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  • 1
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    Interaction Between Dietary Iron Intake and Genetically Determined Iron Overload: Risk of Islet Autoimmunity and Progression to Type 1 Diabetes in the TEDDY Study
    American Diabetes Association ; 2023
    In:  Diabetes Care Vol. 46, No. 5 ( 2023-05-01), p. 1014-1018
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 46, No. 5 ( 2023-05-01), p. 1014-1018
    Abstract: To examine whether iron intake and genetically determined iron overload interact in predisposing to the development of childhood islet autoimmunity (IA) and type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS In The Environmental Determinants of Diabetes in the Young (TEDDY) study, 7,770 genetically high-risk children were followed from birth until the development of IA and progression to T1D. Exposures included energy-adjusted iron intake in the first 3 years of life and a genetic risk score (GRS) for increased circulating iron. RESULTS We found a U-shaped association between iron intake and risk of GAD antibody as the first autoantibody. In children with GRS ≥2 iron risk alleles, high iron intake was associated with an increased risk of IA, with insulin as first autoantibody (adjusted hazard ratio 1.71 [95% CI 1.14; 2.58]) compared with moderate iron intake. CONCLUSIONS Iron intake may alter the risk of IA in children with high-risk HLA haplogenotypes.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc22-1359
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
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  • 2
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    An Age-Related Exponential Decline in the Risk of Multiple Islet Autoantibody Seroconversion During Childhood
    American Diabetes Association ; 2021
    In:  Diabetes Care Vol. 44, No. 10 ( 2021-10-01), p. 2260-2268
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 44, No. 10 ( 2021-10-01), p. 2260-2268
    Abstract: Islet autoimmunity develops before clinical type 1 diabetes and includes multiple and single autoantibody phenotypes. The objective was to determine age-related risks of islet autoantibodies that reflect etiology and improve screening for presymptomatic type 1 diabetes. RESEARCH DESIGN AND METHODS The Environmental Determinants of Diabetes in the Young study prospectively monitored 8,556 genetically at-risk children at 3- to 6-month intervals from birth for the development of islet autoantibodies and type 1 diabetes. The age-related change in the risk of developing islet autoantibodies was determined using landmark and regression models. RESULTS The 5-year risk of developing multiple islet autoantibodies was 4.3% (95% CI 3.8–4.7) at 7.5 months of age and declined to 1.1% (95% CI 0.8–1.3) at a landmark age of 6.25 years (P & lt; 0.0001). Risk decline was slight or absent in single insulin and GAD autoantibody phenotypes. The influence of sex, HLA, and other susceptibility genes on risk subsided with increasing age and was abrogated by age 6 years. Highest sensitivity and positive predictive value of multiple islet autoantibody phenotypes for type 1 diabetes was achieved by autoantibody screening at 2 years and again at 5–7 years of age. CONCLUSIONS The risk of developing islet autoimmunity declines exponentially with age, and the influence of major genetic factors on this risk is limited to the first few years of life.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc20-2122
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
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  • 3
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    Maternal Type 1 Diabetes Reduces Autoantigen-Responsive CD4+ T Cells in Offspring
    American Diabetes Association ; 2020
    In:  Diabetes Vol. 69, No. 4 ( 2020-04-01), p. 661-669
    Details
    In: Diabetes, American Diabetes Association, Vol. 69, No. 4 ( 2020-04-01), p. 661-669
    Abstract: Autoimmunity against pancreatic β-cell autoantigens is a characteristic of childhood type 1 diabetes (T1D). Autoimmunity usually appears in genetically susceptible children with the development of autoantibodies against (pro)insulin in early childhood. The offspring of mothers with T1D are protected from this process. The aim of this study was to determine whether the protection conferred by maternal T1D is associated with improved neonatal tolerance against (pro)insulin. Consistent with improved neonatal tolerance, the offspring of mothers with T1D had reduced cord blood CD4+ T-cell responses to proinsulin and insulin, a reduction in the inflammatory profile of their proinsulin-responsive CD4+ T cells, and improved regulation of CD4+ T cell responses to proinsulin at 9 months of age, as compared with offspring with a father or sibling with T1D. Maternal T1D was also associated with a modest reduction in CpG methylation of the INS gene in cord blood mononuclear cells from offspring with a susceptible INS genotype. Our findings support the concept that a maternal T1D environment improves neonatal immune tolerance against the autoantigen (pro)insulin.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-0751
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
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  • 4
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    1280-P: Improving Type 1 Diabetes (T1D) Prediction by Incorporating Growth Features into Landmark Models
    American Diabetes Association ; 2020
    In:  Diabetes Vol. 69, No. Supplement_1 ( 2020-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 69, No. Supplement_1 ( 2020-06-01)
    Abstract: We explored the association between growth features and T1D development using landmark analysis at different ages. Analysis included individuals from 2 birth cohort studies: DAISY and BABYDIAB (n=2,664; 129 progressed to T1D). Using height and weight measured over time, percentiles for age were calculated. Missing values were imputed using LMS parameters of CDC growth charts. Rates of change of percentiles were computed over the prior year. Twelve ages (1-12 years) were used for landmark analysis with Random Survival Forest to predict probability of T1D onset in the 1- to 19-year follow up windows. The baseline model used HLA risk group, sex, T1D family history and breastfeeding history. The full model added growth features: height and weight percentiles at age and change in percentiles. Performance was measured using C-index and feature importance was ranked. Incorporating growth features significantly improved prediction accuracy of T1D onset for 95% of combinations of landmark ages and prediction window sizes (Table 1, not all ages and windows shown). The order of features from most to least predictive is: HLA group, rates of height and weight changes, height and weight percentiles, family history, breastfeeding and sex. This analysis demonstrates that using growth features can significantly improve prediction of T1D. Table 1: C-Index with and without inclusion of growth features for landmark age of 3 years. Disclosure Z. Li: None. V. Anand: None. J.L. Dunne: None. B.I. Frohnert: None. W. Hagopian: Consultant; Self; Novo Nordisk Inc. H. Hyoty: None. M. Maziarz: None. A. Ziegler: None. J. Toppari: None. Funding JDRF (1-IND-2019-717-I-X, 1-SRA-2019-722-I-X, 1-SRA-2019-720-I-X, 1-SRA-2019-721-I-X, 1-SRA-2019-719-I-X, 1-SRA-2019-723-I-X)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db20-1280-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
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  • 5
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    Autoantibodies to Sympathetic Ganglia, GAD, or Tyrosine Phosphatase in Long-Term IDDM With and Without ECG-Based Cardiac Autonomic Neuropathy
    American Diabetes Association ; 1997
    In:  Diabetes Care Vol. 20, No. 6 ( 1997-06-01), p. 1009-1012
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 20, No. 6 ( 1997-06-01), p. 1009-1012
    Abstract: To evaluate the association of autoantibodies to complement-fixing sympathetic ganglia (CF-SG), and tyrosine phosphatase (IA-2) with electrocardiogram (ECG)-based cardiac autonomic neuropathy (CAN) in long-term IDDM. RESEARCH DESIGN AND METHODS We examined the prevalence of autoantibodies to CF-SG (by complement-fixing indirect immunoflourescence), GAD, and IA-2 (by radioligand assay) and islet cells (by indirect immunofluorescence) in 96 long-term IDDM patients (41 with ECG-based CAN, ≥ 2 of 5 cardiac reflex tests abnormal; 55 without ECG-based CAN). As a control group, 89 healthy nondiabetic subjects were investigated. RESULTS CF-SG autoantibodies were observed more frequently in long-term IDDM patients than in the control group (25 vs. 4%, P = 0.0001). Of the IDDM patients, 14 (34%) with CAN and 10 (18%) without CAN presented with CF-SG autoantibodies (P = 0.06). GAD or IA-2 autoantibodies were detected in 14 (34%) and 17 (41%) IDDM patients with CAN, compared with 24 (44%) and 29 (53%) IDDM patients without CAN (P = 0.2, P = 0.2). Islet cell antibodies were observed in 6 (15%) IDDM patients with and in 9 (16%) IDDM patients without CAN (P = 0.5). CONCLUSIONS In long-term IDDM, the role of CF-SG autoantibodies, which tend to be more frequent in patients with ECG-based CAN, requires further investigations. The persistence of GAD and IA-2 autoantibodies is not related to ECG-based CAN.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/diacare.20.6.1009
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 1997
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  • 6
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    Efficacy and Safety of Dapagliflozin in Patients With Inadequately Controlled Type 1 Diabetes: The DEPICT-1 52-Week Study
    American Diabetes Association ; 2018
    In:  Diabetes Care Vol. 41, No. 12 ( 2018-12-01), p. 2552-2559
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 41, No. 12 ( 2018-12-01), p. 2552-2559
    Abstract: This study evaluated the long-term safety and efficacy of dapagliflozin as an adjunct to adjustable insulin in patients with type 1 diabetes and inadequate glycemic control. RESEARCH DESIGN AND METHODS DEPICT-1 (Dapagliflozin Evaluation in Patients With Inadequately Controlled Type 1 Diabetes) was a randomized (1:1:1), double-blind, placebo-controlled phase 3 study of dapagliflozin 5 mg and 10 mg in patients with type 1 diabetes (HbA1c 7.5–10.5% [58–91 mmol/mol]) (NCT02268214). The results of the 52-week study, consisting of the 24-week short-term and 28-week extension period, are reported here. RESULTS Of the 833 patients randomized into the study, 708 (85%) completed the 52-week study. Over 52 weeks, dapagliflozin 5 mg and 10 mg led to clinically significant reductions in HbA1c (difference vs. placebo [95% CI] −0.33% [−0.49, −0.17] [−3.6 mmol/mol (−5.4, −1.9)] and −0.36% [−0.53, −0.20] [−3.9 mmol/mol (−5.8, −2.2)], respectively) and body weight (difference vs. placebo [95% CI] −2.95% [−3.83, −2.06] and −4.54% [−5.40, −3.66] , respectively). Serious adverse events were reported in 13.4%, 13.5%, and 11.5% of patients in the dapagliflozin 5 mg, 10 mg, and placebo groups, respectively. Although hypoglycemia events were comparable across treatment groups, more patients in the dapagliflozin groups had events adjudicated as definite diabetic ketoacidosis (DKA; 4.0%, 3.4%, and 1.9% in dapagliflozin 5 mg, 10 mg, and placebo groups, respectively). CONCLUSIONS Over 52 weeks, dapagliflozin led to improvements in glycemic control and weight loss in patients with type 1 diabetes, while increasing the risk of DKA.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc18-1087
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 7
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    1445-P: Co-occurrence of Islet, Celiac, and Thyroid Autoimmunity in Children Prospectively Followed from Birth in the TEDDY Study
    American Diabetes Association ; 2024
    In:  Diabetes Vol. 73, No. Supplement_1 ( 2024-06-14)
    Details
    In: Diabetes, American Diabetes Association, Vol. 73, No. Supplement_1 ( 2024-06-14)
    Abstract: Islet autoantibodies (IA) that precede type 1 diabetes, tissue transglutaminase autoantibodies (tTGA) preceding celiac disease, and thyroid peroxidase (TPOA) or thyroglobulin (ThGA) autoantibodies preceding autoimmune thyroid disease may coincide. We aim to describe the order of first appearance of IA, tTGA, or thyroid autoimmunity in children, as well as the role of thyroid autoimmunity in risk of subsequent development of IA or tTGA. Children (n = 5437) with a genetically determined high risk for autoimmune disease from the USA, Finland, Germany, and Sweden were followed from birth to age 14 or type 1 diabetes diagnosis. Cox regression was used for survival analyses. IA, tTGA, and thyroid autoimmunity were the first or only type of autoantibody to develop in 10%, 20%, and 8% of the children, respectively, and 61% remained autoantibody negative (median follow-up 12.0 years). Among autoantibody positive children, a family history of autoimmune thyroid disease was associated with an increased risk of ThGA (OR 2.05, 95% CI 1.48, 2.85, p & lt; 0.001), but not TPOA (OR 1.18, 95% CI 0.71, 1.95, p = 0.53), as the first or only autoantibody. TPOA as the first or only thyroid autoantibody was associated with increased risk of subsequent development of IA (HR 1.94, 95% CI 1.11, 3.41, p = 0.021) and tTGA (HR 1.69, 95% CI 1.04, 2.75, p = 0.036), while there was no association for ThGA-first thyroid autoimmunity with either IA or tTGA. Among children with IA, thyroid autoimmunity status at the time of IA seroconversion was not associated with risk of IAA versus GADA as the first appearing IA (TPOA-first p = 0.73, ThGA-first p = 0.20). The association between thyroid autoimmunity and either IA or tTGA depends on which thyroid autoantibody appears first. A better understanding of the co-occurrence and order of appearance of these three types of autoantibodies may aid in designing a more personalized approach to identifying individuals at highest risk for autoimmune comorbidity. Disclosure J.L. Clasen: None. H.E. Larsson: None. B. Jonsdottir: None. M.J. Haller: Consultant; Sanofi. Advisory Panel; SAB Biotherapeutics, Inc. Consultant; MannKind Corporation. D. Agardh: None. H.M. Parikh: None. K.F. Lynch: None. Å. Lernmark: Advisory Panel; DiaMyd Medical AB, Stockholm, Sweden. M. Rewers: Advisory Panel; Sanofi. Other Relationship; Sanofi. Consultant; Janssen Pharmaceuticals, Inc. Research Support; Juvenile Diabetes Research Foundation (JDRF). Consultant; Provention Bio, Inc. Research Support; Hemsley Charitable Trust, National Institute of Diabetes and Digestive and Kidney Diseases. R. McIndoe: None. J. Toppari: None. A. Ziegler: None. J. Krischer: None. B. Akolkar: None. W. Hagopian: Research Support; Janssen Pharmaceuticals, Inc., Provention Bio, Inc. Consultant; Sanofi-Aventis U.S., Randox R & D. K. Vehik: None. Funding NIH NIDDK (U01 DK63829, U01 DK63861, U01 DK63821, U01 DK63865, U01 DK63863, U01 DK63836, U01 DK63790, UC4 DK63829, UC4 DK63861, UC4 DK63821, UC4 DK63865, UC4 DK63863, UC4 DK63836, UC4 DK95300, UC4 DK100238, UC4 DK106955, UC4 DK112243, UC4 DK117483, U01 DK124166, U01 DK128847, and Contract No. HHSN267200700014C)
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db24-1445-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2024
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  • 8
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    High-Dose Intravenous Insulin Infusion Versus Intensive Insulin Treatment in Newly Diagnosed IDDM
    American Diabetes Association ; 1997
    In:  Diabetes Vol. 46, No. 10 ( 1997-10-01), p. 1607-1611
    Details
    In: Diabetes, American Diabetes Association, Vol. 46, No. 10 ( 1997-10-01), p. 1607-1611
    Abstract: High-dose intravenous insulin infusion at the onset of IDDM has been suggested to improve β-cell function during the 1st year of insulin treatment. To test this hypothesis, we randomly assigned newly diagnosed IDDM patients to receive either an experimental 2-week high-dose intravenous insulin infusion (n = 9; age, 25 ± 7 years; HbA1c, 10.5 ± 2.0%) or an intensive insulin therapy of four injections per day (n = 10; age, 28 ± 7 years; HbA1c, 12.3 ± 3.0%). The experimental-therapy group received three times more insulin (1.2 ± 0.4 U · kg−1 · day−1) than the intensive-therapy group (0.4 ± 0.1 U · kg−1 · day−1, P & lt; 0.0005). By week 3, both groups were treated similarly with intensive insulin therapy and were followed for 1 year, β-cell function was evaluated with fasting plasma C-peptide and glucagon-stimulated and mixed meal-stimulated C-peptide concentrations. In both groups, insulin doses were comparable, and HbA1c levels were near normal during follow-up. At diagnosis of IDDM, fasting C-peptide was 0.40 ± 0.13 nmol/l in the experimental-therapy group and 0.39 ± 0.23 nmol/1 in the intensive-therapy group. Irrespective of treatment, a slight decline of fasting C-peptide was observed in sequential measurements up to 12 months in both groups (Δ, -0.13 and -0.08 nmol/1, respectively; NS). Glucagon-stimulated C-peptide concentrations decreased from 0.54 ± 0.18 and 0.70 ± 0.39 nmol/l at month 0 to 0.41 ± 0.20 and 0.61 ± 0.52 nmol/1, respectively, at month 12. In the experimental-therapy group, mixed meal-stimulated C-peptide concentrations (area under the curve over 2 h) increased from 82.10 ± 43.72 to 101.20 ± 32.53 nmol/L and in the intensive-therapy group, from 75.05 ± 46.01 to 107.20 ± 102.51 nmol/1. Changes in stimulated C-peptide concentrations between month 0 and 12 were not significant in both groups. During follow-up, fasting and stimulated C-peptide concentrations were not significantly different between the experimental-therapy group and the intensive-therapy group. We conclude that as initial treatments of newly diagnosed IDDM, high-dose intravenous insulin infusion and intensive insulin therapy equally preserve β-cell function during the 1st year of insulin therapy.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diacare.46.10.1607
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 1997
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  • 9
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    An Interferon-Induced Helicase ( IFIH1 ) Gene Polymorphism Associates With Different Rates of Progression From Autoimmunity to Type 1 Diabetes
    American Diabetes Association ; 2011
    In:  Diabetes Vol. 60, No. 2 ( 2011-02-01), p. 685-690
    Details
    In: Diabetes, American Diabetes Association, Vol. 60, No. 2 ( 2011-02-01), p. 685-690
    Abstract: Genome-wide association studies have identified gene regions associated with the development of type 1 diabetes. The aim of this study was to determine whether these associations are with the development of autoimmunity and/or progression to diabetes. RESEARCH DESIGN AND METHODS Children (n = 1,650) of parents with type 1 diabetes were prospectively followed from birth (median follow-up 10.20 years) for the development of islet autoantibodies, thyroid peroxidase antibodies, tissue transglutaminase antibodies, and diabetes. Genotyping for single-nucleotide polymorphisms of the PTPN22, ERBB3, PTPN2, KIAA0350, CD25, and IFIH1 genes was performed using the MassARRAY system with iPLEX chemistry. RESULTS Islet autoantibodies developed in 137 children and diabetes developed in 47 children. Type 1 diabetes risk was associated with the IFIH1 rs2111485 single-nucleotide polymorphism (hazard ratio 2.08; 95% CI 1.16–3.74; P = 0.014). None of the other genes were significantly associated with diabetes development in this cohort. IFIH1 genotypes did not associate with the development of islet autoantibodies (P = 0.80) or autoantibodies against thyroid peroxidase (P = 0.55) and tissue transglutaminase (P = 0.66). Islet autoantibody–positive children with the IFIH1 rs2111485 GG genotype had a faster progression to diabetes (31% within 5 years) than children with the type 1 diabetes protective GA or AA genotypes (11% within 5 years; P = 0.006). CONCLUSIONS The findings indicate that IFIH1 genotypes influence progression from autoimmunity to diabetes development, consistent with the notion that protective genotypes downregulate responses to environmental insults after initiation of autoimmunity.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db10-1269
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2011
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  • 10
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    BMI at Age 8 Years Is Influenced by the Type 2 Diabetes Susceptibility Genes HHEX-IDE and CDKAL1
    American Diabetes Association ; 2010
    In:  Diabetes Vol. 59, No. 8 ( 2010-08-01), p. 2063-2067
    Details
    In: Diabetes, American Diabetes Association, Vol. 59, No. 8 ( 2010-08-01), p. 2063-2067
    Abstract: To determine whether HHEX-IDE and CDKAL1 genes, which are associated with birth weight and susceptibility to type 2 diabetes, continue to influence growth during childhood. RESEARCH DESIGN AND METHODS BMI, weight, and height at age 8 years expressed as age- and sex-corrected standard deviation scores (SDS) against national reference data and single-nucleotide polymorphism genotyping of HHEX-IDE and CDKAL1 loci were analyzed in 646 prospectively followed children in the German BABYDIAB cohort. All children were singleton full-term births; 386 had mothers with type 1 diabetes, and 260 had fathers with type 1 diabetes and a nondiabetic mother. RESULTS Type 2 diabetes risk alleles at the HHEX-IDE locus were associated with reduced BMI-SDS at age 8 years (0.17 SDS per allele; P = 0.004). After stratification for birth weight, both HHEX-IDE and CDKAL1 risk alleles were associated with reduced BMI-SDS (0.45 SDS, P = 0.0002; 0.52 SDS, P = 0.0001) and weight-SDS (0.22 SDS, P = 0.04; 0.56 SDS, P = 0.0002) in children born large for gestational age ( & gt;90th percentile) but not children born small or appropriate for gestational age. Within children born large for gestational age, BMI and weight decreased with each additional type 2 diabetes risk allele (∼ −2 kg per allele; & gt;8 kg overall). Findings were consistent in children of mothers with type 1 diabetes (P & lt; 0.0001) and children of nondiabetic mothers (P = 0.008). CONCLUSIONS The type 2 diabetes susceptibility alleles at HHEX-IDE and CDKAL1 loci are associated with low BMI at age 8 years in children who were born large for gestational age.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db10-0099
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2010
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