Insulin Resistance in the Control of Intestinal Lipid Metabolism
| Status: | Recruiting |
|---|---|
| Conditions: | Endocrine |
| Therapuetic Areas: | Endocrinology |
| Healthy: | No |
| Age Range: | 18 - 50 |
| Updated: | 4/21/2016 |
| Start Date: | January 2014 |
| End Date: | December 2016 |
| Contact: | Elizabeth J Parks, PhD |
| Email: | parksej@missouri.edu |
| Phone: | 573-822-5864 |
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.
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.
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.
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.
Inclusion Criteria:
Healthy subjects (age 18-50y) will be categorized as:
- lean/insulin sensitive (IS) (n=8, BMI uU/mL)
- overweight/obese IS (n=8, BMI 26-35 and SI >2.5 min-1 10-4 * per uU/mL)
- overweight/obese insulin resistant (n=8, BMI 26-35 and SI <2.5 min-1 10-4 * per
uU/mL).
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.
- Type 2 diabetic patients (BMI 26-35, and OGTT 2h glucose >/= 140 mg/dL.
Exclusion Criteria:
- BMI over 35 kg/m2: We felt it prudent to limit the additional variability that could
be caused by morbid obesity (and by diabetes), given the early stages of this
research area.
- Unusual eating habits (dietary fat< 30% or >40% of energy, skipping breakfast,
day-long fasting, or allergies to milk). Habitual food intake can influence taste
acuity and milk is used in the formulas to dissolve the isotopes.
- Uncontrolled hypertension, or occasional or regular smoker, use of supplements or
medications that interfere with lipid, protein, or carbohydrate metabolism or impact
taste. For example, the hypertensive drugs thiazides or the supplement chondroitin
sulfate or niacin, can be associated with impaired glucose tolerance. ACE inhibitors
and beta-blockers and smoking can affect taste. Use of insulin in the case of type 2
diabetics.
- Pregnancy (urine test), breastfeeding, or anemia (CBC with diff): Limitations of
blood that can be drawn. Postmenopausal women frequently have increases in blood
lipids since lack of estrogen influences lipid metabolism.
- Alcohol intake: Males >140 g/week, females > 70 g/week. Excess EtOH increases lipid
synthesis and secretion in the liver and whether it also has an impact on intestinal
TG metabolism is unknown.
- Fasting plasma TG >300 mg/dL. Extreme hypertriglyceridemia could be due to either
elevations in VLDL or chylomicrons, either of which would impair our ability to
resolve dietary metabolic processes.
- Exclude those who need to consume acetaminophen-containing medications on a regular
basis. Acetaminophen is administered with meals to assess gastric emptying.
- Postmenopausal women.
We found this trial at
1
site
Columbia, Missouri 65211
(573) 882-2121
Principal Investigator: Elizabeth J. Parks, PhD
Phone: 573-884-1708
University of Missouri T he University of Missouri was founded in 1839 in Columbia, Mo.,...
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