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Fibrates and cholestasis.

Nisanne S Ghonem1, David N Assis2, James L Boyer2

  • 1Department of Pharmaceutical Sciences, School of Pharmacy, MCPHS University, Boston, MA.

Hepatology (Baltimore, Md.)
|February 14, 2015
PubMed
Summary
This summary is machine-generated.

Peroxisome proliferator-activated receptor alpha (PPARα) ligands, like fenofibrate, show promise for treating cholestatic liver diseases such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) when ursodeoxycholic acid (UDCA) is ineffective.

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Area of Science:

  • Hepatology and Gastroenterology
  • Molecular Biology
  • Pharmacology

Background:

  • Cholestatic liver diseases, including primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC), result from impaired bile production, leading to liver fibrosis and failure.
  • Current treatments like ursodeoxycholic acid (UDCA) have limited efficacy, especially in advanced stages or for PSC, necessitating alternative therapeutic strategies.
  • Hepatic transporters regulate bile formation, and nuclear receptors (NRs) are key regulators of these transporters, presenting potential therapeutic targets.

Purpose of the Study:

  • To review the role of peroxisome proliferator-activated receptor alpha (PPARα) in regulating hepatic transporters involved in bile acid homeostasis.
  • To explore the mechanisms by which PPARα influences genes critical for bile acid synthesis and transport.
  • To assess the therapeutic potential of PPARα ligand therapy, such as fenofibrate, for cholestatic liver diseases.

Main Methods:

  • Literature review focusing on the role of nuclear receptors, specifically PPARα, in cholestasis.
  • Analysis of studies investigating PPARα's regulation of genes involved in bile acid metabolism and transport.
  • Examination of the expression patterns of PPARα-regulated genes in cholestatic liver conditions.

Main Results:

  • PPARα plays a central role in maintaining cholesterol, lipid, and bile acid homeostasis by regulating key genes in bile acid synthesis and transport.
  • Expression of many PPARα-regulated genes is altered in cholestatic liver diseases, indicating a disrupted regulatory network.
  • Specific mechanisms of PPARα's effects on certain transporters and enzymes in cholestasis require further investigation.

Conclusions:

  • PPARα is a critical regulator of hepatic transporters and bile acid homeostasis, making it a promising therapeutic target for cholestatic liver diseases.
  • PPARα ligand therapy, exemplified by fenofibrate, offers a potential alternative or adjunctive treatment for patients with PBC and PSC unresponsive to UDCA.
  • Further research into the precise mechanisms of PPARα action in cholestasis is warranted to optimize therapeutic strategies.