African-American (AA) children are hyperinsulinemic and
insulin resistant compared with American White (AW) children. This study investigated 1) whether AA/AW differences in insulinemia are associated with differences in
insulin clearance; 2) whether dietary patterns, mainly
carbohydrate and fat intake, play a role; and 3) whether the quantitative relationship between
insulin sensitivity and secretion is similar between AA and AW children. Forty-four prepubertal children (22 AA and 22 AW) with comparable body composition and visceral adiposity were studied. All underwent a 3-h hyperinsulinemic (40 mU x m(-2) x min(-1))-euglycemic clamp to calculate
insulin sensitivity and
insulin clearance and a 2-h hyperglycemic clamp (12.5 mmol/l) to assess first- and second-phase
insulin responses. Twenty-four-hour food recalls were analyzed for macronutrient intake.
Insulin clearance (19.5 +/- 0.7 vs. 22.9 +/- 1.1 ml x min(-1) x kg(-1) fat-free mass [FFM]; P = 0.011) and
insulin sensitivity were lower in AA versus AW children (14.8 +/- 1.0 vs. 18.9 +/- 1.4 micro mol x min(-1) x kg(-1) FFM; P = 0.021). Both
insulin clearance and
insulin sensitivity correlated inversely with
dietary fat/
carbohydrate ratio, which was higher in AA than in white children. Fasting
C-peptide and
insulin were higher in AA children with no difference in
proinsulin levels. First- and second-phase
insulin concentrations and
glucose disposition index (
insulin sensitivity x first-phase
insulin) were higher in AA than in white children (12.8 +/- 2.1 vs. 7.2 +/- 0.6 micro mol. min(-1) x kg(-1) FFM; P = 0.019). In conclusion, the
hyperinsulinemia observed in AA children is due to both lower
insulin clearance and higher insulin secretion compared with their white peers. The quantitative relationship between insulin secretion and sensitivity is upregulated in AA children. This suggests that increased insulin secretion in AA children is not merely a compensatory response to lower
insulin sensitivity. Dietary factors may have a role. Additional studies are needed to determine whether metabolic/nutritional factors, possibly mediated through
free fatty acids, may play a role in the
hyperinsulinism observed in AA children.