Abstract
Poor maternal nutrition during gestation can negatively affect offspring growth, development, and health pre- and post-natally. Overfeeding during gestation or maternal obesity (MO) results in altered metabolism and imbalanced endocrine hormones in animals and humans which will have long-lasting and detrimental effects on offspring growth and health. In this study, we examined the effects of overnutrition during gestation on autophagy associated pathways in offspring heart muscles at two gestational and one early postnatal time point (n = 5 for treated and untreated male and female heart respectively at each time point). Two-way ANOVA was used to analyze the interaction between treatment and sex at each time point. Our results revealed significant interactions of maternal diet by developmental stages for offspring autophagy signaling. Overfeeding did not affect the autophagy signaling at mid-gestation day 90 (GD90) in both male and female offspring while the inflammatory cytokines were increased in GD90 MO male offsrping; however, overfeeding during gestation significantly increased autophagy signaling, but not inflammation level at a later developmental stage (GD135 and day 1 after birth) in both males and females. We also identified a sexual dimorphic response in which female progeny were more profoundly influenced by maternal diet than male progeny regardless of developmental stages. We also determined the cortisol concentrations in male and female hearts at three developmental stages. We did not observe cortisol changes between males and females or between overfeeding and control groups. Our exploratory studies imply that MO alters autophagy associated pathways in both male and female at later developmental stages with more profound effects in female. This finding need be confirmed with larger sample numbers in the future. Our results suggest that targeting on autophagy pathway could be a strategy for correction of adverse effects in offspring of over-fed ewes.
Highlights
Developmental programming, known as fetal programming, occurs during in utero life whilst the fetus is developing (Widdowson and McCance, 1975)
Other research groups found that over-nutrition and maternal obesity (MO) alters the JUN N-terminal kinase (JNK)-insulin receptor substrate (IRS)-1 signaling cascade and cardiac function in the fetal heart (Wang et al, 2010) and induces fibrosis in fetal myocardium of sheep (Huang et al, 2010)
At day1 after birth, we found that total extracellular signal-regulated kinase (ERK) was increased in MO male neonates compared with control male neonates (p 0.0154)
Summary
Developmental programming, known as fetal programming, occurs during in utero life whilst the fetus is developing (Widdowson and McCance, 1975). Nutrition is one of the major intrauterine environmental factors that can reprogram fetal growth and development during gestation in many species such as cattle, swine and sheep (Bell and Ehrhardt, 2002) Both maternal under- and over-nutrition can lead to intrauterine growth restriction, reduced birth weight, increased fetal and neonatal mortality, and altered postnatal growth rate, decreased carcass quality, feed efficiency, and negative health effects in animals and humans (Barker and Clark, 1997; Godfrey and Barker, 2001; Bell and Ehrhardt, 2002; Wallace et al, 2003; Wu et al, 2006; Ford and Long, 2011; Du et al, 2013; Reed et al, 2014). We used a previously characterized MO sheep model (Pillai et al, 2017) to determine whether autophagy associated cell signaling pathways are changed in fetuses and neonates at different developmental stages in response to MO
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