Some of the affected proteins have previously been associated with effects of prenatal protein undernutrition in mammalian models and will be discussed in more detail. The GLUT proteins are a family of facilitative transport proteins, catalyzing glucose uptake across the plasma membrane, the rate-limiting step in glucose metabolism. In mammals, GLUT1 is expressed ubiquitously and facilitates the basal glucose uptake, which is essential for growth and development in most cells. Expression of GLUT1 has previously been examined in other mammalian models of prenatal undernutrition, but no differences could be detected. Chickens exhibit a peculiar glucose transport and glucose homeostasis, since they are lacking GLUT4, the major insulin-responsive transporter. The mechanism for regulation of blood glucose concentration in chickens is not well understood. Furthermore, no information is available on the roles of the chickens GLUT isoforms in relation to glucose metabolism. Most likely, GLUT1 will act in maintaining basal glucose transport in most chicken cell types as in mammals, however the precise function of GLUT1 in the chicken remains to be elucidated. Chickens maintain an elevated level of blood glucose, which is supported by high rates of gluconeogenesis. In the present study, prenatal protein undernutrition caused an increase in PCK2 protein abundance, as opposite to the decreased FBP1 protein abundance and the decreased glycogen content. The liver glycogen content has previously been shown to change in a reciprocal way to the cytosolic PCK activity. Indeed, there are two forms of PCK found in most species, differing in their cellular localization: cytosolic PCK1 and mitochondrial PCK2. The relative abundance of both isoforms is dependent on the animal species and the growth stage of the animal. In the avian liver, the mitochondrial PCK activity is the most abundant one but during the perinatal period the cytosolic PCK activity increased considerable from a few days before hatching to 4 days after hatching. As PCK1 is the most abundant form in rats and has been linked previously with effects of prenatal protein undernutrition, the expression of both PCK1 and PCK2 was measured. Both genes were present in similar amounts in the liver at hatch, but were not influenced by the applied treatment. Rats and mice have been used extensively to examine the effects of the maternal diet on the programming of the progeny. In rat dams fed a protein-restricted diet an increase in PCK1 mRNA and increased activity was detected in liver of the progeny until 11 months of age, suggesting that programming of the metabolism also extends to the regulation of gene expression. A persistent increase in the gene expression of hepatic PCK, catalyzing the first, committed step of gluconeogenesis, leads to reduced ability of insulin to suppress hepatic glucose output.