Race Adiposity Interactions Regulate Mechanisms Determining Insulin Sensitivity
| Status: | Completed |
|---|---|
| Conditions: | Neurology, Endocrine |
| Therapuetic Areas: | Endocrinology, Neurology |
| Healthy: | No |
| Age Range: | 19 - 45 |
| Updated: | 7/18/2018 |
| Start Date: | January 8, 2014 |
| End Date: | June 30, 2018 |
This research study will examine how ethnic/racial background, body composition (%body fat),
and the location of body fat affect the ability of the hormone insulin to promote uptake of
blood sugar in persons who are 19 to 45 years of age. When insulin is ineffective in
promoting blood sugar uptake, this condition is termed "insulin resistance." Insulin
resistance plays a major role in the development of chronic metabolic diseases (such as type
2 diabetes, cardiovascular disease, and cancer), many of which differ with race. Previous
studies suggest that insulin resistance is higher in African-Americans (AA) vs.
European-Americans (EA). However, results from these studies remain unclear due to different
testing measures used for insulin resistance as well as differences in body fat between
individuals. Results from this research study may help explain why insulin resistance differs
with genetic background and may guide development of personalized treatment strategies with
implications for several chronic metabolic diseases (e.g., type 2 diabetes, cardiovascular
disease, and cancer).
and the location of body fat affect the ability of the hormone insulin to promote uptake of
blood sugar in persons who are 19 to 45 years of age. When insulin is ineffective in
promoting blood sugar uptake, this condition is termed "insulin resistance." Insulin
resistance plays a major role in the development of chronic metabolic diseases (such as type
2 diabetes, cardiovascular disease, and cancer), many of which differ with race. Previous
studies suggest that insulin resistance is higher in African-Americans (AA) vs.
European-Americans (EA). However, results from these studies remain unclear due to different
testing measures used for insulin resistance as well as differences in body fat between
individuals. Results from this research study may help explain why insulin resistance differs
with genetic background and may guide development of personalized treatment strategies with
implications for several chronic metabolic diseases (e.g., type 2 diabetes, cardiovascular
disease, and cancer).
Insulin resistance plays a major role in the etiology of chronic metabolic diseases, many of
which differ with race/ethnicity. Previous studies using mainly indirect methods suggest that
insulin sensitivity is lower in AA vs. EA. Our preliminary data using the reference standard
glucose clamp indicate that in lean individuals, insulin sensitivity is lower among AA, while
in obese individuals, insulin sensitivity is higher among AA. We hypothesize that this
race/body mass index (BMI) interaction may be explained in part by significantly lower
visceral and hepatic fat accumulation in AA. Conversely, based on our preliminary data, we
hypothesize that inherently greater oxidative stress impairs insulin sensitivity even in AA,
explaining lower insulin sensitivity in lean AA vs. EA. We propose to test these hypotheses
by prospectively comparing skeletal muscle and hepatic insulin sensitivity in healthy lean,
overweight, and obese AA and EA using the hyperinsulinemic isoglycemic glucose clamp.
Analysis of ancestral genes will permit simultaneous assessment of the contribution of
ancestry to main outcomes.
which differ with race/ethnicity. Previous studies using mainly indirect methods suggest that
insulin sensitivity is lower in AA vs. EA. Our preliminary data using the reference standard
glucose clamp indicate that in lean individuals, insulin sensitivity is lower among AA, while
in obese individuals, insulin sensitivity is higher among AA. We hypothesize that this
race/body mass index (BMI) interaction may be explained in part by significantly lower
visceral and hepatic fat accumulation in AA. Conversely, based on our preliminary data, we
hypothesize that inherently greater oxidative stress impairs insulin sensitivity even in AA,
explaining lower insulin sensitivity in lean AA vs. EA. We propose to test these hypotheses
by prospectively comparing skeletal muscle and hepatic insulin sensitivity in healthy lean,
overweight, and obese AA and EA using the hyperinsulinemic isoglycemic glucose clamp.
Analysis of ancestral genes will permit simultaneous assessment of the contribution of
ancestry to main outcomes.
Inclusion Criteria:
- African American or Caucasian
- Body Mass Index 19-45
- Do NOT have diabetes
- Exercise less than 2 hours per week
- Are willing to travel to UAB for 2 screens and 4 testing visits
Exclusion Criteria:
- Diabetes
- Any major medical conditions or medications that interfere with study outcomes
We found this trial at
1
site
1720 2nd Ave S
Birmingham, Alabama 35233
Birmingham, Alabama 35233
(205) 934-4011
Phone: 205-934-4386
University of Alabama at Birmingham The University of Alabama at Birmingham (UAB) traces its roots...
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