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Related Experiment Videos

Liver metabolism in CRF.

Miroslaw J Smogorzewski1, Shaul G Massry

  • 1Division of Nephrology and the Department of Medicine, University of Southern California, Los Angeles, USA. smogorze@hsc.usc.edu

American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
|March 4, 2003
PubMed
Summary

Liver dysfunction in chronic renal failure (CRF) is linked to altered calcium signaling in hepatocytes. Elevated cytosolic calcium (Ca2+) in CRF may downregulate key hepatic receptors and protein synthesis.

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Area of Science:

  • Nephrology
  • Hepatology
  • Molecular Biology

Background:

  • Uremic syndrome typically does not present with liver function alterations.
  • However, experimental uremia and chronic renal failure (CRF) show varying degrees of liver dysfunction.
  • This review covers two decades of research on hepatic metabolism and molecular regulation in uremia.

Purpose of the Study:

  • To summarize data on protein, carbohydrate, and lipid metabolism in the liver during uremia.
  • To explore molecular regulation of lipid and protein synthesis in the liver in CRF.
  • To highlight the role of cytosolic calcium ([Ca(2+)](i)) and signal transduction in hepatocytes during CRF.

Main Methods:

  • Literature review of studies over the past 20 years.
  • Analysis of data on hepatic metabolism (protein, carbohydrate, lipid) in uremia.
  • Focus on molecular mechanisms, including calcium signaling pathways.

Main Results:

  • Elevated parathyroid hormone (PTH) increases hepatocyte [Ca(2+)](i) in CRF.
  • Increased [Ca(2+)](i) may downregulate hepatic receptors for PTH, PTHrP, vasopressin, and angiotensin II.
  • Elevated basal [Ca(2+)](i) might affect mRNA for other hormone receptors and liver proteins.

Conclusions:

  • Altered hepatic calcium homeostasis is a key feature of chronic renal failure.
  • PTH-mediated calcium signaling plays a significant role in regulating hepatic gene expression and receptor function in CRF.
  • These molecular changes in hepatocytes contribute to liver dysfunction in patients with chronic renal failure.

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