Between a low birth weight and type diabetes or impaired glucose tolerance has been found around the time of the famine

This means that poor nutrition in utero may lead to permanent changes in insulinglucose metabolism. Indeed, by restricting the nutrient supply during the prenatal period, the fetus adapts to a low nutrient environment and makes metabolic adaptations to survive. However, when nutrition is adequate or overabundant in the postnatal life, a conflict between the programming and the postnatal conditions arises. The latter is referred to as the ‘fetal origins’ hypothesis, which states that it is the conflict between the prenatal metabolic programming and the postnatal conditions that leads to disease and malfunction. Prenatal protein undernutrition has been studied in several animal models. In these models, the maternal diet is manipulated, exerting MLN4924 direct nutritional effects as well as indirect effects such as hormonal changes on the fetus. As proposed by, the approach of albumen removal in avian eggs, as a model of prenatal protein undernutrition, offers a unique avian model to investigate the direct effect of reduced protein availability during embryogenesis on growth and metabolism. Recently, the effect of a low protein diet provided to the hens on metabolic programming of the offspring was investigated in the chicken. Both the investigation of the direct and indirect animals models of prenatal protein deprivation can contribute to unraveling the prenatal programming effects. Several studies have already been conducted examining the effects of albumen removal in chicken for various reasons. A long-term study was previously conducted to examine the importance of albumen as a protein source during embryonic development in the chicken. Before sexual maturation, the body weight and feed intake were reduced. In contrast, during adulthood, an increased body weight was accompanied by reduced reproduction performance, indicating long-lasting programming effects. The objective of the present study was to investigate if the chicken model of prenatal protein undernutrition already displays significant differences during the perinatal period, before the conflict between the prenatal and postnatal conditions arises and whether it is possible to detect effects on programming on the protein and gene expression during this period. For this purpose, 3 mL of albumen was removed from layer-type eggs and replaced with saline. During the perinatal period, the present model showed little differences in growth, hormones and metabolites and hepatic glycogen content, supporting the ‘fetal origins’ hypothesis. However, metabolic programming caused by prenatal protein undernutrition was revealed by the observed hepatic proteome changes related with amino acids catabolism and glucose metabolism. Interestingly, the differential protein expression of these enzymes was not accompanied by a differential mRNA expression, suggesting that the observed proteome changes are related.

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