Premium
Novel Insights into the Role of Soluble Epoxide Hydrolase in Adipogenesis
Author(s) -
Alquraishi Mohammed,
Puckett Dexter L.,
Chahed Samah L.,
BAETTAIEB AHMED
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09709
Subject(s) - epoxide hydrolase 2 , adipogenesis , adipose tissue , adipocyte , peroxisome proliferator activated receptor gamma , chemistry , biochemistry , biology , enzyme , gene , peroxisome proliferator activated receptor
Obesity is a growing epidemic that presents a major health problem worldwide. The past decade has seen advances in the identification of specific factors that contribute to this condition. However, despite these strides, there is still much to be learned about the underlying mechanisms. A better understanding of these biochemical mechanisms will enhance our ability to prevent and treat obesity. This study demonstrates that modulation of epoxy fatty acids (EpFA) metabolism in mouse white adipocytes alters cell cycle progression and clonal expansion. In addition, CRISPR/Cas9‐mediated deletion of soluble epoxide hydrolase (sEH), a cytosolic enzyme which hydrolyzes epoxy fatty acids (EpFA) into less active diols, resulted in alterations in adipogenesis. Similar findings were obtained using a selective sEH inhibitor 1‐trifluoromethoxyphenyl‐3‐(1‐propionylpiperidin‐4‐yl) urea (TPPU). Importantly, mice with specific deletion of sEH in the adipose tissue were resistant to high fat feeding and exhibited increased energy expenditure. Taken together, the present study demonstrates that modulation of sEH activity in white adipocytes alters adipocyte differentiation and improves glycemic control. Additionally, our findings suggest that sEH is a physiological modulator of adipogenesis and a potential target for the development of novel anti‐obesity therapeutic strategies. Support or Funding Information This work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (R00DK100736) to A.B.