PMID- 26621325
OWN - NLM
STAT- MEDLINE
DCOM- 20170109
LR  - 20220408
IS  - 1753-0407 (Electronic)
IS  - 1753-0407 (Linking)
VI  - 8
IP  - 3
DP  - 2016 May
TI  - Soluble epoxide hydrolase: A potential target for metabolic diseases.
PG  - 305-13
LID - 10.1111/1753-0407.12358 [doi]
AB  - Epoxyeicosatrienoic acids (EETs), important lipid mediators derived from 
      arachidonic acid, have many beneficial effects in metabolic diseases, including 
      atherosclerosis, hypertension, cardiac hypertrophy, diabetes, non-alcoholic fatty 
      liver disease, and kidney disease. Epoxyeicosatrienoic acids can be further 
      hydrolyzed to less active diols by the enzyme soluble epoxide hydrolase (sEH). 
      Increasing evidence suggests that inhibition of sEH increases levels of EETs, 
      which have anti-inflammatory effects and can prevent the development of 
      hypertension, atherosclerosis, heart failure, fatty liver, and multiple organ 
      fibrosis. Arachidonic acid is the most abundant omega-6 polyunsaturated fatty 
      acid (PUFA) and shares the same set of enzymes with omega-3 PUFAs, such as 
      docosahexaenoic acid and eicosapentaenoic acid. The omega-3 PUFAs and 
      metabolites, such as regioisomeric epoxyeicosatetraenoic acids and 
      epoxydocosapentaenoic acids, have been reported to have strong vasodilatory and 
      anti-inflammatory effects. Therefore, sEH may be a potential therapeutic target 
      for metabolic disorders. In this review, we focus on our and other recent studies 
      of the functions of sEH, including the effects of its eicosanoid products from 
      both omega-3 and omega-6 PUFAs, in various metabolic diseases. We also discuss 
      the possible cellular and molecular mechanisms underlying the regulation of sEH.
CI  - (c) 2015 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and John 
      Wiley & Sons Australia, Ltd.
FAU - He, Jinlong
AU  - He J
AD  - Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of 
      Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Wang, Chunjiong
AU  - Wang C
AD  - Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of 
      Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Zhu, Yi
AU  - Zhu Y
AD  - Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of 
      Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Ai, Ding
AU  - Ai D
AD  - Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of 
      Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20160109
PL  - Australia
TA  - J Diabetes
JT  - Journal of diabetes
JID - 101504326
RN  - EC 3.3.2.- (Epoxide Hydrolases)
SB  - IM
MH  - Animals
MH  - Epoxide Hydrolases/*antagonists & inhibitors/metabolism
MH  - Humans
MH  - Metabolic Diseases/enzymology/*prevention & control
OTO - NOTNLM
OT  - arachidonic acid
OT  - epoxyeicosatrienoic acids
OT  - metabolic disease
OT  - polyunsaturated fatty acids
OT  - soluble epoxide hydrolase
OT  - 代谢性疾病
OT  - 可溶性表氧化物水解酶
OT  - 多不饱和脂肪酸
OT  - 环氧-二十碳三烯酸
OT  - 花生四烯酸
EDAT- 2015/12/02 06:00
MHDA- 2017/01/10 06:00
CRDT- 2015/12/02 06:00
PHST- 2015/07/15 00:00 [received]
PHST- 2015/11/16 00:00 [revised]
PHST- 2015/11/22 00:00 [accepted]
PHST- 2015/12/02 06:00 [entrez]
PHST- 2015/12/02 06:00 [pubmed]
PHST- 2017/01/10 06:00 [medline]
AID - 10.1111/1753-0407.12358 [doi]
PST - ppublish
SO  - J Diabetes. 2016 May;8(3):305-13. doi: 10.1111/1753-0407.12358. Epub 2016 Jan 9.