ABSTRACTS: Oral Presentation Abstracts
Introduction: Maternal nutrition is one of the determining factors for the intrauterine environment, which plays an important role in fetal and placental development. Among these dietary fatty acids, especially the long-chain polyunsaturated fatty acids, are essential. Whereas the effects on fetal development of changes in the availability of lipid components, like those produced by changes in dietary fatty acids, are widely established, little is known about their influence on placental development and function. This study investigated the effects of dietary fatty acids on placental development in rat.
Methods: Sprague-Dawley rats were fed diets containing 10% (wt/wt) of palm- (saturated), sunflower- (18:2), olive- (18:1) or fish (w-3) oil. At day 20 of gestation, placental fatty acid composition and protein expression levels of the cell cycle regulating proteins PCNA (S-phase), p21 (inhibitor of G2M & G1S transition), cyclin E (G1-phase), p53 (masterswitch for apoptosis) and PARP (split 89 & unsplit 116 kDa) were determined. The proteins were also immunolocalized and the proportion of labelled cells was counted.
Results: Litter size, placental weight and gross morphology were unaltered by the diet. Placental fatty acid composition in the phospholipid and triglyceride fractions reflected the diet composition except for saturated fatty acids. PCNA levels do not differ between the groups. The higher proportion of labyrinthine-trophoblasts (fetal side) in G1 (cyclin E) in the fish oil group was associated with low p21, but unaltered PCNA levels, suggesting p21-independent control of the G1/S transition. p21 absence in spongiotrophoblasts (maternal side) demonstrates that cell cycle must be regulated by other inhibitors. The higher p53 levels in sunflower and olive oil groups were associated with a higher level of apoptosis, low levels of apoptosis in the fish oil group were associated with low p53 levels. This contrasts the palm oil group, in which a high level of apoptosis was found despite relatively lower levels of p53, suggesting other p53 independent control mechanisms to account for this effect.
Conclusion: Dietary fatty acids do not have gross effects on reproductive performance and placental development. However, subtle changes of the cell cycle and apoptosis do occur, which are most pronounced when the oils contain long-chain polyunsaturatd fatty acids. These appear to protect the placenta from apoptosis.