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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.
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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.
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Inclusion criteria
Healthy subjects (age 18-50y) will be categorized as:
Overweight/obese insulin resistant subjects will have a family history of diabetes as defined as at least one parent or grandparent with type 2 diabetes, or at least one other family member with type 2 diabetes.
Exclusion criteria
22 participants in 3 patient groups
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Data sourced from clinicaltrials.gov
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