To examine the phases of acute insulin release and glucose homeostasis in people of African descent with and without a positive family history of type II diabetes who reside in geographically diverse environments. The prevalence of type II diabetes in people of African descent varies considerably depending on the country of habitat. Family history is recognized as an important risk factor for the development of the disease.
We studied serum glucose and insulin concentrations—before and after intravenous glucose challenge—in glucosetolerant, first-degree relatives of African-American (n = 18) and Nigerian (n = 20) type II diabetic patients and their respective healthy control subjects (African American, n = 9; Nigerian, n = 18) living in their native countries. The acute first- (t = 0 – 5 min) and second-phase (t = 10–60 min) insulin releases were calculated as the sum of incremental insulin responses to the intravenous glucose stimulation.
Mean serum glucose levels and glucose decay constant (KG were not different in the African Americans and Nigerians. Fasting serum insulin in the African-American relatives was significantly greater than the Nigerian relatives (16.0 ± 3.0 vs. 5.8 ± 1.7 mU/L, P < 0.05). In contrast, FSI levels in the African- American control subjects were similar to Nigerian control subjects (6.3 ± 1.4 vs. 4.5 ± 1.8 mU/L). Acute first- and second-phase insulin levels were 2–3 times (P < 0.01) greater in African Americans than Nigerians, irrespective of family history of diabetes. Comparing the African-American relatives with healthy control subjects, we found significantly (P < 0.05) higher FSI in the relatives; whereas the acute first- (272 ± 44 vs. 222 ± 55 mU/L) and second-phase (388 ± 61 vs. 235 ± 53 mU/L) serum insulin release tended to be greater, but not significantly different in the relatives. In contrast, the acute first (101 ± 15 vs. 120 ± 20 mU/L) and secondphases (88 ± 14 vs. 111 ± 17 mU/1) of insulin release were slightly lower, but not significantly different, in the Nigerian relatives versus the Nigerian healthy control subjects. In a subgroup of nonobese African-American (n = 11) and Nigerian (n = 11) relatives, and African-American (n = 8) and Nigerian (n = 7) healthy control subjects with a body mass index <30 kg/m2, the mean fasting and poststimulation serum glucose were not different. However, serum insulin concentrations in the African Americans were significantly different from those of the Nigerians. The pattern of insulin responses in the nonobese subjects was similar to those of the respective African- American and Nigerian groups.
Our preliminary study demonstrates greater serum insulin responses and, perhaps, insulin resistance in glucose-tolerant African Americans than in their Nigerian counterparts, irrespective of family history of diabetes and obesity. We conclude that the antecedent lesions leading to the development of type II diabetes may be different in the first-degree relatives of African- American and Nigerian diabetic patients.