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Postprandial effect to decrease soluble epoxide hydrolase activity: roles of insulin and gut microbiota.

Jun Yang1, Young Taek Oh2, Debin Wan1

  • 1Department of Entomology and Nematology, University of California, Davis, CA, USA.

The Journal of Nutritional Biochemistry
|September 2, 2017
PubMed
Summary

Soluble epoxide hydrolase (sEH) activity significantly decreases after meals in rats, but not due to insulin. Gut bacteria appear to mediate this reduction in sEH activity, impacting metabolic and cardiovascular health.

Keywords:
Cardiovascular diseaseDiabetesDietary potassiumFFA epoxidesOxylipin analysis

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Area of Science:

  • Biochemistry
  • Metabolic Health
  • Cardiovascular Physiology

Background:

  • Epoxides of free fatty acids (FFAs), like epoxyeicosatrienoic acids (EETs), are crucial lipid mediators for metabolic and cardiovascular health.
  • Soluble epoxide hydrolase (sEH) rapidly metabolizes these beneficial FFAs into less active diols.
  • Inhibiting sEH increases EET levels, offering a potential therapeutic strategy for diabetes and cardiovascular diseases.

Purpose of the Study:

  • To investigate the impact of postprandial states on soluble epoxide hydrolase (sEH) activity in rats.
  • To determine if insulin action mediates the observed changes in sEH activity post-meal.
  • To explore the role of gut microbiota in regulating postprandial sEH activity.

Main Methods:

  • Analysis of plasma levels of 17 sEH products (FFA diols) in rats before and after a meal.
  • Calculation of sEH product to substrate (sEH P/S) ratios as an indicator of sEH activity.
  • Performance of hyperinsulinemic-euglycemic clamps to assess insulin's effect on sEH P/S ratios.
  • Evaluation of postprandial sEH P/S ratios in rats treated with antibiotics to deplete gut bacteria.

Main Results:

  • Plasma levels of sEH products and sEH P/S ratios significantly decreased in postprandial states in rats.
  • Hyperinsulinemic-euglycemic clamps showed minimal increase, not a decrease, in sEH P/S ratios, indicating insulin is not the mediator.
  • Antibiotic treatment completely abolished the postprandial decrease in sEH P/S ratios, implicating gut bacteria.

Conclusions:

  • Postprandial reduction in sEH activity is a significant physiological event in rats.
  • Insulin action does not account for the observed decrease in sEH activity after a meal.
  • Gut bacteria-derived factors likely play a critical role in modulating sEH activity in the postprandial state, warranting further investigation.