The overall objective of this study is to determine if genetic, immunological, and clinical variables can be utilized to distinguish between black gestational diabetes mellitus (GDM) individuals who will subsequently become a non-insulin dependent diabetic, insulin dependent diabetic, or remain normal. Over 400 black women who presented with GDM to one of seven prenatal clinics operated by the Department of Public Health, Jefferson County, Alabama have been studied for the past four years with regard to risk factors for development of the disease.
The aim i s to continue to accrue new patients who present to these clinics as well as to follow all patients accrued longitudinally to determine if parity, obesity, body fat distribution, fetal outcome, hypertension, thyroid disorders, family history of diabetes and/or heart disease, HLA-DR, DQ and Bf phenotypes, presence of autoantibody, restriction fragment length polymorphisms (RFLPs) within the DR/DQ region, RFLPs within the apolipoprotein A-I/C- III gene complex and the insulin receptor gene are risk factors for these women developing overt diabetes. The relationship of lifestyle, socioeconomic, dietary habits, and personality traits as assessed by a health hazard appraisal type of instrument to the development of subsequent overt diabetes, will also be assessed. There is the opportunity to collect information from this population that might shed light on the etiological relationship of other diseases to diabetes and diabetes to other diseases such as hypertension and cardiovascular diseases. Therefore, in order to address these issues the women will be assesed at their yearly follow-up visits with regard to the serum levels of cholesterol, triglycerides, HDL, LDL, Apo-A, and Apo-B. In addition, RFLPs within or flanking the Apo-A-II, B, and E gene regions will also be assessed. All variables will be analyzed with regard to whether they predict overt diabetes or other disease states such as thyroid disorders and cardiovascular diseases. This study is an opportunity to utilize a large population based sample of black women in order to more clearly understand risk factors for subsequent development of non-insulin dependent diabetes, insulin dependent diabetes, as well as other diseases that often coexist with diabetes. The data obtained should help to more clearly define the etiological factors of diabetes in blacks. This information may be applicable to other races as well.
|Giger, Joyce Newman; Strickland, Ora L; Weaver, Michael et al. (2005) Genetic predictors of coronary heart disease risk factors in premenopausal African-American women. Ethn Dis 15:221-32|
|Barton, E H; West, P A; Rivers, C A et al. (2001) Transferrin receptor-2 (TFR2) mutation Y250X in Alabama Caucasian and African American subjects with and without primary iron overload. Blood Cells Mol Dis 27:279-84|
|Acton, R T; Barton, J C; Bell, D S et al. (2001) HFE mutations in African-American women with non-insulin-dependent diabetes mellitus. Ethn Dis 11:578-84|
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|Barton, J C; Sawada-Hirai, R; Rothenberg, B E et al. (1999) Two novel missense mutations of the HFE gene (I105T and G93R) and identification of the S65C mutation in Alabama hemochromatosis probands. Blood Cells Mol Dis 25:147-55|
|Barton, J C; Shih, W W; Sawada-Hirai, R et al. (1997) Genetic and clinical description of hemochromatosis probands and heterozygotes: evidence that multiple genes linked to the major histocompatibility complex are responsible for hemochromatosis. Blood Cells Mol Dis 23:135-45; discussion 145a-b|
|Acton, R T; Bell, D S; Collins, J et al. (1997) Genes within and flanking the major histocompatibility region are risk factors for diabetes, insulin resistance, hypertension, and microalbuminuria in African-American women. Transplant Proc 29:3710-2|
|Acton, R T (1997) Molecular genetic testing for adult-onset disorders: the evolving laboratory, physician, patient interface. J Clin Lab Anal 11:23-7|
|Barton, J C; Harmon, L; Rivers, C et al. (1996) Hemochromatosis: association of severity of iron overload with genetic markers. Blood Cells Mol Dis 22:195-204|
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