Animal Science Department

 

Date of this Version

3-14-2018

Citation

The Author(s) 2018. Published by Oxford University Press on behalf of the American Society of Animal Science.

Comments

Transl. Anim. Sci. 2018.2:S14–S18 doi: 10.1093/tas/txy047

Abstract

Intrauterine growth restriction (IUGR) is linked to metabolic dysfunction in offspring, but the mediating mechanisms are still under investigation (Barker et al., 1993). IUGR fetuses adapt to their poor intrauterine environment by repartitioning nutrients to organs critical for survival (i.e., brain, heart) at the expense of tissues such as muscle (Yates et al., 2012c). These developmental adaptations help the fetus to survive in utero but have lifelong consequences in offspring; persistent reduction of highly metabolic muscle mass is detrimental to glucose homeostasis (DeFronzo et al., 1981). Glucose metabolism is regulated primarily by insulin, and nutrient depravation is associated with impaired β-cell mass, insulin secretion, and insulin action in the IUGR fetus (Limesand et al., 2006). Moreover, inflammation disrupts insulin action and aids in the development of insulin resistance (Bach et al., 2013). We recently showed that inflammatory cytokines acutely stimulate glucose metabolism despite their antagonistic effects on insulin signaling (Cadaret et al., 2017b). However, we hypothesize that chronic exposure alters responsiveness to cytokines and results in basal cytokine concentrations having a greater inhibitory tone. Furthermore, chronic maternal inflammation may induce fetal inflammatory adaptations that impair muscle growth and metabolism. Therefore, our objective was to determine the effects of sustained maternal inflammation on fetal growth, islet function, and muscle glucose metabolism.

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