Abstract
Increased maternal food intake is considered a normal pregnancy adjustment. However, the overavailability of nutrients may lead to dysregulated fetal development and increased adiposity, with long-lasting effects on offspring in later life. Several gut-hormone molecules regulate maternal appetite, with both their orexigenic and anorectic effects being in a state of sensitive equilibrium. The aim of this manuscript is to systematically review literature on the effects of maternal gut-hormone molecules on fetal growth and metabolism, birth weight and the later metabolic health of offspring. Maternal serum ghrelin, leptin, IGF-1 and GLP-1 appear to influence fetal growth; however, a lack of consistent and strong correlations of maternal appetite axis hormones with birth weight and the concomitant correlation with fetal and birth waist circumference may suggest that these molecules primarily mediate fetal energy deposition mechanisms, preparing the fetus for survival after birth. Dysregulated intrauterine environments seem to have detrimental, sex-dependent effects on fetal energy stores, affecting not only fetal growth, fat mass deposition and birth weight, but also future metabolic and endocrine wellbeing of offspring.
Highlights
Our aim was to explore the effects of maternal gut-hormone molecules during pregnancy on intrauterine fetal growth, anthropometric measurements at birth and the longer-term metabolic health of offspring
In a prospective cohort study of 574 healthy pregnancies, Walsh et al [30] reported that ultrasound-estimated fetal weight at 32 weeks of gestation was related to maternal serum leptin levels at booking [30]
It is possible that enhanced maternal appetite during gestation may reflect not just a mother’s own nutrient supply needs as measured by ghrelin or other gut hormonal levels and the rising energy needs of the developing fetus, affecting its future metabolic health
Summary
According to the Barker et al hypothesis of developmental origins of health and disease (DOHaD), fetal development is vulnerable during the antenatal period [1,2]. This process of “fetal developmental programming” can have a long-lasting or even permanent impact on the offspring’s health trajectory through structural and functional disorders within the developing fetus [2]. Dutch famine suggest that in-utero fetal exposure to malnutrition was associated with a variety of adverse metabolic phenotypes in offspring, such as elevations in BMI and serum cholesterol and worsening insulin resistance. Exposure to malnutrition during mid or late gestation resulted in lower birth weight and decreased head circumference [3,4]
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