Bettaieb_2013_J.Biol.Chem_288_14189

Reference

Title : Soluble Epoxide Hydrolase Deficiency or Inhibition Attenuates Diet-induced Endoplasmic Reticulum Stress in Liver and Adipose Tissue - Bettaieb_2013_J.Biol.Chem_288_14189
Author(s) : Bettaieb A , Nagata N , Aboubechara D , Chahed S , Morisseau C , Hammock BD , Haj FG
Ref : Journal of Biological Chemistry , 288 :14189 , 2013
Abstract :

Soluble epoxide hydrolase (sEH) is a cytosolic enzyme whose inhibition has beneficial effects in cardiovascular, inflammatory, and metabolic diseases in murine models. Mice with targeted deletion or pharmacological inhibition of sEH exhibit improved insulin signaling in liver and adipose tissue. Herein, we assessed the role of sEH in regulating endoplasmic reticulum (ER) stress in liver and adipose tissue. We report that sEH expression was increased in the livers and adipose tissue of mice fed a high fat diet, the adipose tissue of overweight humans, and palmitate-treated cells. Importantly, sEH deficiency or inhibition in mice attenuated chronic high fat diet-induced ER stress in liver and adipose tissue. Similarly, pharmacological inhibition of sEH in HepG2 cells and 3T3-L1 adipocytes mitigated chemical-induced ER stress and activation of JNK, p38, and cell death. In addition, insulin signaling was enhanced in HepG2 cells treated with sEH substrates and attenuated in cells treated with sEH products. In summary, these findings demonstrate that sEH is a physiological modulator of ER stress and a potential target for mitigating complications associated with obesity.

PubMedSearch : Bettaieb_2013_J.Biol.Chem_288_14189
PubMedID: 23576437

Related information

Inhibitor TUPS

Citations formats

Bettaieb A, Nagata N, Aboubechara D, Chahed S, Morisseau C, Hammock BD, Haj FG (2013)
Soluble Epoxide Hydrolase Deficiency or Inhibition Attenuates Diet-induced Endoplasmic Reticulum Stress in Liver and Adipose Tissue
Journal of Biological Chemistry 288 :14189

Bettaieb A, Nagata N, Aboubechara D, Chahed S, Morisseau C, Hammock BD, Haj FG (2013)
Journal of Biological Chemistry 288 :14189