| Description |
Despite advances in the medical field, bronchopulmonary dysplasia (BPD) remains a major concern for preterm infants. A hallmark characteristic of BPD is impaired alveolar formation. Contributing to impaired alveolar formation and the development of BPD is respiratory support as well as poor postnatal growth and inadequate nutrition. The contribution of respiratory support has been well characterized in the development of BPD; however, the role that postnatal growth restriction (PGR) plays in impaired alveolar formation and the development of BPD is less understood. Our study focused on determining the downstream molecular mediators of altered essential long-chain fatty acids in alveolar formation, peroxisome proliferator activated receptor gamma (PPARγ), and fatty acid binding protein 4 (FABP4). We hypothesize that PGR decreases circulating essential fatty acids in the rat, in association with increased lung mRNA and protein levels of FABP4, and reduced levels of lung PPARγ protein. To test this hypothesis, PGR was induced in our rat model using variation in litter size by cross-fostering newborn rat pups into rat dams with litter sizes of 16 (PGR) or 8 (control). Rat pup weights were measured every other day from birth to day of life 21 (d21). GC-MS was used to measure serum and lung fatty acid profiles at d21. RT-PCR was used to measure PPARγ, and FABP4 mRNA abundance in the lung at d21. Western blotting was used to measure PPARγ, and FABP4 protein abundance in the lung at d21. PGR reduced serum LA, AA, ALA, and DHA in male rat pups compared to sex-matched controls. PGR significantly decreased PPARγ protein abundance in male rat pups compared to sex-matched controls. PGR also increased FABP4 mRNA, and FABP4 protein abundance in male rat pups compared to sex-matched controls. We conclude that PGR alters serum fatty acid profiles, as well as PPARγ, and FABP4 levels in a sex-divergent manner. The effects that PGR has on serum fatty acid profiles, PPARγ, and FABP4 may have a potential impact on the development of BPD. We speculate that PGR causes alterations in serum fatty acids, which inhibit nutrient responsive signaling pathways that are vital for alveolar formation. |
