) gene and LPL activity following a two-thirds hepatectomy and during liver regeneration. In most of the tissues studied, LPL activity increased a few hours after partial hepatectomy, but soon returned to normal levels. The greatest increase was found in the adrenal glands, plasma and liver. This increase in LPL activity in the liver could be partially due to an increase in the influx of the enzyme from extrahepatic tissues. There is, however, also a re-expression of LPL mRNA in the liver after partial hepatectomy (during the first hours). It is well known that LPL is expressed in the liver of neonatal animals, but progressively decreases during post-natal development, to reach adult levels around the time of weaning. Our results show by the first time that the remaining liver re-expresses LPL gene during the regeneration process and that the hepatocytes de-differentiate and acquire some of the neonatal characteristics. The increase in LPL mRNA will contribute to the rise in LPL activity after hepatectomy. This presence of LPL could enable the liver to take up fatty acids from the circulating triacylglycerols, which are needed as energetic and plastic substrates during the process of hepatic regeneration.

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Changes in lipoprotein binding and uptake by hepatocytes during rat liver regeneration

Cited by 10 publications

References 36 publications

Biosynthesis and secretion of triacylglycerol in rat liver after partial hepatectomy

Biosynthesis and secretion of triacylglycerol in rat liver after partial hepatectomy

Serum acute phase reactants hallmark healthy individuals at risk for acetaminophen-induced liver injury

Hepatic regeneration induces changes in lipoprotein lipase activity in several tissues and its re-expression in the liver

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