Histomorphogenesis of human pancreatic islets amidst maternal anaemia: a critical insight.

Abstract

Maternal anaemia, the most common nutritional deficiency, adversely affects the growth and development of the fetus as a whole and the fetal pancreas in particular. These changes lead to the young onset of diabetes in the near future. To understand the pathophysiology behind this, present study investigates the histomorphogenesis of human fetal pancreatic islets and the impact of maternal anaemia on islet dimension, area proportion, and cellular composition across various gestational weeks using immunohistochemistry. The research was conducted on 18 human fetal pancreases obtained from spontaneous abortions or stillbirths between 17 to 36 weeks of gestation, categorized into normal (n=10) and anaemic (n=8) maternal groups. Results revealed a larger islet diameter in fetuses from anaemic mothers compared to the non-anaemic group (P=0.039). The beta cell percentage was significantly lower in the anaemic group across all gestational ages (P=0.003), while the alpha cell proportion remained unchanged in the anaemic group but increased significantly in the non-anaemic group after 20 weeks (P=0.006). The non-alpha/beta cell proportion in anaemic group was consistently higher than in the non-anaemic group. In conclusion, maternal anaemia results in the reprogramming of fetal pancreatic islets, characterized by a reduction in beta cell proportion, an increase in non-alpha/beta cells, and a disruption in the alpha-to-beta cell ratio. These changes may impair fetal pancreatic function and predispose the offspring to glucose intolerance and diabetes in later life. Ensuring adequate maternal nutrition through iron and folic acid supplementation during pregnancy is essential to prevent these developmental disruptions.