ABCs

In Infants (Asian Indian Beta-Cells in Infants) Maternal Nutritional Status and Pancreatic Beta Cell Function in Asian Indian Infants

92%

Follow-up Completion Rate

44–50%

Cell Variation at Birth

0–6 Months

First 6 Months Matter

Overview

This study explores the relationship between maternal weight and early pancreatic beta cell function in infants. Pancreatic beta cells play a critical role in insulin production and regulation of blood glucose levels, which are essential for metabolic health.

The research highlights how maternal health, particularly weight status, may influence the metabolic functioning of infants from an early stage of life. By examining these early-life determinants, the study contributes to a better understanding of the origins of metabolic disorders such as diabetes.

This work reflects the growing focus on maternal and child health as a key component in preventing non-communicable diseases and improving long-term health outcomes.

Aim

To investigate the impact of maternal nutritional status on early pancreatic beta cell function and metabolic health outcomes in infants.

Objectives

To examine the association of maternal nutritional status [i.e., first trimester body mass index (BMI); and pregnancy weight gain] with beta cell function of their infants at 6-months of age.

Outcome measures will be collected at two time points:

Birth - At birth, cord blood will be analyzed for glucose, c-peptide, and insulin and will be used to calculate maternal and fetal glycemia, insulin resistance, static insulin secretion, and insulin clearance
6-months postpartum. - At 6 months of age, infants will undergo an oral glucose tolerance test, with samples analyzed for glucose, C-peptide, and insulin to assess pancreatic beta-cell function, measured by the oral disposition index. Other calculated measures at 6 months will include insulin resistance, static insulin secretion, and insulin clearance.

Results

Of the 155 enrolled women, 135 (92%) completed the 7-month follow-up, resulting in 63 underweight, 43 normal weight, and 29 overweight mother–infant dyads. Maternal age, pregnancy glucose levels, and gestational age at delivery were similar across groups. At birth, infants of underweight and overweight mothers had approximately 44–50% higher cord HOMA2-B values compared to those of normal weight mothers, demonstrating a U-shaped association between maternal BMI and beta cell function, while HOMA2-IR did not differ. At 7 months, infants of overweight mothers showed higher fasting insulin, C-peptide, and sustained insulin resistance, whereas infants of underweight mothers exhibited the greatest improvement in insulin resistance and the highest disposition index. Regression analyses confirmed a significant association between maternal weight group and beta cell function at birth.

Conclusion

This study provides evidence of specific early-life endocrine features associated with the maternal nutritional environment. Compared to infants born to normal weight mothers, infants from underweight mothers and overweight mothers exhibit similar patterns of beta cell function at birth. During the first 7 months of postnatal life, changes to metabolic measures were most dramatic for infants born to underweight mothers. After an oral glucose tolerance test, infants born to underweight mothers had the highest levels of dynamic beta cell function compared to infants born to normal weight or overweight mothers, suggesting a compensatory response. Future research should assess the long-term implications of heightened insulin secretion in infancy compared to infants born to normal weight mothers. The totality of findings here warrants further examination of intergenerational risk of pancreatic poor beta cell structure and function.