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Role of a Proline Insertion in the Insulin Promoter Factor 1 (IPF1) Gene in African Americans With Type 2 Diabetes

¹ Endocrinology Section, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas
² Division of Endocrinology, Department of Medicine, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas
³ Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas
⁴ Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina
⁵ Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina
⁶ Division of Endocrinology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland
⁷ Geriatric Research and Education Clinical Center, Baltimore Veterans Administration Medical Center, Baltimore, Maryland
⁸ Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland
⁹ Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland

Address correspondence and reprint requests to Steven C. Elbein, MD, Professor of Medicine, Division of Endocrinology 111J-1/LR, John L. McClellan Veterans Hospital, 4300 West 7th St., Little Rock, AR 72205-5446. E-mail: elbeinstevenc{at}uams.edu

Abbreviations: AIR, acute insulin response; ARIC, Atherosclerosis Risk in Communities; FSIGT, frequently sampled intravenous glucose tolerance test; MODY, maturity-onset diabetes of the young

African Americans have twice the prevalence of type 2 diabetes as Caucasians and much greater genetic diversity. We identified an inframe insertion of a proline in the insulin promoter factor 1 (IPF1) gene (InsCCG243), which was relatively common (minor allele frequency 0.08) in African Americans and showed a trend to association with type 2 diabetes in preliminary studies. An earlier French study identified InsCCG243 as a cause of autosomal dominant diabetes. To determine the role of this variant in African Americans, we examined an additional population from North Carolina (n = 368) and a subset of African-American participants from the Atherosclerosis Risk in Communities (ARIC) study (n = 1,741). We also looked for segregation in 66 African-American families and for a role in insulin secretion in 112 nondiabetic subjects. InsCCG243 did not increase the risk of type 2 diabetes (P = 0.16 in North Carolina; P = 0.97 in the ARIC study) and did not segregate with type 2 diabetes in families. However, we found suggestive evidence for reduced insulin response to glucose (P = 0.05). Neither indirect measures of ß-cell mass nor ß-cell compensation were altered (P > 0.1). InsCCG243 does not act in a dominant, highly penetrant fashion in African Americans and is not a significant risk factor for type 2 diabetes in this population.

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