Diet in late pregnancy and glucose‐insulin metabolism of the offspring 40 years later

• Published in: BJOG : an international journal of obstetrics and gynaecology Vol. 107; no. 7; pp. 890 - 895
• Main Authors: Shiell, A. W., Campbell, D. M., Hall, M. H., Barker, D. J. P.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-07-2000
• Subjects: Adult; Birth Weight - physiology; Blood Glucose - metabolism; Blood Pressure - physiology; Body Mass Index; Diet; Dietary Carbohydrates - administration & dosage; Dietary Fats - administration & dosage; Dietary Proteins - administration & dosage; Energy Intake - physiology; Female; Follow-Up Studies; Humans; Insulin - blood; Male; Middle Aged; Pregnancy - metabolism; Scotland - epidemiology; Scotland
• ISSN: 1470-0328; 1471-0528
• DOI: 10.1111/j.1471-0528.2000.tb11088.x

Objective
To determine how diets of women in pregnancy influence the glucose‐insulin metabolism of their offspring in adult life.
Design
A follow up study of men and women born during 1948–1954 whose mothers had taken part in a survey of diet in late pregnancy.
Setting
Aberdeen, Scotland.
Population
One hundred and sixty‐eight men and women born in the Aberdeen Maternity Hospital.
Main outcome measure
Plasma glucose and insulin concentrations, fasting and after a standard oral glucose challenge.
Results
The offspring of women who had high intakes of fat and protein in late pregnancy had a reduced plasma insulin increment between fasting and 30 min with a 7.0% decrease in increment (P= 0.007) per 10 g increase in protein intake and a 4.9% decrease (P= 0.002) per 10 g increase in fat intake. This was independent of the mother's body mass index or weight gain in pregnancy. A low maternal body mass index in early or late pregnancy was associated with a raised fasting plasma insulin concentration with a decrease of 2.4% (P= 0.05) per 1 kg/m2 increase of maternal body mass.
Conclusion
High intakes of protein and fat during pregnancy may impair development of the fetal pancreatic beta cells and lead to insulin deficiency in the offspring. The offspring of thin mothers tend to be insulin resistant.