ABSTRACT
It has been suggested that the absence of a specific malformation pattern for diabetic embryopathy signals the presence of several teratological factors and mechanisms in diabetic pregnancy. The maternal non esterified fatty acids and fatty acids from triglycerides cross the placenta and reach the embryo and fetus. Branched-chain amino acids are transported to the embryo/fetus and used as fuel and for protein synthesis. This class of amino acids is increased in the serum of diabetic individuals, in the serum of diabetic pregnant rats, where this increase correlates with embryo dysmorphogenesis. Rat embryos cultured in inositol-depleted serum develop neural tube defects, which demonstrate the teratogenic capacity of inositol deficiency. The combined observations support a role for nitrosative stress in diabetic embryopathy, apparently as a consequence of oxidative stress. There is also a growing understanding of the diabetes-induced alterations in genetic and epigenetic systems, which will, again, increase our knowledge and, hopefully, inspire to develop new ways to block diabetic embryopathy.
