Abstract
Aims/hypothesisWe aimed to identify critical periods and specific longitudinal growth patterns from fetal life onwards associated with childhood insulin and C-peptide levels.MethodsIn a prospective population-based cohort study of 4328 children, we repeatedly measured (femur) length and (estimated fetal) weight from the second trimester of fetal life until 6 years of age. BMI was calculated from 6 months onwards. Insulin and C-peptide levels were measured at 6 years of age.ResultsPreterm birth and small or large size for gestational age at birth were not associated with childhood insulin levels. Conditional growth modelling showed that, independent of growth in other time intervals, weight growth in each time interval from birth onwards, length growth from 6 months onwards and BMI growth from 12 months onwards were positively associated with childhood insulin levels. The strongest associations were present for weight and BMI growth between 48 and 72 months of age. Repeated measurement analyses showed that, compared with children in the lowest quartile of childhood insulin, those in the highest quartile had a higher length from birth onwards and a higher weight and BMI from 24 months onwards. These differences increased with age. No associations were observed for fetal growth characteristics. Similar results were observed for C-peptide levels.Conclusions/interpretationOur results suggest that rapid length, weight and BMI growth from birth onwards, but not during fetal life, is associated with higher insulin levels in childhood.
Highlights
A large body of evidence suggests that adverse exposures in early life influence the risk of type 2 diabetes in later life [1]
Conclusions/interpretation Our results suggest that rapid length, weight and BMI growth from birth onwards, but not during fetal life, is associated with higher insulin levels in childhood
No or minor differences in childhood growth characteristics were observed between the groups
Summary
A large body of evidence suggests that adverse exposures in early life influence the risk of type 2 diabetes in later life [1]. Multiple previous studies have shown that adults born with either a low or high birthweight are at increased risk of type 2 diabetes [2, 3]. Since birthweight is the result of different fetal growth patterns and is the starting point of infant growth, Diabetologia (2017) 60:81–88 birthweight is not a causal factor per se in the development of type 2 diabetes. Studies assessing the associations of directly measured fetal growth characteristics with measures of glucose or insulin metabolism in later life are scarce and focused on measures of growth during specific trimesters only [4, 5]. As the development of the endocrine pancreas starts as early as the first trimester [6], fetal life might be a critical period for glucose and insulin metabolism, and the development of type 2 diabetes in later life
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