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

Children’s Hospital of Pittsburgh, Pennsylvania, Division of Pediatric Endocrinology, Metabolism and Diabetes Mellitus (F.B., R.S., N.G., S.A.A.); and Division of Biostatistics, Department of Family Medicine and Clinical Epidemiology (J.J.), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

Address all correspondence and requests for reprints to: Silva A. Arslanian, M.D., Division of Endocrinology, Children’s Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto Street, Pittsburgh, Pennsylvania 15213. E-mail: Silva.Arslanian{at}chp.edu.

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 x 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.

This work was supported by USPHS Grants RO1-HD-27503, K24-HD-01357, and MO1-RR-00084, the General Clinical Research Center, and Eli Lilly \|[amp ]\| Co. Parts of this work were presented at the 62nd Scientific Sessions of the American Diabetes Association.

Abbreviations: AA, African-American; BMI, body mass index; BOA, black obese adolescents; CT, computed tomography; CVD, cardiovascular disease; FFA, free fatty acids; HDL, high density lipoprotein; LDL, low density lipoprotein; SAT, sc abdominal adipose tissue; TAT, total abdominal adipose tissue; T2DM, type 2 diabetes mellitus; VAT, visceral adiposity; WOA, white obese adolescents.

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