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Meat Science

University of Nebraska - Lincoln

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Adaptive fetal programming

Articles 1 - 6 of 6

Full-Text Articles in Animal Sciences

Dousing The Flame: Reviewing The Mechanisms Of Inflammatory Programming During Stress-Induced Intrauterine Growth Restriction And The Potential For Ω-3 Polyunsaturated Fatty Acid Intervention, Melanie White, Dustin T. Yates Sep 2023

Dousing The Flame: Reviewing The Mechanisms Of Inflammatory Programming During Stress-Induced Intrauterine Growth Restriction And The Potential For Ω-3 Polyunsaturated Fatty Acid Intervention, Melanie White, Dustin T. Yates

Department of Animal Science: Faculty Publications

Intrauterine growth restriction (IUGR) arises when maternal stressors coincide with peak placental development, leading to placental insufficiency. When the expanding nutrient demands of the growing fetus subsequently exceed the capacity of the stunted placenta, fetal hypoxemia and hypoglycemia result. Poor fetal nutrient status stimulates greater release of inflammatory cytokines and catecholamines, which in turn lead to thrifty growth and metabolic programming that benefits fetal survival but is maladaptive after birth. Specifically, some IUGR fetal tissues develop enriched expression of inflammatory cytokine receptors and other signaling cascade components, which increases inflammatory sensitivity even when circulating inflammatory cytokines are no longer elevated …


Primary Myoblasts From Intrauterine Growth-Restricted Fetal Sheep Exhibit Intrinsic Dysfunction Of Proliferation And Differentiation That Coincides With Enrichment Of Inflammatory Cytokine Signaling Pathways, Robert J. Posont, Micah S. Most, Caitlin Cadaret, Eileen Marks-Nelson, Kiristen A. Beede, Sean W. Limesand, Ty B. Schmidt, Jessica L. Petersen, Dustin T. Yates Aug 2022

Primary Myoblasts From Intrauterine Growth-Restricted Fetal Sheep Exhibit Intrinsic Dysfunction Of Proliferation And Differentiation That Coincides With Enrichment Of Inflammatory Cytokine Signaling Pathways, Robert J. Posont, Micah S. Most, Caitlin Cadaret, Eileen Marks-Nelson, Kiristen A. Beede, Sean W. Limesand, Ty B. Schmidt, Jessica L. Petersen, Dustin T. Yates

Department of Animal Science: Faculty Publications

Intrauterine growth restriction (IUGR) is linked to lifelong reductions in muscle mass due to intrinsic functional deficits in myoblasts, but the mechanisms underlying these deficits are not known. Our objective was to determine if the deficits were associated with changes in inflammatory and adrenergic regulation of IUGR myoblasts, as was previously observed in IUGR muscle. Primary myoblasts were isolated from IUGR fetal sheep produced by hyperthermia-induced placental insufficiency (PI-IUGR; n = 9) and their controls (n = 9) and from IUGR fetal sheep produced by maternofetal inflammation (MI-IUGR; n = 6) and their …


The Price Of Surviving On Adrenaline: Developmental Programming Responses To Chronic Fetal Hypercatecholaminemia Contribute To Poor Muscle Growth Capacity And Metabolic Dysfunction In Iugr-Born Offspring, Rachel L. Gibbs, Dustin T. Yates Dec 2021

The Price Of Surviving On Adrenaline: Developmental Programming Responses To Chronic Fetal Hypercatecholaminemia Contribute To Poor Muscle Growth Capacity And Metabolic Dysfunction In Iugr-Born Offspring, Rachel L. Gibbs, Dustin T. Yates

Department of Animal Science: Faculty Publications

Maternofetal stress induces fetal programming that restricts skeletal muscle growth capacity and metabolic function, resulting in intrauterine growth restriction (IUGR) of the fetus. This thrifty phenotype aids fetal survival but also yields reduced muscle mass and metabolic dysfunction after birth. Consequently, IUGR-born individuals are at greater lifelong risk for metabolic disorders that reduce quality of life. In livestock, IUGR-born animals exhibit poor growth efficiency and body composition, making these animals more costly and less valuable. Specifically, IUGR-associated programming causes a greater propensity for fat deposition and a reduced capacity for muscle accretion. This, combined with metabolic inefficiency, means that these …


Going Up Inflame: Reviewing The Underexplored Role Of Inflammatory Programming In Stress-Induced Intrauterine Growth Restricted Livestock, Zena M. Hicks, Dustin T. Yates Nov 2021

Going Up Inflame: Reviewing The Underexplored Role Of Inflammatory Programming In Stress-Induced Intrauterine Growth Restricted Livestock, Zena M. Hicks, Dustin T. Yates

Department of Animal Science: Faculty Publications

The impact of intrauterine growth restriction (IUGR) on health in humans is well-recognized. It is the second leading cause of perinatal mortality worldwide, and it is associated with deficits in metabolism and muscle growth that increase lifelong risk for hypertension, obesity, hyperlipidemia, and type 2 diabetes. Comparatively, the barrier that IUGR imposes on livestock production is less recognized by the industry. Meat animals born with low birthweight due to IUGR are beset with greater early death loss, inefficient growth, and reduced carcass merit. These animals exhibit poor feed-to-gain ratios, less lean mass, and greater fat deposition, which increase production costs …


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 Feb 2019

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.


Chronic Maternal Inflammation During Late Gestation Impairs Subsequent Β-Cell Function But Not Islet Growth In Fetal Sheep, M.D. Abebe, C.N. Cadaret, T.B. Barnes, K.A. Beede, D. T. Yates Jan 2018

Chronic Maternal Inflammation During Late Gestation Impairs Subsequent Β-Cell Function But Not Islet Growth In Fetal Sheep, M.D. Abebe, C.N. Cadaret, T.B. Barnes, K.A. Beede, D. T. Yates

Department of Animal Science: Faculty Publications

Intrauterine growth restriction (IUGR) greatly increases perinatal mortality and morbidity rates, and leads to much greater risk for metabolic complications later in life. One such complication is the development of glucose intolerance or diabetes, which typically develops concurrently with abhorrent patterns of insulin secretions due to diminished β-cell mass and impaired function as well as an overall reduction in pancreatic endocrine tissue. The mechanisms by which IUGR causes problems with health and function of the pancreatic islets are not well understood. Therefore, our goal for this study was to determine how materno-fetal inflammation (MI) affects β-cell growth and function. To …