Matthew A Sabin1, Costan G Magnussen2, Markus Juonala3, Julian P H Shield4, Mika Kähönen5, Terho Lehtimäki6, Tapani Rönnemaa7, Juha Koskinen8, Britt-Marie Loo9, Mikael Knip10, Nina Hutri-Kähönen5, Jorma S A Viikari7, Terence Dwyer11, Olli T Raitakari12. 1. Murdoch Childrens Research Institute, Royal Children's Hospital and University of Melbourne, Melbourne, Australia; matthew.sabin@mcri.edu.au. 2. Research Centre of Applied and Preventive Cardiovascular Medicine, and Menzies Research Institute Tasmania, University of Tasmania, Hobart, Australia; 3. Research Centre of Applied and Preventive Cardiovascular Medicine, and Medicine, University of Turku and Division of Medicine, Turku University Hospital, Turku, Finland; 4. National Institute for Health Research, Bristol Biomedical Research Unit in Nutrition, University of Bristol and Royal Hospital for Children, Bristol, United Kingdom; 5. Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Tampere, Finland; 6. Department of Clinical Chemistry, Finlab Laboratories, University of Tampere School of Medicine, Tampere, Finland; 7. Medicine, University of Turku and Division of Medicine, Turku University Hospital, Turku, Finland; 8. Research Centre of Applied and Preventive Cardiovascular Medicine, and. 9. National Institute for Health and Welfare, Department of Chronic Disease Prevention, Population Studies Unit, Turku, Finland; and. 10. Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland. 11. Murdoch Childrens Research Institute, Royal Children's Hospital and University of Melbourne, Melbourne, Australia; 12. Research Centre of Applied and Preventive Cardiovascular Medicine, and Departments of Clinical Physiology and Nuclear Medicine, and.
Abstract
BACKGROUND AND OBJECTIVES: Fasting insulin concentrations are increasingly being used as a surrogate for insulin resistance and risk for type 2 diabetes (T2DM), although associations with adult outcomes are unclear. Our objective was to determine whether fasting insulin concentrations in childhood associate with later T2DM. METHODS: Fasting insulin values were available from 2478 participants in the longitudinal Cardiovascular Risk in Young Finns Study at baseline age 3 to 18 years, along with data on adult T2DM (N = 84, mean age = 39.6 years). RESULTS: Among 3- to 6-year-olds, a 1-SD increase in fasting insulin was associated with a relative risk (RR) of 2.04 (95% confidence interval [CI], 1.54-2.70) for later T2DM, which remained significant after we adjusted for BMI and parental history of T2DM. For those aged 9 to 18 years, a 1-SD increase in insulin was associated with an RR of 1.32 (95% CI, 1.06-1.65) for T2DM, but this became nonsignificant after we adjusted for BMI and parental history of T2DM. In the latter age group, a 1-SD increase in BMI was associated with an RR of 1.45 (95% CI, 1.21-1.73) for T2DM, with adjustment for insulin and parental history of T2DM not improving this association. BMI in younger children was not associated with later T2DM. In life course analyses, those with T2DM had higher fasting insulin levels in early childhood and later adulthood but not in peripubertal years. CONCLUSIONS: Elevated fasting insulin concentrations in early childhood, but not adolescence, are independently associated with an elevated risk of T2DM in adulthood.
BACKGROUND AND OBJECTIVES: Fasting insulin concentrations are increasingly being used as a surrogate for insulin resistance and risk for type 2 diabetes (T2DM), although associations with adult outcomes are unclear. Our objective was to determine whether fasting insulin concentrations in childhood associate with later T2DM. METHODS: Fasting insulin values were available from 2478 participants in the longitudinal Cardiovascular Risk in Young Finns Study at baseline age 3 to 18 years, along with data on adult T2DM (N = 84, mean age = 39.6 years). RESULTS: Among 3- to 6-year-olds, a 1-SD increase in fasting insulin was associated with a relative risk (RR) of 2.04 (95% confidence interval [CI], 1.54-2.70) for later T2DM, which remained significant after we adjusted for BMI and parental history of T2DM. For those aged 9 to 18 years, a 1-SD increase in insulin was associated with an RR of 1.32 (95% CI, 1.06-1.65) for T2DM, but this became nonsignificant after we adjusted for BMI and parental history of T2DM. In the latter age group, a 1-SD increase in BMI was associated with an RR of 1.45 (95% CI, 1.21-1.73) for T2DM, with adjustment for insulin and parental history of T2DM not improving this association. BMI in younger children was not associated with later T2DM. In life course analyses, those with T2DM had higher fasting insulin levels in early childhood and later adulthood but not in peripubertal years. CONCLUSIONS: Elevated fasting insulin concentrations in early childhood, but not adolescence, are independently associated with an elevated risk of T2DM in adulthood.
Authors: Tian Hu; David R Jacobs; Alan R Sinaiko; Lydia A Bazzano; Trudy L Burns; Stephen R Daniels; Terry Dwyer; Nina Hutri-Kähönen; Markus Juonala; Kari A Murdy; Ronald J Prineas; Olli T Raitakari; Elaine M Urbina; Alison Venn; Jessica G Woo; Julia Steinberger Journal: Diabetes Care Date: 2020-09-01 Impact factor: 19.112
Authors: Marie-Jeanne Buscot; Simon S Wotherspoon; Costan G Magnussen; Markus Juonala; Matthew A Sabin; David P Burgner; Terho Lehtimäki; Jorma S A Viikari; Nina Hutri-Kähönen; Olli T Raitakari; Russell J Thomson Journal: BMC Med Res Methodol Date: 2017-06-06 Impact factor: 4.615