People whose parents have type 2 diabetes see no ethnic disparities in how they regulate glucose or whether they get type 2 diabetes themselves, according to a study recently published in The Journal of Clinical Endocrinology and Metabolism.
A study reported by Ebenezer Nyenwe, MD, FWACP, FACP, FACE as part of a research project directed by Sam Dagogo-Jack, MD, DM, MSc, FRCP, of the University of Tennessee Health Science Center in Memphis, that ethic minorities are disproportionately affected by type 2 diabetes. African Americans are nearly twice as likely to have type 2 diabetes than Caucasians. However, there haven’t been many studies looking at the role of genetics in modifying ethnic effects in normoglycemic African Americans and Caucasians. “Therefore,” the authors write, “we investigated glucoregulation in normoglycemic African-Americans and Caucasians with or without parental diabetes.”
The researchers evaluated data from 100 healthy, normoglycemic African-Americans and Caucasians, 50 people with parental diabetes and 50 people whose parents did not have diabetes, matched in age, sex, ethnicity, and BMI. The mean age was 40.5 ± 11.6 years, BMI 28.7 ± 5.9 kg/m2, fasting plasma glucose 90.2 ± 5.9 mg/dL, and 2-hour postglucose 120.0 ± 26.8 mg/dL. The patients underwent a 75-g oral glucose tolerance test (OGTT), physical examination, anthropometry, biochemistries, indirect calorimetry and assessment of body composition, insulin sensitivity by euglycemic clamp (Si-clamp), and beta-cell function by Disposition index.
Subjects with parental diabetes showed higher glycemic excursion during OGTT-area under the curve-glucose, lower Si-clamp, and lower Disposition index. Beta cell function was lower in subjects whose parents have diabetes (by 30% in lean subjects with parental diabetes and 40% in obese subjects with parental diabetes). African Americans without parental diabetes had ∼40% lower insulin, twofold higher acute insulin secretion, but ∼30% lower Disposition index compared with Caucasians without parental diabetes, the authors write. “Remarkably,” they continue,” there were no significant differences by ethnicity in these glucoregulatory measures among subjects with parental diabetes.”
Based on these results, the authors conclude: “Offspring with parental diabetes harbor substantial impairments in glucoregulation compared with individuals without parental diabetes. Ethnic disparities in glucoregulation were abrogated by parental diabetes.” They go on to note that these results represent the earliest glucoregulatory defect in the evolution of dysglycemia in high-risk individuals.
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