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Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...

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Fat Preference: A Novel Model of Eating Behavior in Rats
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EET agonist prevents adiposity and vascular dysfunction in rats fed a high fat diet via a decrease in Bach 1 and an

Komal Sodhi1, Nitin Puri, Kazuyoshi Inoue

  • 1Department of Physiology and Pharmacology, The University of Toledo College of Medicine, Health Education Building, 3000 Arlington Avenue, Toledo, OH 43614-2598, USA.

Prostaglandins & Other Lipid Mediators
|January 3, 2012
PubMed
Summary

Epoxyeicosatrienoic acids (EETs) and the heme oxygenase (HO) system protect against diet-induced obesity. An EET agonist reversed obesity-related cardio-metabolic dysfunction by enhancing HO-1 expression.

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Syndrome
  • Obesity Research

Background:

  • Epoxyeicosatrienoic acids (EETs) and heme oxygenase (HO) system involvement in adipogenesis is reported.
  • EET agonists' potential in obesity and cardio-metabolic dysfunction requires investigation.

Purpose of the Study:

  • To investigate the effectiveness of an EET agonist (NUDSA) on diet-induced obesity and associated cardio-metabolic dysfunction in rats.
  • To elucidate the role of the interplay between EETs and the HO system in mediating these effects.

Main Methods:

  • Rats were fed a high-fat (HF) diet for 16 weeks, with or without an EET agonist (NUDSA) and an HO inhibitor (SnMP).
  • Physiological, biochemical, and molecular markers of oxidative stress, inflammation, adiposity, and energy homeostasis were assessed.

Main Results:

  • HF diet induced oxidative stress, inflammation, and metabolic dysfunction, with reduced EETs and HO-1.
  • NUDSA treatment reversed these adverse effects, improving blood pressure, fat content, inflammation, and endothelial function.
  • NUDSA enhanced HO-1 expression via Bach 1 suppression, indicating EET-HO system interaction.

Conclusions:

  • EETs stimulate HO-1 expression through Bach 1 suppression.
  • The interplay between EETs and HO system provides vascular and metabolic protection against diet-induced obesity.