Open Access. Powered by Scholars. Published by Universities.®
Articles 1 - 2 of 2
Full-Text Articles in Life Sciences
Postnatal Nutrient Repartitioning Due To Adaptive Developmental Programming, Robert J. Posont, Dustin T. Yates
Postnatal Nutrient Repartitioning Due To Adaptive Developmental Programming, Robert J. Posont, Dustin T. Yates
Department of Animal Science: Faculty Publications
The consequences of prenatal stress on lifelong metabolic function and health was first proposed by David Barker and Nicholas Hales with the publication of their Thrifty Phenotype Hypothesis in the early 1990s.1,2 Subsequent studies in humans and animals have further demonstrated that stress-induced adaptive fetal programming leads to tissue-specific changes in metabolic function and growth capacity.3,4 Developmental adaptations to the intrauterine nutrient restriction that accompanies most maternofetal stressors target regulatory pathways for nutrient utilization in non-essential tissues such as skeletal muscle.4-6 This aids intrauterine survival by re-appropriating nutrients to support neural, cardiac, and endocrine tissue function but reduces metabolic efficiency …
Maternal Inflammation At Midgestation Impairs Subsequent Fetal Myoblast Function And Skeletal Muscle Growth In Rats, Resulting In Intrauterine Growth Restriction At Term, Caitlin N. Cadaret, Robert J. Posont, Kristin A. Beede, Hannah E. Riley, John Dustin Loy, Dustin T. Yates
Maternal Inflammation At Midgestation Impairs Subsequent Fetal Myoblast Function And Skeletal Muscle Growth In Rats, Resulting In Intrauterine Growth Restriction At Term, Caitlin N. Cadaret, Robert J. Posont, Kristin A. Beede, Hannah E. Riley, John Dustin Loy, Dustin T. Yates
Department of Animal Science: Faculty Publications
Maternal inflammation induces intrauterine growth restriction (MI-IUGR) of the fetus, which compromises metabolic health in human offspring and reduces value in livestock. The objective of this study was to determine the effect of maternal inflammation at midgestation on fetal skeletal muscle growth and myoblast profiles at term. Pregnant Sprague-Dawley rats were injected daily with bacterial endotoxin (MI-IUGR) or saline (controls) from the 9th to the 11th day of gestational age (dGA; term = 21 dGA). At necropsy on dGA 20, average fetal mass and upper hindlimb cross-sectional areas were reduced (P < 0.05) in MI-IUGR fetuses compared with controls. MyoD+ and myf5+ myoblasts were less abundant (P < 0.05), and myogenin+ myoblasts were more abundant (P < 0.05) in MI-IUGR hindlimb skeletal muscle compared with controls, indicating precocious myoblast differentiation. Type I and Type II hindlimb muscle fibers were smaller (P < 0.05) in MI-IUGR fetuses than in controls, but fiber type proportions did not differ between experimental groups. Fetal blood plasma TNFα concentrations were below detectable amounts in both experimental groups, but skeletal muscle gene expression for the cytokine receptors TNFR1, IL6R, and FN14 was greater (P < 0.05) in MI-IUGR fetuses than controls, perhaps indicating enhanced sensitivity to these cytokines. Maternal blood glucose concentrations at term did not differ between experimental groups, but MI-IUGR fetal blood contained less (P < 0.05) glucose, cholesterol, and triglycerides. Fetal-to-maternal blood glucose ratios were also reduced (P < 0.05), which is indicative of placental insufficiency. Indicators of protein catabolism, including blood plasma urea nitrogen and creatine kinase, were greater (P < 0.05) in MI-IUGR fetuses than in controls. From these findings, we conclude that maternal inflammation at midgestation causes muscle-centric fetal programming that impairs myoblast function, increases protein catabolism, and reduces skeletal muscle growth near term. Fetal muscle sensitivity to inflammatory cytokines appeared to be enhanced after maternal inflammation, which may represent a mechanistic target for improving these outcomes in MI-IUGR fetuses.