Pharmacological inhibition of soluble epoxide hydrolase ameliorates diet-induced metabolic syndrome in rats

Iyer, Abishek, Kauter, Kathleen, Alam, Md. Ashraful, Hwang, Sung Hee, Morisseau, Christophe, Hammock, Bruce D. and Brown, Lindsay (2011) Pharmacological inhibition of soluble epoxide hydrolase ameliorates diet-induced metabolic syndrome in rats. Experimental Diabetes Research, 2012 758614.1-758614.11. doi:10.1155/2012/758614

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Author Iyer, Abishek
Kauter, Kathleen
Alam, Md. Ashraful
Hwang, Sung Hee
Morisseau, Christophe
Hammock, Bruce D.
Brown, Lindsay
Title Pharmacological inhibition of soluble epoxide hydrolase ameliorates diet-induced metabolic syndrome in rats
Journal name Experimental Diabetes Research   Check publisher's open access policy
ISSN 1687-5214
1687-5303
Publication date 2011-10-01
Year available 2012
Sub-type Article (original research)
DOI 10.1155/2012/758614
Open Access Status DOI
Volume 2012
Start page 758614.1
End page 758614.11
Total pages 11
Place of publication New York, NY, United States
Publisher Hindawi Publishing Corporation
Language eng
Subject 2712 Endocrinology, Diabetes and Metabolism
1210 Music
Abstract The signs of metabolic syndrome following chronic excessive macronutrient intake include body weight gain, excess visceral adipose deposition, hyperglycaemia, glucose and insulin intolerances, hypertension, dyslipidaemia, endothelial damage, cardiovascular hypertrophy, inflammation, ventricular contractile dysfunction, fibrosis, and fatty liver disease. Recent studies show increased activity of soluble epoxide hydrolase (sEH) during obesity and metabolic dysfunction. We have tested whether sEH inhibition has therapeutic potential in a rat model of diet-induced metabolic syndrome. In these high-carbohydrate, high-fat-fed rats, chronic oral treatment with trans-4-[4-(3-adamantan-1-ylureido)-cyclohexyloxy]-benzoic acid (t-AUCB), a potent sEH inhibitor, alleviated the signs of metabolic syndrome in vivo including glucose, insulin, and lipid abnormalities, changes in pancreatic structure, increased systolic blood pressure, cardiovascular structural and functional abnormalities, and structural and functional changes in the liver. The present study describes the pharmacological responses to this selective sEH inhibitor in rats with the signs of diet-induced metabolic syndrome. Copyright
Formatted abstract
The signs of metabolic syndrome following chronic excessive macronutrient intake include body weight gain, excess visceral adipose deposition, hyperglycaemia, glucose and insulin intolerances, hypertension, dyslipidaemia, endothelial damage, cardiovascular hypertrophy, inflammation, ventricular contractile dysfunction, fibrosis, and fatty liver disease. Recent studies show increased activity of soluble epoxide hydrolase (sEH) during obesity and metabolic dysfunction. We have tested whether sEH inhibition has therapeutic potential in a rat model of diet-induced metabolic syndrome. In these high-carbohydrate, high-fat-fed rats, chronic oral treatment with trans-4-[4-(3-adamantan-1-ylureido)-cyclohexyloxy]-benzoic acid (t-AUCB), a potent sEH inhibitor, alleviated the signs of metabolic syndrome in vivo including glucose, insulin, and lipid abnormalities, changes in pancreatic structure, increased systolic blood pressure, cardiovascular structural and functional abnormalities, and structural and functional changes in the liver. The present study describes the pharmacological responses to this selective sEH inhibitor in rats with the signs of diet-induced metabolic syndrome.
Keyword Endocrinology & Metabolism
Medicine, Research & Experimental
Endocrinology & Metabolism
Research & Experimental Medicine
ENDOCRINOLOGY & METABOLISM
MEDICINE, RESEARCH & EXPERIMENTAL
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Article ID 758614, pp. 1-11.

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2012 Collection
School of Biomedical Sciences Publications
 
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Created: Fri, 21 Oct 2011, 20:03:04 EST by Bacsweet Kaur on behalf of School of Biomedical Sciences