Interpretive Summary: Maternofetal inflammation induced for 2 wk in late gestation reduced birth weight and impaired neonatal growth and skeletal muscle glucose metabolism in lambs.
By: Dr. Emily Taylor
Authors of the current study previously reported that sustained maternofetal inflammation resulted in intrauterine growth-restricted (MI-IR) fetuses having asymmetric body composition, impaired muscle glucose metabolism, heightened inflammatory tone, and b-cell dysfunction near term (Yates et a., 2018). Therefore, the objective of the current study was to determine if the growth and metabolic deficits observed in near-term MI-IUGR fetuses persisted in MI-IUGR neonates due to the inflammatory programming of skeletal muscle.
Twenty commercial Polypay ewes either received serial lipopolysaccharide (MI-IUGR) or saline (Control) injections in the first 2 wk of the third trimester to produce intrauterine growth restriction. Cell function, glucose metabolism of the hindlimb and flexor digitorum superficialis muscle (FDS), and daily blood parameters were recorded.
Lambs experiencing MI-IURG had asymmetric body composition as neonates and continued to be lighter than controls through 31 days of age; however, body and cannon bone lengths did not differ at either age. Smaller FDS muscles, reduced glucose oxidation, and Akt phosphorylation were observed, though both treatments experienced similar glucose uptake when incubated in basal or insulin-spiked media. MI-IURG lambs also exhibited a reduction in circulating urea nitrogen and cholesterol, with an increase in triglycerides, high-density lipoprotein cholesterol, and glucose-to-insulin rations. Greater monocyte and granulocyte concentrations reduced plasma TNFa, and greater concentrations of TNFR1 and IkBa protein content in FDS muscle were observed.
Data from the current study suggests that sustained maternofetal inflammation in late gestation results in tissue-specific fetal programming and alters neonatal growth rates, body composition, and metabolism. MI-IUGR lambs exhibited growth and metabolic phenotypes consistent with IUGR born humans and animals. This data supports the author's hypothesis that inflammation-induced programming is a mechanism for IUGR phenotype.
This article is available on the Journal of Animal Science website.