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Full-Text Articles in Animal Sciences
The Role Of Inflammatory Pathways In Development, Growth, And Metabolism Of Skeletal Muscle In Iugr Offspring; Blood Gene Expression Of Inflammatory Factors As Novel Biomarkers For Assessing Stress And Wellbeing In Exotic Species., Robert J. Posont
Department of Animal Science: Dissertations, Theses, and Student Research
Our first study identified the effects of maternal inflammation-induced intrauterine growth restriction (MI-IUGR) on growth and muscle glucose metabolism in offspring supplemented with curcumin. MI-IUGR lambs exhibited asymmetric growth restriction at birth and 30d of age, but normal glucose-stimulated insulin secretion. Hindlimb glucose oxidation was reduced by MI-IUGR and not improved by curcumin supplementation. Ex vivo muscle glucose oxidation was reduced by MI-IUGR but improved somewhat by curcumin. These finding indicate that fetal programming responses to MI contribute to neonatal growth and metabolic deficits. Neonatal curcumin supplementation had minimal effect on growth deficits but may improve glucose metabolism. …
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.