Abstract
Different animal models have been used to study the effects of prenatal protein undernutrition and the mechanisms by which these occur. In mammals, the maternal diet is manipulated, exerting both direct nutritional and indirect hormonal effects. Chicken embryos develop independent from the hen in the egg. Therefore, in the chicken, the direct effects of protein deficiency by albumen removal early during incubation can be examined. Prenatal protein undernutrition was established in layer-type eggs by the partial replacement of albumen by saline at embryonic day 1 (albumen-deprived group), compared to a mock-treated sham and a non-treated control group. At hatch, survival of the albumen-deprived group was lower compared to the control and sham group due to increased early mortality by the manipulation. No treatment differences in yolk-free body weight or yolk weight could be detected. The water content of the yolk was reduced, whereas the water content of the carcass was increased in the albumen-deprived group, compared to the control group, indicating less uptake of nutrients from the yolk. At embryonic day 16, 20 and at hatch, plasma triiodothyronine (T3), corticosterone, lactate or glucose concentrations and hepatic glycogen content were not affected by treatment. At embryonic day 20, the plasma thyroxine (T4) concentrations of the albumen-deprived embryos was reduced compared to the control group, indicating a decreased metabolic rate. Screening for differential protein expression in the liver at hatch using two-dimensional difference gel electrophoresis revealed not only changed abundance of proteins important for amino acid metabolism, but also of enzymes related to energy and glucose metabolism. Interestingly, GLUT1, a glucose transporter, and PCK2 and FBP1, two out of three regulatory enzymes of the gluconeogenesis were dysregulated. No parallel differences in gene expressions causing the differences in protein abundance could be detected pointing to post-transcriptional or post-translational regulation of the observed differences.
Highlights
Studies of the Dutch Hunger Winter (1944–1945) clearly showed that reduced growth in utero has detrimental effects on health in later life [1]
When nutrition is adequate or overabundant in the postnatal life, a conflict between the programming and the postnatal conditions arises [3,4]. The latter is referred to as the ‘fetal origins’ hypothesis’ [5], which states that it is the conflict between the prenatal metabolic programming and the postnatal conditions that leads to disease and malfunction
The albumen-deprived group had a lower survival compared to both the control (P,0.001)) and the sham group (P,0.001)
Summary
Studies of the Dutch Hunger Winter (1944–1945) clearly showed that reduced growth in utero has detrimental effects on health in later life [1]. An association between a low birth weight and type II diabetes or impaired glucose tolerance has been found in people born around the time of the famine [2]. This means that poor nutrition in utero may lead to permanent changes in insulinglucose metabolism. When nutrition is adequate or overabundant in the postnatal life, a conflict between the programming and the postnatal conditions arises [3,4] The latter is referred to as the ‘fetal origins’ hypothesis’ [5], which states that it is the conflict between the prenatal metabolic programming and the postnatal conditions that leads to disease and malfunction
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