ESPE Yearbook of Paediatric Endocrinology

To read the full abstract: J Clin Endocrinol Metab. Vol 104, Issue 9, September 2019, Pages 3785–3794. PMID: 31127822

Maternal vitamin D status during pregnancy has been associated with markers of fetal growth and development. The circulating form of vitamin D, 25-hydroxyvitamin D [25(OH)D], crosses the placenta, and the developing fetus relies on the mother for its vitamin D source. Maternal vitamin D insufficiency during pregnancy has been linked to impaired fetal growth, increased risk of gestational diabetes mellitus (GDM), and adverse postnatal growth patterns and insulin resistance in the offspring (1). Thus, maternal vitamin D status may contribute to prenatal programming of the insulin axis and glucose regulation. However, some observational studies have not found associations of maternal 25(OH)D concentrations during pregnancy with markers of fetal growth or fetal insulin production (2,3). Although adequate vitamin D status seems to influence glycemic control in adults, the association of vitamin D with insulin secretion during fetal life is unclear. As both vitamin D and adequate nutrient supply are important for fetal adiposity and weight gain, vitamin D may play a different role in insulin secretion and beta-cell function during the prenatal period than in childhood and adulthood.

This study examined the associations of measures of prenatal vitamin D (cord blood vitamin D) status with markers of fetal insulin secretion. The authors included two pre-birth cohorts of mother-newborn pairs based in high-latitude regions where there is high risk of 25(OH)D deficiency, which allowed the replication of findings in two similar but independent populations. Among mother-child pairs with high prevalence of vitamin D insufficiency, newborn cord blood 25(OH)D levels were positively associated with cord blood insulin and c-peptide concentrations, but maternal 25(OH) status itself showed a non-linear relationship with cord blood insulin and c-peptide. These results suggest that vitamin D may play a role in regulating fetal beta-cell function, with a potential long-term impact on post-natal glucose regulation and growth. The same results were obtained when adjusting for maternal pre-pregnancy BMI and gestational weight gain, which would also impact cord blood insulin and c-peptide levels. Thus, cord blood 25(OH)D concentration might be a more accurate measure of fetal vitamin D status and that fetal vitamin D status is directly related to fetal insulin secretion, whereas the relationship with maternal vitamin D status is more complex. Further studies should explore the role of cord blood 25(OH)D in fetal beta-cell function and glucose physiology.

References:

1. Chiu KC, Chu A, Go VLW, Saad MF. Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Am J Clin Nutr. 2004;79(5):820–825.

2. Roth DE, Leung M, Mesfin E, Qamar H, Watterworth J, Papp E. Vitamin D supplementation during pregnancy: state of the evidence from a systematic review of randomised trials. BMJ. 2017;359:j5237.

3. Leffelaar ER, Vrijkotte TGM, van Eijsden M. Maternal early pregnancy vitamin D status in relation to fetal and neonatal growth: results of the multi-ethnic Amsterdam Born Children and their Development cohort. Br J Nutr. 2010;104(1):108–117.