Title: Type 2 diabetes in youth: Are there racial differences in beta-cell responsiveness relative to insulin sensitivity? Authors
|Bacha, Fida -|
|Gungor, Neslihan -|
|Lee, Sojung -|
|Arslanian, Silva -|
Submitted to: Pediatric Diabetes
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 22, 2011
Publication Date: May 1, 2012
Citation: Bacha, F., Gungor, N., Lee, S., Arslanian, S.A. 2012. Type 2 diabetes in youth: Are there racial differences in beta-cell responsiveness relative to insulin sensitivity? Pediatric Diabetes. 13(3):259-265. Interpretive Summary: Type 2 diabetes and its complications are known to be more prevalent in minority ethnic groups, specifically African Americans, than in American Caucasians. Whether this is prevalence is due to insulin secretion levels or insulin sensitivity is unclear. We conducted a study of adolescents with Type 2 diabetes to see if we could distinguish any differences in insulin secretion or sensitivity that could be associated with race. Our findings showed that there appears to be a race differential in the pathophysiological mechanisms responsible for youth Type 2 diabetes; there is greater impairment in insulin sensitivity in African Americans and greater impairment in insulin secretion in whites. Our research observations provide important insight into the need for potentially different approaches in the prevention and treatment of youth Type 2 diabetes in the different racial groups.
Technical Abstract: Non-diabetic African American (AA) youth have an upregulated insulin secretion relative to insulin sensitivity (IS) compared with their American White (AW) peers. We investigated if similar racial differences exist in youth with T2DM. Fourteen AAs and 14 AWs T2DM adolescents underwent evaluation of IS and clearance (hyperinsulinemic-euglycemic clamp), first- and second-phase insulin and C-peptide secretion (hyperglycemic clamp); body composition (DEXA); and abdominal adiposity (CT). AA and AW T2DM had similar HbA1c, diabetes duration, BMI, and % body fat, with lower visceral fat in AAs (p = 0.013). While insulin-stimulated glucose disposal was similar in AA and AW (7.5 +/- 1.0 vs. 7.3 +/- 0.9 mg/kg FFM/min), IS tended to be lower (2.5 +/- 0.4 vs. 3.8 +/- 0.6 mg/kg FFM/min per microU/mL, p = 0.081). First-phase insulin (175.7 +/- 52.9 vs. 66.6 +/- 10.8 microU/mL, p = 0.01) and second-phase insulin (236.2 +/- 40.7 vs. 105.1 +/- 17.9 microU/mL, p = 0.008), and first-phase C-peptide (8.2 +/- 1.2 vs. 5.0 +/- 0.3 ng/mL, p = 0.02) and second-phase C-peptide (10.8 +/- 0.9 vs. 7.6 +/- 0.6 ng/mL, p = 0.012) were higher in AA. Beta-cell function relative to IS was higher in AA vs. AW (259.5 +/- 35.3 vs. 168.8 +/- 25.1 mg/kg FFM/min, p = 0.043). Racial differences in insulin secretion can be demonstrated with the clamp technique in obese adolescents with T2DM. Similar to non-diabetic youth, AA adolescents with T2DM compared with their AW counterparts have an upregulated beta-cell function relative to IS, the reasons for which remain to be investigated.