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Impact of Family History of Diabetes and Ethnicity on β-Cell Function in Obese, Glucose-Tolerant Individuals

Research and Medical Services (N.R., S.C.E.), Central Arkansas Veterans Healthcare System, Little Rock, Arkansas 72205; and Division of Endocrinology, Department of Internal Medicine (N.R., A.A.R., S.C.E.) and Department of Biostatistics (H.J.S.), University of Arkansas for Medical Sciences, College of Medicine, Little Rock, Arkansas 72205

Address all correspondence and requests for reprints to: Neda Rasouli, M.D., Central Arkansas Veterans Healthcare System, 111J LR, 4300 West 7th Street, Little Rock, Arkansas 72205. E-mail: rasoulineda{at}uams.edu.

Context: The increased insulin secretion in response to reduced insulin sensitivity (S_I) is heritable, but whether the genetic predisposition is restricted to members of high-risk Caucasian families is unknown. Furthermore, the relative importance of insulin resistance and defective β-cell compensation in the increased prevalence of type 2 diabetes (T2DM) in African-American compared with Caucasian individuals is uncertain.

Objectives: We tested whether obese individuals with a family history of T2DM have decreased β-cell compensation compared with obese controls without a family history of T2DM. In addition, we compared S_I and insulin secretion measures in African-American and Caucasian individuals.

Design: S_I, acute insulin response to iv glucose (AIR_g), maximally potentiated insulin response to arginine (AIR_max), and disposition indexes (DIs) (DI = S_I * AIR_g; DI_max = S_I * AIR_max) were compared among nondiabetic Caucasian and African-American individuals with and without a family history of diabetes.

Setting: This study was performed in an Ambulatory General Clinical Research Center.

Subjects: Subjects were healthy, nondiabetic individuals with or without a family history of T2DM.

Interventions: There were no interventions.

Main Outcome Measures: Comparison of S_I, AIR_g, AIR_max, DI, and DI_max between Caucasians and African-Americans with or without a strong family history of T2DM were made.

Results: Obese subjects did not differ in S_I, AIR_g, or DI by family history of diabetes. African-Americans had 8% lower S_I (P < 0.001), but 68% higher AIR_g (P < 0.001) and 46% higher DI (P = 0.001) than age, gender, body mass index-matched Caucasian individuals. However, African-Americans had lower DI_max compared with Caucasians.

Conclusions: We found no reduction in insulin secretion in obese subjects with a family history of T2DM compared with controls, but in general, African-Americans were more insulin resistant and had lower maximal β-cell response (DI_max). The paradoxical increased DI could be explained by the reduced hepatic insulin extraction.

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