A Lauria1, A Barker1, N Schloot1, N Hosszufalusi1, J Ludvigsson1, C Mathieu1, D Mauricio1, M Nordwall2, B Van der Schueren1, T Mandrup-Poulsen2, W A Scherbaum1, I Weets2, F K Gorus2, N Wareham1, R D Leslie1, P Pozzilli2. 1. Department of Endocrinology and DiabetesUniversity Campus Bio-Medico, Via Alvaro del Portillo, Rome 21 00128, ItalyMRC Epidemiology UnitCambridge, UKInstitute for Clinical DiabetologyGerman Diabetes Centre, Leibniz-Institute for Diabetes Research and Clinic for Metabolic Diseases Heinrich Heine University, Dusseldorf, GermanySemmelweis University3rd Department of Internal Medicine, Linkoping University, Linkoping, SwedenDivision of PediatricsDepartment of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, SwedenLaboratory for Experimental Medicine and EndocrinologyKatholieke Universiteit Leuven, Leuven, BelgiumDepartment EndocrinologyHospital Arnau de Vilanova, Lleida, SpainPediatric ClinicVrinnevi Hospital, Norrköping, SwedenDepartment of Biomedical SciencesUniversity of Copenhagen, Copenhagen, DenmarkDepartment of EndocrinologyDiabetes and Rheumatology, Heinrich Heine University, Dusseldorf, GermanyDiabetes Research Center and Academic Hospital (UZ Brussel)Vrije Universiteit Brussel (VUB), Brussel, BelgiumBelgian Diabetes Registry (BDR)Brussels, BelgiumCentre of DiabetesBlizard Institute, Barts and The London School of Medicine, Queen Mary University of London, London, UKDepartment of Molecular Medicine and SurgeryKarolinska Institutet, Stockholm, Sweden. 2. Department of Endocrinology and DiabetesUniversity Campus Bio-Medico, Via Alvaro del Portillo, Rome 21 00128, ItalyMRC Epidemiology UnitCambridge, UKInstitute for Clinical DiabetologyGerman Diabetes Centre, Leibniz-Institute for Diabetes Research and Clinic for Metabolic Diseases Heinrich Heine University, Dusseldorf, GermanySemmelweis University3rd Department of Internal Medicine, Linkoping University, Linkoping, SwedenDivision of PediatricsDepartment of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, SwedenLaboratory for Experimental Medicine and EndocrinologyKatholieke Universiteit Leuven, Leuven, BelgiumDepartment EndocrinologyHospital Arnau de Vilanova, Lleida, SpainPediatric ClinicVrinnevi Hospital, Norrköping, SwedenDepartment of Biomedical SciencesUniversity of Copenhagen, Copenhagen, DenmarkDepartment of EndocrinologyDiabetes and Rheumatology, Heinrich Heine University, Dusseldorf, GermanyDiabetes Research Center and Academic Hospital (UZ Brussel)Vrije Universiteit Brussel (VUB), Brussel, BelgiumBelgian Diabetes Registry (BDR)Brussels, BelgiumCentre of DiabetesBlizard Institute, Barts and The London School of Medicine, Queen Mary University of London, London, UKDepartment of Molecular Medicine and SurgeryKarolinska Institutet, Stockholm, Sweden Department of Endocrinology and DiabetesUniversity Campus Bio-Medico, Via Alvaro del Portillo, Rome 21 00128, ItalyMRC Epidemiology UnitCambridge, UKInstitute for Clinical DiabetologyGerman Diabetes Centre, Leibniz-Institute for Diabetes Research and Clinic for Metabolic Diseases Heinrich Heine University, Dusseldorf, GermanySemmelweis University3rd Department of Internal Medicine, Linkoping University, Linkoping, SwedenDivision of PediatricsDepartment of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, SwedenLaboratory for Experimental Medicine and EndocrinologyKatholieke Universiteit Leuven, Leuven, BelgiumDepartme
Abstract
OBJECTIVE: Body weight-related insulin resistance probably plays a role in progression to type 1 diabetes, but has an uncertain impact following diagnosis. In this study, we investigated whether BMI measured at diagnosis was an independent predictor of C-peptide decline 1-year post-diagnosis. DESIGN: Multicentre longitudinal study carried out at diagnosis and up to 1-year follow-up. METHODS: Data on C-peptide were collected from seven diabetes centres in Europe. Patients were grouped according to age at diagnosis (<5 years, n=126; >5 years <10 years, n=295; >10 years <18 years, n=421; >18 years, n=410). Linear regression was used to investigate whether BMI was an independent predictor of change in fasting C-peptide over 1 year. Models were additionally adjusted for baseline insulin dose and HbA1c. RESULTS: In individuals diagnosed between 0 and 5 years, 5 and 10 years and those diagnosed >18 years, we found no association between BMI and C-peptide decline. In patients aged 10-18 years, higher BMI at baseline was associated with a greater decline in fasting C-peptide over 1 year with a decrease (β 95% CI; P value) of 0.025 (0.010, 0.041) nM/kg per m(2) higher baseline BMI (P=0.001). This association remained significant after adjusting for gender and differences in HbA1c and insulin dose (β=0.026, 95% CI=0.0097, 0.042; P=0.002). CONCLUSIONS: These observations indicate that increased body weight and increased insulin demand are associated with more rapid disease progression after diagnosis of type 1 diabetes in an age group 10-18 years. This should be considered in studies of β-cell function in type 1 diabetes.
OBJECTIVE: Body weight-related insulin resistance probably plays a role in progression to type 1 diabetes, but has an uncertain impact following diagnosis. In this study, we investigated whether BMI measured at diagnosis was an independent predictor of C-peptide decline 1-year post-diagnosis. DESIGN: Multicentre longitudinal study carried out at diagnosis and up to 1-year follow-up. METHODS: Data on C-peptide were collected from seven diabetes centres in Europe. Patients were grouped according to age at diagnosis (<5 years, n=126; >5 years <10 years, n=295; >10 years <18 years, n=421; >18 years, n=410). Linear regression was used to investigate whether BMI was an independent predictor of change in fasting C-peptide over 1 year. Models were additionally adjusted for baseline insulin dose and HbA1c. RESULTS: In individuals diagnosed between 0 and 5 years, 5 and 10 years and those diagnosed >18 years, we found no association between BMI and C-peptide decline. In patients aged 10-18 years, higher BMI at baseline was associated with a greater decline in fasting C-peptide over 1 year with a decrease (β 95% CI; P value) of 0.025 (0.010, 0.041) nM/kg per m(2) higher baseline BMI (P=0.001). This association remained significant after adjusting for gender and differences in HbA1c and insulin dose (β=0.026, 95% CI=0.0097, 0.042; P=0.002). CONCLUSIONS: These observations indicate that increased body weight and increased insulin demand are associated with more rapid disease progression after diagnosis of type 1 diabetes in an age group 10-18 years. This should be considered in studies of β-cell function in type 1 diabetes.
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