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Fetal overnutrition and offspring insulin resistance and β-cell function: the Exploring Perinatal Outcomes among
K A Sauder1, C W Hockett2, B M Ringham3
1Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO, USA.
Insights
Maternal diabetes and obesity during pregnancy increase offspring insulin resistance. This study highlights the long-term metabolic effects of fetal overnutrition on children and adolescents.
Area of Science:
- Endocrinology
- Metabolic Health
- Pediatric Health
Background:
- Maternal diabetes and obesity are growing global health concerns.
- Intrauterine environment significantly influences offspring metabolic programming.
- Understanding these associations is crucial for early intervention strategies.
Purpose of the Study:
- To investigate the link between maternal diabetes and obesity in utero and offspring insulin resistance, beta-cell function, and oral disposition index.
- To analyze these associations in a diverse pediatric cohort over time.
- To determine if these effects persist after accounting for offspring body mass index.
Main Methods:
- Longitudinal observational study of 445 offspring.
- Two fasting blood measurements and oral glucose tolerance tests were conducted.
- Linear mixed models and general linear univariate models were used to analyze data.
Main Results:
- Intrauterine exposure to maternal diabetes was associated with increased offspring insulin resistance (higher HOMA2-IR, lower Matsuda index).
- Increased maternal pre-pregnancy BMI also predicted higher offspring insulin resistance and beta-cell function.
- After adjusting for offspring BMI, maternal diabetes remained significantly associated with insulin resistance.
Conclusions:
- Intrauterine exposure to maternal diabetes or obesity is linked to elevated insulin resistance in offspring.
- These findings support the hypothesis that fetal overnutrition leads to metabolic dysfunction.
- Early life metabolic programming has lasting implications for childhood and adolescent health.
Aims:
To examine the associations of intrauterine exposure to maternal diabetes and obesity with offspring insulin resistance, β-cell function and oral disposition index in a longitudinal observational study of ethnically diverse offspring.
Methods:
A total of 445 offspring who were exposed (n=81) or not exposed (n=364) to maternal diabetes in utero completed two fasting blood measurements at mean (sd) ages of 10.5 (1.5) and 16.5 (1.2) years, respectively, and an oral glucose tolerance test at the second visit. We used linear mixed models and general linear univariate models to evaluate the associations of maternal diabetes and pre-pregnancy BMI with offspring outcomes.
Results:
Maternal diabetes in utero predicted increased insulin resistance [18% higher updated homeostatic model assessment of insulin resistance (HOMA2-IR), P=0.01; 19% lower Matsuda index, P=0.01 and 9% greater updated homeostatic model assessment of β-cell function (HOMA2-β), P=0.04]. Each 5-kg/m2 increase in pre-pregnancy BMI predicted increased insulin resistance (11% greater HOMA2-IR, P<0.001; 10% lower Matsuda index, P<0.001; 6% greater HOMA2-β, P<0.001). Similar results were obtained in a combined model with both exposures. After adjustment for offspring BMI, only maternal diabetes was associated with higher HOMA2-IR (β=1.12, P=0.03) and lower Matsuda index (β=0.83, P=0.01). Neither exposure was associated with early insulin response or oral disposition index.
Conclusions:
Intrauterine exposure to diabetes or obesity is associated with greater offspring insulin resistance than non-exposure, supporting the hypothesis that fetal overnutrition results in metabolic abnormalities during childhood and adolescence.
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