Obesity, Regional Fat Distribution, and Syndrome X in Obese Black Versus White Adolescents: Race Differential in Diabetogenic and Atherogenic Risk Factors

• Published in: The journal of clinical endocrinology and metabolism 2003-06, Vol.88 (6), p.2534-2540
• Main Authors: Bacha, Fida, Saad, Rola, Gungor, Neslihan, Janosky, Janine, Arslanian, Silva A.
• Format: Article
• Language: English
• Subjects: Adipose Tissue - diagnostic imaging; Adolescent; Arteriosclerosis - etiology; Black or African American; Black People; Blood Pressure; Body Composition; Diabetes Mellitus, Type 2 - etiology; Female; Humans; Insulin - metabolism; Insulin Resistance; Insulin Secretion; Male; Metabolic Syndrome - etiology; Obesity - complications; Obesity - diagnostic imaging; Obesity - ethnology; Obesity - pathology; Obesity - physiopathology; Risk Factors; Tomography, X-Ray Computed; Viscera; White People
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.2002-021267

The incidence of type 2 diabetes mellitus in children is increasing with the increasing prevalence of obesity, particularly in African-American children. We hypothesized that African-American obese adolescents are more insulin resistant than their white peers, but have lower insulin secretion, thus increasing their risk of type 2 diabetes mellitus. The present study investigated insulin sensitivity and secretion, visceral adiposity (VAT), and cardiovascular disease (CVD) risk profile in black obese adolescents (BOA) vs. white obese adolescents (WOA). Twenty-four BOA and 26 WOA underwent a hyperinsulinemic-euglycemic clamp to assess insulin sensitivity, a hyperglycemic clamp to determine insulin secretion, dual energy x-ray absorptiometry for body composition and computed tomography scan at L4–L5 to measure VAT and sc abdominal adipose tissue. Fasting lipid and automated blood pressure measurements were obtained. The WOA and BOA groups were divided into low VAT and high VAT groups. BOA compared with WOA of similar body mass index and percent body fat had less visceral adiposity, lower hepatic glucose production, and lower lipid levels. Visceral adiposity was associated with lower insulin sensitivity in both groups [low vs. high VAT; BOA, 2.9 ± 0.4 vs. 1.7 ± 0.2 μmol/kg·min per pmol/liter (P = 0.016); WOA, 2.6 ± 0.5 vs. 1.5 ± 0.1 (P = 0.032)]. However, this was compensated by higher insulin secretion in whites (low VAT, 934.8 ± 121.8; high VAT, 1590.6 ± 232.8 pmol/liter; P = 0.037), but not in blacks (low VAT, 1398.9 ± 214.0; high VAT, 1423.7 ± 108.7 pmol/liter). Glucose disposition index (insulin sensitivity × first phase insulin) was lower in high VAT vs. low VAT BOA, but not in WOA. In each racial group, high VAT groups had elevation of systolic and diastolic blood pressure, but dyslipidemia was worse in WOA with high VAT. In conclusion, a given level of body mass index confers different metabolic risks for WOA vs. BOA. Although differences in fat patterning may help explain the more atherogenic risk profile in whites, the cause of the more diabetogenic insulin sensitivity/secretion profile in blacks remains unknown and needs to be investigated further.