Results from a large, ongoing epidemiologic study demonstrated a positive association between African ancestry and fasting glucose in individuals without diagnosed diabetes.
"This association is not substantively diminished by accounting for body mass index or available socioeconomic status measures, suggesting that differences between African Americans and whites in diabetes risk might include genetic/biologically mediated differences in glucose homeostasis," Dr. James B. Meigs reported at the annual scientific sessions of the American Diabetes Association.
Dr. James B. Meigs
Dr. Meigs, who directs the Massachusetts General Hospital Clinical Research Program’s Disease Management Research Unit, presented findings from 1,545 individuals without diagnosed diabetes who are enrolled in the Boston Area Community Health (BACH) Pre-Diabetes Study, an ongoing, community-based, random-sample cohort study. During morning in-home interviews, the researchers collected data on body mass index and socioeconomic status, and took samples for analysis of fasting glucose and DNA for genotyping 63 markers that discriminate between European, African, and Native American ancestry.
To test the hypothesis that the degree of African ancestry is associated with fasting glucose levels in individuals without diagnosed diabetes independent of socioeconomic factors, the researchers used three different linear regression models predicting fasting glucose. Model 1 included terms for age, gender, percent African, and percent Native American ancestry. Model 2 added BMI as a measure, and model 3 added socioeconomic status as a measure (income, education, and occupation).
Dr. Meigs, who is also an associate professor of medicine at Harvard Medical School in Boston, reported that the mean age- and gender-adjusted fasting glucose levels were 103 mg/dL in those with 100% African ancestry and 97 mg/dL in those with 100% European ancestry. When the researchers applied model 1, each 10% increase in percentage of African ancestry was associated with a fasting glucose increase of 0.53 mg/dL (P = .005). In model 2, adjustment for BMI weakened the association with fasting glucose (0.42 mg/dL; P = .02), while in model 3 additional adjustment for socioeconomic factors did not further diminish the association (0.46 mg/dL; P = .02).
Although the clinical application of genetics in diabetes is a long way off, a lot is being learned about the mechanisms underlying type 2 diabetes, Dr. Meigs said. "We’re looking for the differences between whites, who have been studied principally so far, and other ancestral groups, in terms of the specific mutations that alter levels of diabetes risk."
To accomplish this, the BACH Prediabetes Study is attempting to exhaust all other social and environmental factors, such as employment, insurance status, access to care, nutritional environment, and detailed neighborhood characteristics, he said.
BACH is supported by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Meigs said that he had no relevant financial disclosures to make.