Diabetologia

, Volume 37, Issue 2, pp 150–154

Thinness at birth and insulin resistance in adult life

  • D. I. W. Phillips
  • D. J. P. Barker
  • C. N. Hales
  • S. Hirst
  • C. Osmond
Article

DOI: 10.1007/s001250050086

Cite this article as:
Phillips, D.I.W., Barker, D.J.P., Hales, C.N. et al. Diabetologia (1994) 37: 150. doi:10.1007/s001250050086

Summary

Type 2 (non-insulin-dependent) diabetes mellitus may originate through impaired development in fetal life. Both insulin deficiency and resistance to the action of insulin are thought to be important in its pathogenesis. Although there is evidence that impaired fetal development may result in insulin deficiency, it is not known whether insulin resistance could also be a consequence of reduced early growth. Insulin resistance was therefore measured in 81 normoglycaemic subjects, and 22 subjects with impaired glucose tolerance, who were born in Preston, UK, between 1935 and 1943. Their birth measurements had been recorded in detail. Insulin resistance was measured by the insulin tolerance test which uses the rate of fall in blood glucose concentrations after intravenous injection of insulin as an index of insulin resistance. Men and women who were thin at birth, as measured by a low ponderal index, were more insulin resistant. The association was statistically significant (p = 0.01) and independent of duration of gestation, adult body mass index and waist to hip ratio and of confounding variables including social class at birth or currently. Thinness at birth and in adult life has opposing effects such that resistance fell with increasing ponderal index at birth but rose with increasing adult body mass index. It is concluded that insulin resistance is associated with impaired development in fetal life.

Key words

Type 2 (non-insulin-dependent) diabetes mellitus insulin resistance fetal growth metabolic programming 

Copyright information

© Springer-Verlag 1994

Authors and Affiliations

  • D. I. W. Phillips
    • 1
  • D. J. P. Barker
    • 2
  • C. N. Hales
    • 3
  • S. Hirst
    • 1
  • C. Osmond
    • 2
  1. 1.Metabolic Programming GroupUniversity of Southampton, Southampton General HospitalSouthamptonUK
  2. 2.MRC Environmental Epidemiology UnitUniversity of Southampton, Southampton General HospitalSouthamptonUK
  3. 3.Department of Clinical BiochemistryUniversity of Cambridge, Addenbrooke’s HospitalCambridgeUK
  4. 4.Metabolic Programming Group, MRC Environmental Epidemiology UnitSouthampton General HospitalSouthamptonUK

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