La hipótesis de Pedersen no es suficiente: Otros nutrientes además de la glucosaexplicarían la macrosomía fetal enpacientes diabéticas gestacionales consobrepeso y buen control glicémico / Nutrients other than glucose might explain fetal overgrowth in gestationaldiabetic pregnancies

ABSTRACT

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-gestationaloverweight not suffering from GDM still have a higher frequency of fetal macrosomia. Furthermore, pregnant women with GDM, despite being subjected to optimalglycemic control, still show unacceptably high frequencies of fetal macrosomia, aphenomenon that is concentrated in pregnancies with overweight or obesity priorto pregnancy. If glucose is not the single nutrient responsible for fetal macrosomiain pregnant women with gestational diabetes that undergo strict glycemic control,other nutrients may cause excessive fetal growth in pre-pregnancy overweightmothers. In this review, we propose that triglycerides (TG) could be responsible forthis accelerated fetal growth. If this hypothesis is validated in animal models andclinical studies, then normal and pathological ranges of TG should be defined, andmonitoring of triglyceride levels during pregnancy should be advised as a possiblenew alternative, besides a good glycemic control, for the management of fetal macrosomia in GDM women with overweight prior to pregnancy.