Low-dose cadmium (Cd) exposure in early pregnancy is associated with more than double the risk of developing gestational diabetes mellitus (GDM).
Cadmium promotes placental syncytiotrophoblast differentiation and alters mitochondrial metabolism, skewing glucose utilization and enhancing insulin-resistance hormone production.
Mechanistic insights reveal that environmental Cd may drive GDM risk via placental metabolic reprogramming rather than direct maternal glucose dysregulation alone.
