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Five-Year Glycemic Trajectories Among Healthy African-American and European-American Offspring of Parents With Type 2 Diabetes

  • Laleh N Razavi
    Affiliations
    Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, Tennessee

    Division of Endocrinology, Case Western Reserve University, Cleveland, Ohio
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  • Sotonte Ebenibo
    Affiliations
    Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, Tennessee
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  • Chimaroke Edeoga
    Affiliations
    Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, Tennessee
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  • Jim Wan
    Affiliations
    Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
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  • Samuel Dagogo-Jack
    Correspondence
    Correspondence: Samuel Dagogo-Jack, MD, DSc, Department of Medicine, Division of Endocrinology, Diabetes and Metabolism; University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163
    Affiliations
    Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, Tennessee

    General Clinical Research Center, University of Tennessee Health Science Center, Memphis, Tennessee
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      ABSTRACT

      Background

      Cross-sectional surveys report a higher prevalence of diagnosed type 2 diabetes mellitus (T2DM) in African Americans (AA) than European Americans (EA). We studied 5-year glycemic excursions among AA and EA in the Pathobiology of Prediabetes in A Biracial Cohort study, to assess ethnic disparities.

      Materials and Methods

      Pathobiology of Prediabetes in A Biracial Cohort followed normoglycemic offspring of parents with T2DM for 5 years, with serial assessments of oral glucose tolerance test , anthropometry, body fat, insulin sensitivity and beta-cell function. The primary outcome was progression to prediabetes (impaired fasting glucose and/or impaired glucose tolerance). We further analyzed 5-year changes in fasting (FPG) and 2-hour plasma glucose (2hrPG).

      Results

      One hundred and one (52 AA, 49 EA) out of 343 subjects developed prediabetes during follow-up. The change in FPG ranged from −24 mg/dl to +38 mg/dl. The FPG remained stable (± 5 mg/dl from baseline) in 50% of EA and 46.8% of AA and the 2hrPG remained stable (± 25 mg/dl from baseline) in 73.7% of EA and 71.0 % of AA during follow-up. The proportions with change in FPG of 5mg/dl to >25 mg/dl and 2hrPG of 25 mg/dl to >50 mg/dl were similar in EA and AA offspring, as were the 10th - 90th percentiles of the distribution of 5-year changes in FPG and 2hrPG.

      Conclusions

      During 5 years of follow-up, black and white offspring of parents with T2DM exhibited remarkable phenotypic concordance of glycemic trajectories. Thus, parental history of T2DM may be a stronger factor than race/ethnicity in the prediction of longitudinal glycemic trends.

      Key Indexing Terms

      INTRODUCTION

      Data from cross-sectional surveys indicate that the prevalence of diagnosed type 2 diabetes (T2DM) is nearly 2-fold higher in African Americans (AA) compared with European-Americans (EA).

      Centers for Disease Control and Prevention. National diabetes statistics report, 2017: estimates of diabetes and its burden in the United States. Available at: https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Accessed November 4, 2019.

      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999–2002.
      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and high risk for diabetes using A1C criteria in the U.S. population in 1988–2006.
      However, the chronology of ethnic disparities in the pathogenesis of T2DM is unclear. Notably, the rate of progression from impaired glucose tolerance(IGT) (prediabetes) to T2DM was similar among individuals from U.S. racial/ethnic groups enrolled in the Diabetes Prevention Program.
      • Knowler WC
      • Barrett-Connor E
      • Fowler SE
      • et al.
      Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.
      Furthermore, a previous report from our Pathobiology of Prediabetes in a Biracial Cohort (POP-ABC) study showed a similar rate of incident prediabetes (impaired fasting glucose [IFG] or IGT) among initially normoglycemic AA and EA with parental history of T2DM followed for 5 years.
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      In that report, the primary outcome of incident prediabetes was assessed as a binary event (progressors versus [vs.] nonprogressors). Thus, participants whose serial fasting plasma glucose (FPG) levels increased substantially from baseline but fell short of 100 mg/dl (5.5 mmol/l) were classified as nonprogressors. A similar classification applied to those whose 2-hour plasma glucose (2hrPG) level during serial oral glucose tolerance tests (OGTT) increased from baseline but fell shy of 140 mg/dl (7.8 mmol/l).
      As plasma glucose is a continuous, rather than a discrete, biological variable, the dichotomous determination of glycemic status (progression to prediabetes vs. nonprogression), based on reaching a conventional diagnostic cut-off level, may mask otherwise important excursions in serial glucose measurements. For example, a participant whose FPG level increased from 80 mg/dl to 95 mg/dl would be classified as a nonprogressor, whereas another participant whose FPG increased from 95 mg/dl to 101 mg/dl would be classified as a progressor to IFG (prediabetes). Moreover, POP-ABC was an observational study that offered no behavioral or pharmacological intervention. As such, biological measures, such as body weight and plasma glucose levels, were subject to the expected fluctuations of the free-living state. Given the overall objective of the POP-ABC study—namely, elucidation of the pathobiology of early dysglycemia in AA and EA—it would be informative to determine if ethnic disparities occur in the magnitude and direction of glycemic excursions during transition to dysglycemia. In the present report, we analyzed glycemic trajectories among initially normoglycemic AA and EA during 5 years of follow-up in the POP-ABC study.

      SUBJECTS AND METHOD

      The POP-ABC study design, recruitment and retention strategies and baseline characteristics of the enrolled cohort have been published.
      • Dagogo-Jack S
      • Edeoga C
      • Nyenwe E
      • et al.
      Pathobiology of prediabetes in a biracial cohort (POP-ABC): design and methods.
      • Ebenibo S
      • Edeoga E
      • Ammons A
      • et al.
      Pathobiology of prediabetes in a biracial cohort (POP-ABC): retention strategies.
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Pathobiology of prediabetes in a biracial cohort (POP-ABC) study: baseline characteristics of enrolled subjects.
      In brief, we recruited 376 normoglycemic offspring (218 black, 158 white) of parents with T2DM and followed them for 5 years (mean 2.62 years). Serial assessments included anthropometry, body fat measurements (DEXA), OGTT, insulin sensitivity and beta-cell function. The body mass index (BMI) was calculated as the weight in kg divided by the height in meter squared. Prediabetes was diagnosed as IFG or IGT, using the revised American Diabetes Association diagnostic criteria.
      American Diabetes Association
      Standards of care in diabetes —2019.
      We measured FPG quarterly and HbA1c, OGTT and body fat annually. For the present analysis we defined changes in FPG and 2hrPG during OGTT (2hrPG) as the difference between enrollment value and the value obtained at the end of study. The homeostasis model of insulin resistance (HOMA-IR) and of beta-cell function (HOMA-B) were derived from FPG and insulin levels.
      • Matthews DR
      • Hosker JP
      • Rudenski AS
      • et al.
      Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.
      Plasma glucose was measured with a glucose oxidase method (Yellow Spring Instruments, Yellow Spring, OH). Plasma insulin level was measured immunochemically in our Endocrine Research Laboratory, using commercial ELISA kits. HbA1c was measured in a contract clinical laboratory. The POP-ABC study was approved by the University of Tennessee institutional review board and conducted at the University of Tennessee General Clinical Research Center. A written informed consent was obtained from all participants before initiation of the study.

      Statistical Analysis

      Data are reported as means ± SD unless otherwise specified. Significance level was set as P < 0.05. Frequency histograms and percentile plots were generated to compare the distribution of 5-year change in FPG and 2hrPG from baseline in EA and AA participants. Group differences were analyzed using unpaired t tests for continuous variables and the chi squared test for categorical variables. The relationship between change in FPG or 2hrPG and metabolic variables was analyzed using linear regression models and Pearson's correlation coefficients. Group distributions were analyzed by Kolmogorov-Smirnov test. Statistical analyses were performed with the use of SAS statistical software, version 9.4 (SAS Institute, Cary, NC).

      RESULTS

      Table 1 summarizes the baseline characteristics in participants. The mean age of the cohort was 44.2 years and mean BMI was 30.2kg/m2. At enrollment, the FPG was 93.2 ± 6.51 mg/dl in EA offspring vs. 90.8 ± 6.80 mg/dl in AA offspring (P = 0.0008); 2-hrPG was 125 ± 23.4 mg/dl in EA offspring vs. 123 ± 27.4 mg/dl in AA offspring (P = 0.408) and the BMI was 28.8 ± 6.80 kg/m2 in EA offspring vs. 31.2 ± 7.39 kg/m2 in AA offspring (P = 0.0008). Compared with the EA offspring, AA offspring had a lower mean age and higher BMI and higher HbA1c level (but lower FPG and similar 2hrPG levels). Baseline HOMA-IR and HOMA-B and body fat mass were not significantly different in 2 groups.
      TABLE 1Baseline characteristics of European-American and African-American offspring of parents with type 2 diabetes.
      European AmericanAfrican AmericanP Value
      Number158218
      Age (yr)46.6 ± 10.542.5 ± 10.30.0002
      BMI (kg/m2)28.8 ± 6.8031.2 ± 7.390.001
      Waist circumference (cm)
        Women90.1 ± 15.994.6 ± 15.10.02
        Men98.9 ± 10.797 ± 17.90.54
      FPG (mg/dl)93.2 ± 6.5190.8 ± 6.800.0008
      2hrPG (mg/dl)125 ± 23.4123 ± 27.40.408
      HbA1c (%)5.44 ± 0.385.66 ± 0.47<0.0001
      Total fat mass (kg)29.3 ± 13.331.8 ± 13.70.11
      Trunk fat mass (kg)14.7 ± 7.015.4 ± 7.50.44
      HOMA-IR1.93 ± 1.621.86 ± 1.530.70
      HOMA-B92.7 ± 76.292.8 ± 62.20.99
      2hrPG, 2-hour plasma glucose during oral glucose tolerance test; FPG, fasting plasma glucose; HOMA-IR, homeostasis model of insulin resistance; HOMA-B, homeostasis model of beta-cell function.
      As reported in the main results from the cohort, a total of 101 (52 black, 49 white) out of 343 subjects (192 black, 151 white) with evaluable data developed prediabetes during 5 years of follow-up (mean 2.62 years).
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      The incidence rate of prediabetes was 12.5 cases per 100 person-years in white offspring and 10.3 cases per 100 person-years in black offspring, without any significant difference by race/ethnicity (Log rank sum P = 0.3745 before and P = 0.8630 after adjustment for baseline variables.
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      Furthermore, the proportion of subjects who reached the prediabetes endpoint by IFG (42.6% vs 46%), IGT (34% vs 36.2%) or IFG and IGT (20.0% vs 21.3%) criteria was similar in black vs white participants.
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      In the present report we determined whether ethnic disparities would be discernible in the trajectories of FPG and 2hrPG during the 5-year follow-up of progressors and nonprogressors to prediabetes. Analyzed as continuous variables, the change in FPG during follow-up ranged from −24 mg/dl to +45 mg/dl and the change in 2hrPG ranged from −65 mg/dl to +84 mg/dl. Comparing EA vs. AA offspring, there was no significant difference in the mean change in FPG (2.07 ± 9.35 mg/dl vs. 1.85 ± 8.94 mg/dl, P = 0.83), or the range (−24 mg/dl to +45 mg/dl vs. −20 mg/dl to +33 mg/dl) or interquartile range (9.00 mg/dl vs. 9.70 mg/dl) of the distribution of change in FPG.
      Comparing EA vs. AA offspring, there was no significant difference in the mean change in 2hrPG (6.67 ± 27.8 mg/dl vs. 8.25 ± 27.3 mg/dl, P = 0.79), or the range (−68 mg/dl to +76 mg/dl vs. −69 mg/dl to +83 mg/dl) or interquartile range (36.2 mg/dl vs. 31.8 mg/dl) of the distribution of change in 2hrPG.
      The frequency distribution of 5-year change in FPG from enrollment was similar for EA and AA participants (Figure 1A, B). The FPG remained stable (± 5 mg/dl from baseline) in 50% of EA offspring and 46.8% of AA offspring during 5 years of follow-up (Table 2). The proportions of subjects who experienced increases or decreases in FPG ranging from 5mg/dl to >25 mg/dl during the 5 years of follow-up were almost identical between EA and AA offspring (Table 2). Similarly, the 2hrPG remained stable (±25 mg/dl from baseline) in 73.7% of EA and 71.0 % of AA during 5 years of follow-up, and the proportions of participants who experienced increases or decreases in 2hrPG ranging from <25 mg/dl to >50 mg/dl were similar in EA and AA offspring (Table 2). Furthermore, the 10th, 25th, 50th, 75th and 90th percentiles of the distributions of 5-year change in FPG and 2hPG were similar in EA and AA offspring (Table 2 and Figure 1C, D). In multivariable regression models, the significant predictors of the change in FPG and 2hrPG were the baseline BMI, FPG, 2hrPG and HbA1c levels along with markers of insulin resistance (HOMA-IR) and insulin secretion (HOMA-B) (P = 0.0034- <0.0001).
      FIGURE 1
      FIGURE 1Frequency distribution of 5-year change in fasting plasma glucose (FPG) from enrollment to end of study in European-American (A) and African-American (B) subjects, and percentile plots of changes in FPG (C) and 2hrPG (D) in European Americans (blue) and African-Americans (red)(C).
      TABLE 2Five-year changes in fasting and 2-hour post-load plasma glucose levels in European-American and African-American offspring of parents with type 2 diabetes.
      European AmericanAfrican AmericanP value
      5-year changes in FPG0.077
      Decreased ≥25 mg/dl (%)5.1012.8
      Decreased 5 to <25 mg/dl (%)17.115.6
      Decreased ≤5 mg/dl (%)28.520.2
      Increased ≤ 5 mg/dl (%)21.526.6
      Increased 5 to <25 mg/dl (%)24.721.6
      Increased ≥ 25 mg/dl (%)3.163.2
      Percentiles of FPG change0.80
      10th percentile (mg/dl)−7.00−8.00
      25th percentile (mg/dl)−3.00−3.70
      50th percentile (mg/dl)0.751.75
      75th percentile (mg/dl)6.006.00
      90th percentile (mg/dl)11.511.0
      5-year changes in 2hrPG0.52
      Decreased ≥25 mg/dl (%)15.811.0
      Decreased 0 to <25 mg/dl (%)24.225.0
      Increased 0 to <25 mg/dl (%)33.735.0
      Increased 25 to ≤50 mg/dl (%)17.922.0
      Increased ≥50 mg/dl (%)6.316.00
      Percentiles of 2hrPG change0.11
      10th percentile (mg/dl)−30.0−30.5
      25th percentile (mg/dl)−15.0−5.80
      50th percentile (mg/dl)7.006.50
      75th percentile (mg/dl)23.826.0
      90th percentile (mg/dl)40.042.0
      2hrPG, 2-hour plasma glucose during oral glucose tolerance tes; FPG, fasting plasma glucose.

      DISCUSSION

      Our previous report from the POP-ABC study showed that initially normoglycemic African-American and EA offspring of parents with T2DM developed incident prediabetes at a similar rate during 5 years of follow-up.
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      Per current standards, prediabetes is defined specifically by threshold plasma glucose levels for IFG and IGT. Thus, the primary outcome of the POP-ABC study was a binary or dichotomous determination of the presence or absence of incident prediabetes during follow-up. Accordingly, our finding of lack of racial disparity in incident prediabetes was a qualitative observation. However, as plasma glucose is a continuous variable, the qualitative dichotomous classification of prediabetes status does not capture quantitative longitudinal glycemic excursions among study subjects in the comparison groups.
      Thus, to glean further insight into quantitative changes in glycemia during follow-up, we compared several parameters of glucose trajectories among the black and white offspring in our study cohort. We found that the 5-year trajectories in FPG and 2hrPG in the 2 groups overlapped considerably. As the POP-ABC was a natural history study, no pharmacological or lifestyle interventions were offered to our free-living participants. Using an arbitrary 5% change from baseline FPG cut-off, we observed that approximately 70% of participants experienced either a decrease or minimal change in FPG, whereas ∼30% experienced an increase. The standard deviation of the change in 2hrPG was ∼27 mg/dl, and ∼70% of our study cohort experienced 5-year excursions within ± 25 mg/dl from baseline 2hPG value. Interestingly, concordant with our previous report of similar incidence of prediabetes,
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      the 5-year glycemic trajectories were almost identical in black and white offspring of parents with T2DM. Baseline glycemia, adiposity, insulin sensitivity and insulin secretion were significant predictors of the 5-year changes in FPG and 2hrPG, which is pathophysiologically congruent, as the natural history of the transition from normoglycemia to dysglycemia involves progressive insulin resistance and β-cell dysfunction.
      • Weyer C
      • Bogardus C
      • Mott DM
      • et al.
      The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus.
      ,
      • Dagogo-Jack S
      Editorial: The continuum of dysglycemia: predicting progression from prediabetes to type 2 diabetes.
      Several reports have indicated a higher prevalence of diagnosed T2DM in AA and other ethnic/racial groups than European Americans.

      Centers for Disease Control and Prevention. National diabetes statistics report, 2017: estimates of diabetes and its burden in the United States. Available at: https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Accessed November 4, 2019.

      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999–2002.
      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and high risk for diabetes using A1C criteria in the U.S. population in 1988–2006.
      ,
      • Dagogo-Jack S
      Ethnic disparities in type 2 diabetes: pathophysiology and implications for prevention and management.
      • Egede LE
      • Dagogo-Jack S
      Epidemiology of type 2 diabetes: focus on ethnic minorities.

      Centers for Disease Control and Prevention. 2011 National Diabetes Fact Sheet. Diagnosed and undiagnosed diabetes in the United States, all ages, 2010. Available at:https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed November 4, 2019

      • Cowie CC
      • Rust KF
      • Ford ES
      • et al.
      Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006.
      Our finding of similar longitudinal glucose excursions among black and white subjects with a parental history of T2DM diabetes indicates that race/ethnicity, per se, may not be a major determinant of early glucose abnormalities. The data on racial/ethnic patterns in the prevalence of diagnosed diabetes in the U.S. were derived from cross-sectional surveys based on self-report, whereas the data for undiagnosed diabetes rates were obtained from direct glucose measurement in a sub-sample of the surveyed population.

      Centers for Disease Control and Prevention. National diabetes statistics report, 2017: estimates of diabetes and its burden in the United States. Available at: https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Accessed November 4, 2019.

      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999–2002.
      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and high risk for diabetes using A1C criteria in the U.S. population in 1988–2006.
      ,
      • Dagogo-Jack S
      Ethnic disparities in type 2 diabetes: pathophysiology and implications for prevention and management.
      • Egede LE
      • Dagogo-Jack S
      Epidemiology of type 2 diabetes: focus on ethnic minorities.

      Centers for Disease Control and Prevention. 2011 National Diabetes Fact Sheet. Diagnosed and undiagnosed diabetes in the United States, all ages, 2010. Available at:https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed November 4, 2019

      • Cowie CC
      • Rust KF
      • Ford ES
      • et al.
      Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006.
      For example, the 2011 Centers for Disease Control and Prevention (CDC estimates for diagnosed and undiagnosed diabetes among U.S. adults were 10.2% in non-Hispanic whites and 18.7% in non-Hispanic blacks.

      Centers for Disease Control and Prevention. 2011 National Diabetes Fact Sheet. Diagnosed and undiagnosed diabetes in the United States, all ages, 2010. Available at:https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed November 4, 2019

      The race/ethnicity-specific estimates for diagnosed diabetes were derived from 2007 to 2009 National Health Interview Survey
      • Cowie CC
      • Rust KF
      • Ford ES
      • et al.
      Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006.
      that relied on self-report.
      Remarkably, estimates of the prevalence of undiagnosed diabetes and prediabetes, which relied on measured blood glucose levels, showed no racial/ethnic differences.

      Centers for Disease Control and Prevention. 2011 National Diabetes Fact Sheet. Diagnosed and undiagnosed diabetes in the United States, all ages, 2010. Available at:https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed November 4, 2019

      A similar pattern of ∼2-fold higher prevalence of self-reported diabetes in AA than EA, unsupported by measured glucose levels showing no racial/ethnic difference in the prevalence of undiagnosed diabetes and prediabetes, has been well documented.

      Centers for Disease Control and Prevention. National diabetes statistics report, 2017: estimates of diabetes and its burden in the United States. Available at: https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf. Accessed November 4, 2019.

      ,
      • Cowie CC
      • Rust KF
      • Byrd-Holt DD
      • et al.
      Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999–2002.
      ,

      Centers for Disease Control and Prevention. 2011 National Diabetes Fact Sheet. Diagnosed and undiagnosed diabetes in the United States, all ages, 2010. Available at:https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Accessed November 4, 2019

      • Cowie CC
      • Rust KF
      • Ford ES
      • et al.
      Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006.
      • Benjamin SM
      • Valdez R
      • Geiss LS
      • et al.
      Estimated number of adults with prediabetes in the US in 2000: opportunities for prevention.
      • Williams DE
      • Cadwell BL
      • Cheng YJ
      • et al.
      Prevalence of impaired fasting glucose and its relationship with cardiovascular disease risk factors in US adolescents, 1999-2000.
      In a related report, Menke et al analyzed demographic distributions of FPG and 2-hrPG in the 2005-2010 NHANES cohort that included U.S. adults with and without diabetes.
      • Menke A
      • Rust KF
      • Savage PJ
      • et al.
      Hemoglobin A1c, fasting plasma glucose, and 2-hour plasma glucose distributions in U.S. population subgroups: NHANES 2005-2010.
      The results showed that, compared with non-Hispanic whites, the distributions of FPG and 2-hrPG were shifted lower for non-Hispanic blacks and higher for Mexican-Americans.
      • Menke A
      • Rust KF
      • Savage PJ
      • et al.
      Hemoglobin A1c, fasting plasma glucose, and 2-hour plasma glucose distributions in U.S. population subgroups: NHANES 2005-2010.
      Those findings, like our present report, are not consistent with the expectation of greater hyperglycemia in non-Hispanic blacks from national surveys.
      Clearly, complex genetic and environmental factors contribute to the dysregulation of glucose and occurrence of dysglycemia in different populations.
      • Dagogo-Jack S
      Ethnic disparities in type 2 diabetes: pathophysiology and implications for prevention and management.
      ,
      • Egede LE
      • Dagogo-Jack S
      Epidemiology of type 2 diabetes: focus on ethnic minorities.
      ,
      • Hivert MF
      • Jablonski KA
      • Perreault L
      • et al.
      Updated genetic score based on 34 confirmed type 2 diabetes loci is associated with diabetes incidence and regression to normoglycemia in the diabetes prevention program.
      However, the evidence for significant racial differences in major diabetes risk alleles of genome-wide significance has not been compelling.
      • Hivert MF
      • Jablonski KA
      • Perreault L
      • et al.
      Updated genetic score based on 34 confirmed type 2 diabetes loci is associated with diabetes incidence and regression to normoglycemia in the diabetes prevention program.
      ,
      • Dagogo-Jack S
      Predicting diabetes: our relentless quest for genomic nuggets.
      We have shown in the present report that African-American and EA offspring of parents with T2DM exhibited remarkable phenotypic concordance of long-term glycemic trajectories. Along with the prior report of similar incidence of prediabetes among initially normoglycemic subjects in our biracial cohort,
      • Dagogo-Jack S
      • Edeoga C
      • Ebenibo S
      • et al.
      Lack of racial disparity in incident prediabetes and glycemic progression among black and white offspring of parents with type 2 diabetes: the pathobiology of prediabetes in a biracial cohort (POP-ABC) study.
      the present findings indicate that parental history of T2DM may be a stronger factor than race/ethnicity in the prediction of longitudinal changes in glycemia.

      ROLE OF FUNDING SOURCES

      The funding sources had no role in the design and execution of the POP-ABC study, or analysis and publication of the data obtained from the study.

      AUTHOR CONTRIBUTIONS

      All authors materially participated in the research and article preparation and gave final approval for the version submitted. SD-J conceived of and designed the study, analyzed data; SDJ and LNR drafted manuscript; SE, CE collected data, reviewed and revised manuscript; JW performed statistical analysis, reviewed and revised manuscript.

      ACKNOWLEDGMENTS

      We are indebted to the participants who volunteered for this study and to the research staff at the GCRC for their expert support during the execution of the study.

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