» Articles » PMID: 8601111

Relation of Size at Birth to Non-insulin Dependent Diabetes and Insulin Concentrations in Men Aged 50-60 Years

Overview
Journal BMJ
Specialty General Medicine
Date 1996 Feb 17
PMID 8601111
Citations 129
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: To establish whether the relation between size at birth and non-insulin dependent diabetes is mediated through impaired beta 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 the 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 beta cell function and to depend on an interaction with obesity in adult life.

Citing Articles

Neonatal outcomes after in utero exposure to antipsychotics: a systematic review and meta-analysis.

Joseph-Delaffon K, Eletri L, Dechartres A, Nordeng H, Richardson J, Elefant E Eur J Epidemiol. 2024; 39(10):1073-1096.

PMID: 39352602 DOI: 10.1007/s10654-024-01156-y.


Reduced type 2 diabetes incidence reflecting end of post‑World War II calorie restrictions in Germany. Reply to Nilsson PM, Vaag A [letter].

Lehner C, Schauberger G, Klug S Diabetologia. 2024; 67(10):2369-2370.

PMID: 39153072 PMC: 11446940. DOI: 10.1007/s00125-024-06255-9.


Reduced type 2 diabetes incidence reflecting end of post-World War II calorie restrictions in Germany.

Nilsson P, Vaag A Diabetologia. 2024; 67(10):2367-2368.

PMID: 39145881 DOI: 10.1007/s00125-024-06195-4.


Preeclampsia and the Antiphospholipid Syndrome.

Mayer-Pickel K, Nanda M, Gajic M, Cervar-Zivkovic M Biomedicines. 2023; 11(8).

PMID: 37626793 PMC: 10452741. DOI: 10.3390/biomedicines11082298.


[Short stature due to intrauterine growth retardation. Clinical and hormonal-metabolic features, possibilities of growth-stimulating therapy].

Nagaeva E Probl Endokrinol (Mosk). 2022; 68(5):4-13.

PMID: 36337013 PMC: 9762449. DOI: 10.14341/probl13178.


References
1.
Miller H, Hassanein K . Fetal malnutrition in white newborn infants: maternal factors. Pediatrics. 1973; 52(4):504-12. View

2.
Paneth N, Susser M . Early origin of coronary heart disease (the "Barker hypothesis"). BMJ. 1995; 310(6977):411-2. PMC: 2548810. DOI: 10.1136/bmj.310.6977.411. View

3.
Matthews D, Hosker J, Rudenski A, Naylor B, Treacher D, Turner R . Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28(7):412-9. DOI: 10.1007/BF00280883. View

4.
Gluckman P . The role of pituitary hormones, growth factors and insulin in the regulation of fetal growth. Oxf Rev Reprod Biol. 1986; 8:1-60. View

5.
Reaven G . Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988; 37(12):1595-607. DOI: 10.2337/diab.37.12.1595. View