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- Title
Ethnicity but not Family History of Diabetes Affects Beta Cell Compensation for Insulin Resistance in Non Diabetic Subjects.
- Authors
Rasouli, Neda; Spencer III, Horace J.; Rashidi, Amir Adel; Elbein, Steven C.
- Abstract
Genetic predisposition increases the risk of type 2 diabetes (T2DM). Disposition index (DI), a measure β-cell compensation for insulin resistance, is heritable. Hence, reduced DI may predate abnormal glucose metabolism. We investigated insulin sensitivity (S[sub I]) and insulin secretion in 333 healthy nondiabetic African Americans (AA) and Caucasians (C) who were matched for age, sex, body mass index (BMI) and waist circumference. To investigate the role of family history (FH) of T2DM, we compared insulin secretion and sensitivity measures in an obese subgroup (BMI≥30; n=141) of subjects selected for either a strong FH of T2DM or no FH. We compared oral glucose tolerance (OGT), S[sub I], acute insulin response to IV glucose (AIR[sub g]), insulin response to glucose potentiated arginine stimulation (AIR[sub max]) and disposition indexes (DI, DI[sub max]) with respect to FH and ethnicity. Among the obese subgroup, individuals with and without a FH did not differ by age, sex, or obesity measures. We found no differences in S[sub I], AIR[sub g], AIR[sub max], DI or DI[sub max] (S[sub I] * AIR[sub max]) by FH in either C or AA tested separately or together. When the larger cohort of lean and obese individuals was examined without regard to FH, AA subjects were more insulin resistant (S[sub I] = 3.85 ± 3.87 vs. 4.22 ± 3.29, p<0.0001, AA vs. C) and had markedly greater AIR[sub g] and DI than Caucasians (AA vs C; AIR[sub g]: 806.5 ± 626.7 vs. 478.7 ± 361.0, p<0.0001; DI: 2331.8 ± 1970.2 vs. 1597.9 ±1220.4, p=0.0104), despite matching for age, sex, and obesity measures. Interestingly, AIR[sub max] did not differ among ethnic groups, and DI[sub max], a measure of β-cell reserve, was lower in AA compared to C. Fasting glucose and fasting and 2 h insulin levels were similar between groups, but AA had lower 2 h glucose and decreased glucose AUC during OGT. We find no defect in β-cell compensation (DI) related to a FH of T2DM in either ethnic group. Over a wide range of BMI, AA had lower S[sub I], and increased AIR[sub g] and DI than C which over-compensated for decreased S[sub I]. The decreased AIR[sub max] suggested lower β-cell reserve in AA compared to C, which might explain the increased prevalence of T2DM in AA. ADA-Funded Research
- Subjects
ETHNICITY; GENETICS of diabetes; PANCREATIC beta cells; INSULIN resistance; TYPE 2 diabetes; ARGININE
- Publication
Diabetes, 2007, Vol 56, pA383
- ISSN
0012-1797
- Publication type
Article