BMJ 1996;312:406-410 (17 February)

Papers

Relation of size at birth to non-insulin dependent diabetes and insulin concentrations in men aged 50-60 years

Hans O Lithell, professor of geriatrics,a Paul M McKeigue, senior lecturer,b Lars Berglund, statistician,a Rawya Mohsen, programmer,a Ulla-Britt Lithell, assistant professor of history,a David A Leon, senior lecturer b

a Department of Geriatrics, Uppsala University, PO Box 609, S751-25 Uppsala, Sweden, b Epidemiology Unit, London School of Hygiene and Tropical Medicine, London WC1E 7HT

Correspondence to: Dr McKeigue.

Abstract

Objective: To establish whether the relation between size at birth and non-insulin dependent diabetes is mediated through impaired ß cell function or insulin resistance.
Design: Cohort study.
Setting: Uppsala, Sweden.
Subjects: 1333 men whose birth records were traced from a cohort of 2322 men born during 1920-4 and resident in Uppsala in 1970.
Main outcome measures: Intravenous glucose tolerance test at age 50 years and non-insulin dependent diabetes at age 60 years.
Results: There was a weak inverse correlation (r=-0.07, P=0.03) between ponderal index at birth and 60 minute insulin concentrations in the intravenous glucose tolerance test at age 50 years. This association was stronger (r=-0.19, P=0.001) in the highest third of the distribution of body mass index than in the other two thirds (P=0.01 for the interaction between ponderal index and body mass index). Prevalence of diabetes at age 60 years was 8% in men whose birth weight was less than 3250 g compared with 5% in men with birth weight 3250 g or more (P=0.08; 95% confidence interval for difference -0.3% to 6.8%). There was a stronger association between diabetes and ponderal index: prevalence of diabetes was 12% in the lowest fifth of ponderal index compared with 4% in the other four fifths (P=0.001; 3.0% to 12.6%).
Conclusion: These results confirm that reduced fetal growth is associated with increased risk of diabetes and suggest a specific association with thinness at birth. This relation seems to be mediated through insulin resistance rather than through impaired ß cell function and to depend on an interaction with obesity in adult life.

Key messages

  • Key messages

  • There is no evidence that reduced fetal growth is associated with impaired ß cell function at age 50 years (as measured by the insulin response to intravenous glucose)

  • The combination of thinness at birth and overweight in adult life is associated with higher insulin concentration at 1 hour after intravenous glucose, suggesting an effect on insulin resistance

  • Control of obesity in adult life is likely to be especially effective in reducing the risk of noninsulin dependent diabetes in those who were thin at birth


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