Insulin Resistance in the Control of Intestinal Lipid Metabolism

Status Completed

Clinical Trial Summary

America's preferential consumption of high-fat/high-sugar foods is a driving force in the current epidemic of obesity and insulin resistance. Recent scientific observations suggest that the taste of food may play a role in how the body processes the food eaten in a meal. The intestine may play a central role in all aspects of dietary fat metabolism, from initial encounter with taste buds in the mouth to eventual triglyceride (TG) storage in the body.

The investigators hypothesize that elevated blood fats in insulin resistance are a result of elevated intestinal-TG secretion and poor communication of this organ to the rest of the body after meals.

In this study, meal feeding and sensory studies will be performed to determine whether the mechanism of taste-associated intestinal signaling leads to higher levels of blood fats after meals in 24 healthy, insulin resistant and type 2 diabetic subjects. Individuals will consume special meals the night before the tests and participate in sensory tests in the morning to analyze the effect of taste.

The goal of this work is to understand how insulin resistance may cause impaired signaling between the taste buds and the intestine to result in an elevation in blood lipids, which increases the risk for other chronic diseases. This study will generate data for a future study to understand how diabetes treatment affects this process.

Clinical Trial Description

Subjects will participate in two screening visits to determine insulin resistance status and then participate in a single in-patient, clinical research center test.

There are no drugs used in this study. The goal is to test the physiological response to eating. ;

Study Design

Observational Model: Case Control, Time Perspective: Prospective

Related Conditions & MeSH terms

Clinical Trial Details

NCT number	NCT02020343
Study type	Observational
Source	University of Missouri-Columbia
Contact
Status	Completed
Phase	Phase 0
Start date	January 2014
Completion date	August 2016

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