Maternal exercise improves markers of metabolic signaling and reduces inflammation in brown adipose tissue of offspring
Authors: Menon Pooja , Bingaman Sarah , Prentice Danielle , Arnold Amy 
Published: May 2023

Maternal obesity impacts approximately one-third of pregnant people and impacts offspring through the transmission of obesogenic and diabetic traits. Pregnant patients often spend considerable time sedentary, which has been associated with harmful cardiometabolic changes. Our recent data show that compared with sedentary conditions, voluntary exercise during pregnancy in mice shifts adipose distribution of offspring away from energy storing white adipose tissue towards energy burning brown adipose tissue (BAT), which could improve energy metabolism over the lifespan. The objective of this study was to test the hypothesis that voluntary exercise in pregnant mice improves metabolic signaling pathways and reduces markers of inflammation in BAT from offspring. To test this, female C57BL/6J mice were placed on control diet and allocated to sedentary versus voluntary running wheel exercise cages. Voluntary wheel running was allowed for two weeks prior to breeding and throughout weaning. When offspring were 16 weeks of age, they were euthanized for collection of BAT. The study groups were male sedentary (n=9), female sedentary (n=11), male exercise (n=12), female exercise (n=8). Quantitative real-time polymerase chain reaction was used to measure mRNA of fibroblast-growth factor receptors (β-klotho, Fgfr1, Fgfr2) and inflammation markers (IL10, IL1β, TNFα) in BAT. Outcomes were analyzed by two-way ANOVA to assess effects of exercise, sex, and their interaction. Offspring from exercised mothers had a significant decrease in mRNA of IL1β (1.4±0.4 male sedentary vs. 0.4±0.1 male exercise vs. 1.1±0.2 female sedentary vs. 0.8 ±0.2 female exercise; PSex=0.668, PEX=0.006, PInt=0.098) and TNFα (0.9±0.1 male sedentary vs. 0.5±0.1 male exercise vs. 1.3±0.3 female sedentary vs. 0.6 ±0.1 female exercise; PSex=0.126, PEX=0.007, PInt=0.562) and an increase in Fgfr2 (1.1±0.2 male sedentary vs. 1.7±0.3 male exercise vs. 1.3±0.3 female sedentary vs. 3.8 ±1.2 female exercise; PSex=0.063, PEX=0.011, PInt=0.096) in BAT, which was largely independent of sex. There was no significant main effect of either sex or exercise on IL10, Fgfr1, or β-klotho mRNA in BAT. These data suggest that maternal exercise is associated with decreased inflammation and increased protective metabolic signaling in BAT. This could impact energy metabolism given increasing evidence for advantageous metabolic adaptations with increased BAT health and signaling. Additional studies are needed to further understand the impact of maternal exercise on adipose health, energy metabolism, and cardiovascular outcomes in offspring over the lifespan.  American Heart Association Undergraduate Summer Fellowship, Department of Obstetrics and Gynecology at Penn State Milton S Hershey Medical Center, and Dani Peress MD Memorial Fund from the Society of Maternal Fetal Medicine This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.