The offspring of gestational diabetes

Gestational diabetes mellitus (GDM) usually develops in the second half of pregnancy and, in order to address the impact of GDM on the conceptus, several issues must be raised: what are the immediate implications for the fetus and the neonate and why do they happen? What are the consequences for the offspring? What can be done? In a theoretical model the whole pathogenesis and spectrum of fetal and neonatal mortality and morbidity could primarily be attributed to the excessive transferal of glucose from mother to fetus, inducing fetal hyperglycemia, leading to fetal pancreatic islet hypertrophy and beta-cell hyperplasia with a consequent rise in insulin secretion. However, besides, and in addition to glucose, it is quite possible that other metabolic fuels, from amino acids to lipids, may also cross the placenta further contributing to the adverse intrauterine environment. Depending upon the time of gestation during critical developmental stages, the same metabolic fuels would have different effects upon the fetus, the neonate and quite possibly, upon the long-term outcome from neurological and psychosocial impairment to the adult development of metabolic and cardiovascular disorders. Based on clinical and experimental evidence that poor maternal homeostasis is at the core of the problem, it is of paramount importance to identify women at risk of GDM and to keep a tight metabolic control in order to avoid immediate and long-term consequences for their offspring.