Phenylbutyrate and β-cell function: contribution of histone deacetylases and ER stress inhibition

Epigenomics. 2017 May;9(5):711-720. doi: 10.2217/epi-2016-0160. Epub 2017 May 4.

Abstract

Incidences of diabetes are increasing globally due to involvement of genetic and epigenetic factors. Phenylbutyrate (PBA) is a US FDA approved drug for treatment of urea cycle disorder in children. PBA reduces endoplasmic reticulum (ER) stress and is proven as a potent histone deacetylases (HDACs) inhibitor. Chronic ER stress results in unfolding protein response, which triggers apoptosis. Abnormal ER homoeostasis is responsible for defective processing of several genes/proteins and contributes to β-cell death/failure. Accumulated evidences indicated that HDACs modulate key biochemical pathways and HDAC inhibitors improve β-cell function and insulin resistance by modulating multiple targets. This review highlights the role of PBA on β-cell functions, insulin resistance for possible treatment of diabetes through inhibition of ER stress and HDACs.

Keywords: ER stress; HDAC inhibition; diabetes; phenylbutyrate; β-cell.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diabetes Mellitus / drug therapy*
  • Diabetes Mellitus / metabolism
  • Endoplasmic Reticulum Stress*
  • Histone Deacetylase Inhibitors / pharmacology*
  • Histone Deacetylase Inhibitors / therapeutic use
  • Histone Deacetylases / metabolism*
  • Humans
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / metabolism*
  • Phenylbutyrates / pharmacology*
  • Phenylbutyrates / therapeutic use

Substances

  • Histone Deacetylase Inhibitors
  • Phenylbutyrates
  • Histone Deacetylases