Abstract:The maternal nutritional, metabolic, and physiological statuses, as well as exposure to various environmental factors during conception, gestation, and lactation, play a fundamental role in the health programming of the offspring. Therefore, alterations affecting the maternal microbiota could indirectly influence fetal development. In addition, such alterations could be transmitted to the progeny at different stages of the infant development (e.g., pre-conception, pre-natal, post-natal), thereby favoring the d… Show more
“…Several maternal nutritional and pathological conditions, including maternal obesity, have been associated with changes in maternal and neonatal gut-microbiota dysbiosis, which could affect microbial composition and promote metabolic disturbances in the offspring (reviewed in Calatayud et al (120) ). A study by Koren et al (121) that analysed the faecal microbiota in ninety-one healthy pregnant women from the first to the third trimester found that significant changes in microbial diversity occurred during the third trimester, whereas in early pregnancy, the microbiota was similar compared with the normal controls of the Human Microbiome Project.…”
Section: Maternal Microbiota Modulates Fetal Growth and Adipositymentioning
Worldwide obesity is increasing at an alarming rate in children and adolescents, with the consequent emergence of co-morbidities. Moreover, the maternal environment during pregnancy plays an important role in obesity, contributing to transgenerational transmission of the same and metabolic dysfunction. White adipose tissue represents a prime target of metabolic programming induced by maternal milieu. In this article, we review adipose tissue physiology and development, as well as maternal influences during the perinatal period that may lead to obesity in early postnatal life and adulthood. First, we describe the adipose tissue cell composition, distribution and hormonal action, together with the evidence of hormonal factors participating in fetal/postnatal programming. Subsequently, we describe the critical periods of adipose tissue development and the relationship of gestational and early postnatal life with healthy fetal adipose tissue expansion. Furthermore, we discuss the evidence showing that adipose tissue is an important target for nutritional, hormonal and epigenetic signals to modulate fetal growth. Finally, we describe nutritional, hormonal, epigenetic and microbiome changes observed in maternal obesity, and whether their disruption alters fetal growth and adiposity. The presented evidence supports the developmental origins of health and disease concept, which proposes that the homeostatic system is affected during gestational and postnatal development, impeding the ability to regulate body weight after birth, thereby resulting in adult obesity. Consequently, we anticipate that promoting a healthy early-life programming of adipose tissue and increasing the knowledge of the mechanisms by which maternal factors affect the health of future generations may offer novel strategies for explaining and addressing worldwide health problems such as obesity.
“…Several maternal nutritional and pathological conditions, including maternal obesity, have been associated with changes in maternal and neonatal gut-microbiota dysbiosis, which could affect microbial composition and promote metabolic disturbances in the offspring (reviewed in Calatayud et al (120) ). A study by Koren et al (121) that analysed the faecal microbiota in ninety-one healthy pregnant women from the first to the third trimester found that significant changes in microbial diversity occurred during the third trimester, whereas in early pregnancy, the microbiota was similar compared with the normal controls of the Human Microbiome Project.…”
Section: Maternal Microbiota Modulates Fetal Growth and Adipositymentioning
Worldwide obesity is increasing at an alarming rate in children and adolescents, with the consequent emergence of co-morbidities. Moreover, the maternal environment during pregnancy plays an important role in obesity, contributing to transgenerational transmission of the same and metabolic dysfunction. White adipose tissue represents a prime target of metabolic programming induced by maternal milieu. In this article, we review adipose tissue physiology and development, as well as maternal influences during the perinatal period that may lead to obesity in early postnatal life and adulthood. First, we describe the adipose tissue cell composition, distribution and hormonal action, together with the evidence of hormonal factors participating in fetal/postnatal programming. Subsequently, we describe the critical periods of adipose tissue development and the relationship of gestational and early postnatal life with healthy fetal adipose tissue expansion. Furthermore, we discuss the evidence showing that adipose tissue is an important target for nutritional, hormonal and epigenetic signals to modulate fetal growth. Finally, we describe nutritional, hormonal, epigenetic and microbiome changes observed in maternal obesity, and whether their disruption alters fetal growth and adiposity. The presented evidence supports the developmental origins of health and disease concept, which proposes that the homeostatic system is affected during gestational and postnatal development, impeding the ability to regulate body weight after birth, thereby resulting in adult obesity. Consequently, we anticipate that promoting a healthy early-life programming of adipose tissue and increasing the knowledge of the mechanisms by which maternal factors affect the health of future generations may offer novel strategies for explaining and addressing worldwide health problems such as obesity.
“…One of the major determinants of infant gut microbiota composition initially is mode of birth, whereby babies delivered vaginally come into contact with the maternal bacteria through the maternal feces and birth canal, though other factors are important including birth environment, prematurity, hygiene, mother-infant contact and the method of infant feeding. Further, maternal metabolic health can influence the infant gut microbiota composition and its related health outcomes [5]. Breast milk has been found to contain several bacterial groups with Bifidobacteriaceae, Streptococcaceae and Staphylococcaceae families being members of the core breast milk microbiome [6,7].…”
Human breastmilk components, the microbiota and immune modulatory proteins have vital roles in infant gut and immune development. In a population of breastfeeding women (n = 78) of different ethnicities (Asian, Māori and Pacific Island, New Zealand European) and their infants living in the Manawatu–Wanganui region of New Zealand, we examined the microbiota and immune modulatory proteins in the breast milk, and the fecal microbiota of mothers and infants. Breast milk and fecal samples were collected over a one-week period during the six to eight weeks postpartum. Breast milk microbiota differed between the ethnic groups. However, these differences had no influence on the infant’s gut microbiota composition. Based on the body mass index (BMI) classifications, the mother’s breast milk and fecal microbiota compositions were similar between normal, overweight and obese individuals, and their infant’s fecal microbiota composition also did not differ. The relative abundance of bacteria belonging to the Bacteroidetes phylum was higher in feces of infants born through vaginal delivery. However, the bacterial abundance of this phylum in the mother’s breast milk or feces was similar between women who delivered vaginally or by cesarean section. Several immune modulatory proteins including cytokines, growth factors, and immunoglobulin differed between the BMI and ethnicity groups. Transforming growth factor beta 1 and 2 (TGFβ1, TGFβ2) were present in higher concentrations in the milk from overweight mothers compared to those of normal weight. The TGFβ1 and soluble cluster of differentiation 14 (sCD14) concentrations were significantly higher in the breast milk from Māori and Pacific Island women compared with women from Asian and NZ European ethnicities. This study explores the relationship between ethnicity, body mass index, mode of baby delivery and the microbiota of infants and their mothers and their potential impact on infant health.
“…To date, the contribution of alterations in the methylome of fetal and adult tissues to the programming of offspring metabolic phenotype has been most widely studied although other epigenetic factors, such as histone modifications and non-coding RNA are also emerging as key players in this process and require further investigation. However, other mediators such as modification to mitochondrial DNA (which are normally inherited from the mother), de novo point mutations in the germline or somatic cells and vertical transmission of microorganisms to offspring can contribute to the developmental programming of metabolic syndrome postnatally [ 116 , 275 – 277 ]. Fig.…”
The results of different human epidemiological datasets provided the impetus to introduce the now commonly accepted theory coined as 'developmental programming', whereby the presence of a stressor during gestation predisposes the growing fetus to develop diseases, such as metabolic dysfunction in later postnatal life. However, in a clinical setting, human lifespan and inaccessibility to tissue for analysis are major limitations to study the molecular mechanisms governing developmental programming. Subsequently, studies using animal models have proved indispensable to the identification of key molecular pathways and epigenetic mechanisms that are dysregulated in metabolic organs of the fetus and adult programmed due to an adverse gestational environment. Rodents such as mice and rats are the most used experimental animals in the study of developmental programming. This review summarises the molecular pathways and epigenetic mechanisms influencing alterations in metabolic tissues of rodent offspring exposed to in utero stress and subsequently programmed for metabolic dysfunction. By comparing molecular mechanisms in a variety of rodent models of in utero stress, we hope to summarise common themes and pathways governing later metabolic dysfunction in the offspring whilst identifying reasons for incongruencies between models so to inform future work. With the continued use and refinement of such models of developmental programming, the scientific community may gain the knowledge required for the targeted treatment of metabolic diseases that have intrauterine origins.
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