Role of Metabolic Overload in the Initiation of DNA Synthesis following Partial Hepatectomy in the Rat

Kenda, J. F. Ngala; Hemptinne, Bernard de; Lambotte, Luc

doi:10.1159/000128422

Cited by 31 publications

(10 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While portal overflow injures the liver directly through nutrient excess, 17,21,22 endothelial activation 21 , and sinusoidal shear stress 19,23,24 , arterial vasoconstriction introduces secondary ischemic damage 25,26 . Several lines of work indicate that these insults are attenuated by reduction of portal flow.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Hemodynamics and Portal Flow Modulation

et al. 2017

View full text Add to dashboard Cite

Objective A principal aim of the Adult-to-Adult Living Donor Liver Transplantation Cohort Study was to study hepatic blood flow and effect of portal flow modulation on graft outcomes in the setting of increasing use of smaller and left lobe grafts. Methods Recipients of 274 living donor liver transplant were enrolled in A2ALL-2, including 233 (85.0%) right lobes, 40 (14.6%) left lobes, and 1 (0.5%) left lateral section. Hepatic hemodynamics were recorded after reperfusion. A total of 57 portal flow modulations were performed on 52 subjects. Results Modulation lowered portal pressure in 68% of subjects with inconsistent effects on hepatic arterial and portal flow. A higher rate of graft dysfunction was observed in modulated vs. unmodulated subjects (31% vs. 18%; p=0.03); however, graft survival in modulated subjects was not different from unmodulated subjects at 3 years. Conclusions These results suggest the need for a study using a prespecified portal flow modulation protocol with defined indications to better define the effects of these interventions.

show abstract

Section: Discussionmentioning

confidence: 99%

Hepatic Hemodynamics and Portal Flow Modulation

et al. 2017

View full text Add to dashboard Cite

show abstract

“…However, both the decrease of EC and the mitochondrial enhancement following partial hepatectomy are not so significant in this model in comparison with those of other animals [13,27,28]. For that reason, we have adopted a 82% subtotal hepatectomy according to the procedure of Weinbren and Woodward, in which the incorporation of 32p into DNA was delayed, compared with 67% partial hepatectomy [26].…”

Section: Discussionmentioning

confidence: 99%

Effect of cyclosporine on oxidative phosphorylation and adenylate energy charge of regenerating rat liver

et al. 1989

View full text Add to dashboard Cite

The effect of cyclosporin A (CyA) on regenerating liver was investigated in subtotal hepatectomized rats treated with CyA in terms of mitochondrial phosphorylative activity, hepatic energy charge, and serum bilirubin levels. In the CyA-treated hepatectomized group, the energy charge decreased from normal control value of 0.857 to 0.782 at 6 h after hepatectomy. The decreased energy charge, however, gradually increased and returned to 0.842 at 48 h after hepatectomy with no significant changes being observed between CyA-treated and untreated hepatectomized groups. Phosphorylation rate in the CyA-untreated group increased to 142% of the normal control at 24 h and then decreased to 114% at 48 h after hepatectomy. By contrast, phosphorylation rate in the CyA-treated group increased to 144% of the normal control at 24 h, but remained at the high value of 132% (P less than 0.01; compared to the CyA-untreated group) even at 48 h after hepatectomy. Serum total bilirubin levels in the CyA-treated group were significantly higher than those in the CyA-untreated group during all experimental periods. We conclude that CyA does not exert a direct detrimental effect on mitochondrial function and that, despite the marked hyperbilirubinemia induced by CyA, the mitochondrial phosphorylative activity increases adaptively to provide sufficient energy for enhanced ATP-utilizing reactions in an early process of liver regeneration.

show abstract

“…Extending this paradigm, other studies show that either intravenous or enteral dextrose supplementation suppresses both PH- [18–24] and toxin- (CCl 4 , thioacetamide; [25, 26] and J. Huang and D.A. Rudnick, unpublished observations) -induced hepatocellular proliferation.…”

Section: The Metabolic Response To Hepatic Insufficiency and Livermentioning

confidence: 99%

Functional Relationships between Lipid Metabolism and Liver Regeneration

Rudnick

Davidson

2012

International Journal of Hepatology

109

View full text Add to dashboard Cite

The regenerative capacity of the liver is well known, and the mechanisms that regulate this process have been extensively studied using experimental model systems including surgical resection and hepatotoxin exposure. The response to primary mitogens has also been used to investigate the regulation of hepatocellular proliferation. Such analyses have identified many specific cytokines and growth factors, intracellular signaling events, and transcription factors that are regulated during and necessary for normal liver regeneration. Nevertheless, the nature and identities of the most proximal events that initiate hepatic regeneration as well as those distal signals that terminate this process remain unknown. Here, we review the data implicating acute alterations in lipid metabolism as important determinants of experimental liver regeneration and propose a novel metabolic model of regeneration based on these data. We also discuss the association between chronic hepatic steatosis and impaired regeneration in animal models and humans and consider important areas for future research.

show abstract

Role of Metabolic Overload in the Initiation of DNA Synthesis following Partial Hepatectomy in the Rat

Cited by 31 publications

References 9 publications

Hepatic Hemodynamics and Portal Flow Modulation

Hepatic Hemodynamics and Portal Flow Modulation

Effect of cyclosporine on oxidative phosphorylation and adenylate energy charge of regenerating rat liver

Functional Relationships between Lipid Metabolism and Liver Regeneration

Contact Info

Product

Resources

About