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    Paternal insulin resistance and its association with umbilical cord insulin concentrations

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    URI
    https://rde.dspace-express.com/handle/11287/622217
    Author
    Shields, B. M.
    Knight, B.
    Turner, M.
    Wilkins-Wall, B.
    Shakespeare, L.
    Powell, R. J.
    Hannemann, M.
    Clark, P. M.
    Yajnik, C. S.
    Hattersley, A. T.
    Date
    2006-05-17
    Journal
    Diabetologia
    Type
    Multicenter Study
    Publisher
    Springer
    DOI
    10.1007/s00125-006-0282-8
    Rights
    Copyright © 2006, Springer-Verlag
    Metadata
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    Abstract
    AIMS/HYPOTHESIS: Fetal growth is influenced by genetic factors as well as the intra-uterine environment. We hypothesised that some genetic factors may alter fetal insulin secretion and insulin action. SUBJECTS, MATERIALS AND METHODS: To assess this, we analysed plasma insulin concentration in umbilical cord blood from 644 normal, term, UK Caucasian deliveries from the Exeter Family Study of Childhood Health. We tested for associations between cord insulin and each of parental anthropometry, fasting glucose, insulin and lipids. RESULTS: As expected, cord insulin concentrations correlated with all measures of birth size (weight, length, head and arm circumferences, sum of skinfold thicknesses, ponderal index: r=0.16-0.4, p<0.01 for all) and maternal BMI (r=0.11, p=0.005), maternal glucose (r=0.25, p<0.001) and maternal insulin resistance (r=0.23, p<0.001). Paternal fasting insulin and insulin resistance were correlated with cord insulin (r=0.15, p=0.006; r=0.13, p=0.001, respectively), and this was independent of paternal BMI. Multiple linear regression analysis revealed paternal insulin resistance to be a predictor of cord insulin concentrations, independently of maternal factors. CONCLUSION: Our results show an independent relationship between paternal insulin resistance and cord insulin concentrations. This is consistent with heritability of insulin resistance from father to offspring and a compensatory increase in fetal insulin secretion, the latter occurring pre-natally before the homeostatic feedback loop between glucose and insulin is established.
    Publisher URL
    https://doi.org/10.1007/s00125-006-0282-8
    Note
    The article is available via Open Access. Click on the 'Additional link' above to access the full-text.
    Collections
    • Diabetes and endocrinology
    • Maternity and obstetrics (birth and babies)
    • pre-2014 RD&E publications

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