To examine the significance of alterations in insulin sensitivity index (S1), glucose effectiveness (Sg), and β-cell function in the pathogenesis of type II diabetes in African-Americans with varying degrees of glucose intolerance.
A total of 154 African-Americans residing in Franklin County, Ohio, were studied. There were 101 subjects with normal glucose tolerance (NGT), 36 with impaired glucose tolerance (IGT), and 17 with type II diabetes. An oral glucose tolerance test (OGTT) was performed on each subject. S1 and Sg were measured by insulin-modified, frequently sampled intravenous glucose tolerance test (FSIGT).
The mean fasting and postprandial serum glucose levels were significantly greater in the diabetic groups when compared with the IGT and NGT groups. In contrast, while fasting serum insulin and C-peptide levels tended to be greater in the type II diabetic and IGT groups, the postprandial responses were blunted at 30 min in the IGT and type II diabetic groups when compared with the NGT group. The mean acute first-phase insulin release after intravenous glucose was blunted also in the IGT and type II diabetic groups when compared with the NGT group. The S1 was significantly lower in the IGT (1.51 ± 0.19) and type II diabetic (0.61 ± 0.15) groups when compared with the NGT group (2.94 ± 0.20 × 10−4 · min−1 · μU−1 · ml−1). The Sg was not significantly different in the NGT (2.90 ± 0.20), IGT (2.47 ± 0.19), and the type II diabetic (2.35 ± 0.15 × 10−2/min) groups. The glucose effectiveness at theoretical zero insulin concentration (GEZI) followed similar patterns as the Sg. Furthermore, the basal insulin effect (BIE) was significantly lower in the IGT and type II diabetic groups compared with the NGT group. In addition, the glucose decay constant (Kg) was significantly lower (P < 0.001) in the IGT (1.21 ± 0.13) and the type II diabetic (1.07 ± 0.12) groups when compared with the NGT group (2.03 ± 0.10% per minute).
Our present study demonstrates that African-American patients with IGT and mild type II diabetes have significant reduction in β-cell function, insulin sensitivity, and BEI but have normal and intact Sg and GEZI when compared with NGT subjects. We conclude the following: 1) a reduction in Sg does not appear to play a significant role in the pathogenetic mechanism of IGT and type II diabetes in African-American patients, and 2) the intact Sg in the IGT and type II diabetic groups could serve as a compensatory mechanism for hyperglycemia in African-Americans.
