CONTEXT: Although overweight and obese African-Americans (AAs) have less visceral adipose tissue (VAT) and liver fat (LF) than Hispanics, they have a similar risk for type 2 diabetes. OBJECTIVE: We examined ethnic differences in the association between VAT and LF with risk factors for type 2 diabetes to help explain this paradox. DESIGN: We conducted a cross-sectional study in an academic pediatric care facility. SUBJECTS: Subjects were overweight and obese AA (n = 131; 15.5 ± 3.3 years old) and Hispanic adolescents (n = 227; 14.7 ± 3.0 years old). MAIN OUTCOME MEASURES: Outcome measures included insulin sensitivity (SI), acute insulin response (AIR), and disposition index (DI) by frequently sampled i.v. glucose tolerance test and minimal modeling. RESULTS: LF, not VAT, was inversely associated with SI, and the effect of high LF compared with low was more pronounced in AAs (P(interaction) < .05). In Hispanics, high LF was associated with a 24% lower SI (P < .01) and a 31% increase in AIR (P < .01) and was not associated with DI (P = .35). In AAs, high LF was associated with a 49% lower SI (P < .001), was not associated with an increase in AIR (P = .25), and was associated with a 42% lower DI (P < .01), indicating failure of compensatory insulin secretion/clearance in response to insulin resistance. Prediabetes changed the relationship between high/low LF and DI in Hispanics (P(interaction) = .002) but not AAs such that prediabetic Hispanics with high LF had a 43% lower DI (P = .03) with no difference in those without prediabetes (P = .06). CONCLUSIONS: LF has a stronger effect on SI compared with VAT. Our results suggest that the impact of high LF on poor β-cell compensation is more pronounced in AAs. In Hispanics, the combination of high LF and prediabetes contributes to poor β-cell compensation.
CONTEXT: Although overweight and obese African-Americans (AAs) have less visceral adipose tissue (VAT) and liver fat (LF) than Hispanics, they have a similar risk for type 2 diabetes. OBJECTIVE: We examined ethnic differences in the association between VAT and LF with risk factors for type 2 diabetes to help explain this paradox. DESIGN: We conducted a cross-sectional study in an academic pediatric care facility. SUBJECTS: Subjects were overweight and obese AA (n = 131; 15.5 ± 3.3 years old) and Hispanic adolescents (n = 227; 14.7 ± 3.0 years old). MAIN OUTCOME MEASURES: Outcome measures included insulin sensitivity (SI), acute insulin response (AIR), and disposition index (DI) by frequently sampled i.v. glucose tolerance test and minimal modeling. RESULTS: LF, not VAT, was inversely associated with SI, and the effect of high LF compared with low was more pronounced in AAs (P(interaction) < .05). In Hispanics, high LF was associated with a 24% lower SI (P < .01) and a 31% increase in AIR (P < .01) and was not associated with DI (P = .35). In AAs, high LF was associated with a 49% lower SI (P < .001), was not associated with an increase in AIR (P = .25), and was associated with a 42% lower DI (P < .01), indicating failure of compensatory insulin secretion/clearance in response to insulin resistance. Prediabetes changed the relationship between high/low LF and DI in Hispanics (P(interaction) = .002) but not AAs such that prediabetic Hispanics with high LF had a 43% lower DI (P = .03) with no difference in those without prediabetes (P = .06). CONCLUSIONS: LF has a stronger effect on SI compared with VAT. Our results suggest that the impact of high LF on poor β-cell compensation is more pronounced in AAs. In Hispanics, the combination of high LF and prediabetes contributes to poor β-cell compensation.
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