Energy metabolism during mammalian embryogenesis

would suggest that the enzyme responsible for mediumchain fatty acid activation is not active at this time. The lack of antagonism of salicylate and octanoate against the embryotoxic effects of valproate is also compatible with the mechanisms of teratogenicity and hepatotoxicity being fundamentally different. Although these data rule out one possibility, they provide little direct information on the actual biochemical mechanism of VPA teratogenicity. We are currently studying the actions of valproate on the synthesis of fatty acid and other components of embryonic cell membranes. These observations do provide a good example of metabolic differences between embryonic and adult tissues and emphasize the need for a greater understanding of intermediary metabolism in the mammalian organogenesis phase of development.