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PMID |
Sentence |
1 |
2012352
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Toxicity was increased in the presence of an epoxide hydrolase inhibitor (17.5% +/- 0.3% dead cells) and abolished by an inhibitor of cytochrome P-450.
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2 |
19881255
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Diabetes reduced the amount of sEH protein in the liver and insulin restored the level of protein.
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3 |
19881255
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The NADPH oxidase inhibitor, diphenyleneiodonium chloride (DPIC), inhibited decrease in sEH expression at high glucose and hydrogen peroxide suppressed sEH expression.
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4 |
19644452
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Furthermore, peroxisome proliferator-activated receptor gamma (PPARgamma) agonists increased the expression of sEH in mature 3T3-L1 adipocytes in vitro and in adipose tissue in vivo.
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5 |
20439437
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Our aims were to determine whether sEH is involved in the regulation of hyperglycemia in diabetic mice and to investigate the reasons for the regulation of insulin secretion by sEH deletion or inhibition in islets.
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6 |
20439437
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We also examined the effects of sEH KO or t-AUCB on glucose-stimulated insulin secretion (GSIS) and intracellular calcium levels in islets.
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7 |
20439437
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More important, when insulin levels were assessed by hyperglycemic clamp study, sEH KO was found to promote insulin secretion.
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8 |
21757024
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A recent publication has demonstrated that stabilizing the levels of epoxyeicosatrienoic acids (EETs), CYP eicosanoids, by inhibiting or deleting soluble epoxide hydrolase (sEH) improves ?-cell function and reduces ?-cell apoptosis in diabetes.
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9 |
21832210
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Urinary monocyte chemoattractant protein-1 (MCP-1) excretion significantly increased in diabetic WT mice compared with control (868 ± 195 vs. 31.5 ± 7 pg/day), and this increase was attenuated in diabetic Ephx2 KO mice (420 ± 98 pg/day).
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10 |
21832210
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Renal NADPH oxidase and urinary thiobarbituric acid reactive substances excretion were reduced in diabetic Ephx2 KO compared with diabetic WT mice.
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11 |
21832210
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Additionally, our data also suggest that activation of HO-1 contributes to improved renal injury in diabetic Ephx2 KO mice.
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12 |
22007192
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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.
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