Abstract

It has previously been suggested (1) that respiratory modulatio of the action of insulin on glucose metabolism may contribute to macrosomia in neonates from diabetic mothers. It was proposed that this was due to a relative hypoxaemia which resulted in an increase in glucose metabolised through the hexose monophosphate shunt pathway in fetal adipocytes. This could be understood on the basis of the Crabtree-Pasteur Effects. It is now suggested that a similar mechanism may lead, in certain tissues, to an increase in the metabolism of glucose through polyol pathways and that this may play a role in the development of diabetic sequelae.

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