La hipótesis de Pedersen no es suficiente: Otros nutrientes además de la glucosa explicarían la macrosomía fetal en pacientes diabéticas gestacionales con sobrepeso y buen control glicémico

Since 1964, the hypothesis of Pedersen has been used to explain fetal macrosomia observed in gestational diabetes mellitus (GDM), by a mechanism involving maternal hyperglycemia - fetal hyperglycemia - fetal hyperinsulinemia. However, since the 1980-89 decade, it is known that pregnant women with pre-gestational overweight not suffering from GDM still have a higher frequency of fetal macrosomia. Furthermore, pregnant women with GDM, despite being subjected to optimal glycemic control, still show unacceptably high frequencies of fetal macrosomia, a phenomenon that is concentrated in pregnancies with overweight or obesity prior to pregnancy. If glucose is not the single nutrient responsible for fetal macrosomia in pregnant women with gestational diabetes that undergo strict glycemic control, other nutrients may cause excessive fetal growth in pre-pregnancy overweight mothers. In this review, we propose that triglycerides (TG) could be responsible for this accelerated fetal growth. If this hypothesis is validated in animal models and clinical studies, then normal and pathological ranges of TG should be defined, and monitoring of triglyceride levels during pregnancy should be advised as a possible new alternative, besides a good glycemic control, for the management of fetal macrosomia in GDM women with overweight prior to pregnancy.