Diverse environmental factors influence future metabolic health starting with the pre-pregnancy health of the mother, the in utero environment, and early childhood development. Some of these windows of risk are critical with limited opportunity for subsequent recovery and an amplified risk of adult diabetes and associated chronic diseases. Risk factors are diverse including maternal stress, nutrition, environmental pollutants, air quality and lifestyle choices such as recreational drugs and alcohol. Target tissues of these stressors are diverse and include the developing pancreas, liver, kidneys, skeletal muscle, adipose tissue, cardiovascular system and brain. The placenta is a key mediator between maternal metabolic stress and offspring development during pregnancy and can both contribute and protect against future metabolic disorders. Substantial gaps exist in our mechanistic understanding of how individual organs and tissues are modified in both form and function by early life stressors, how limitations in tissue plasticity combine to build risk of adult disease, and where might there be opportunities for metabolic rescue before or after birth.
The goals of this Topic are to illustrate key structural and functional developmental changes to organs that arise in response to sub-optimal environmental conditions before and during pregnancy and during childhood development and how these can mutually build risk for adult metabolic diseases. The mechanisms by which different environmental stressors contribute and accumulate to result in altered embryonic, fetal, neonatal and child development resulting in adult onset of diabetes and metabolic syndrome are poorly understood. These are likely to involve lineage changes to tissue-specific stem cell populations, altered hormone, growth factor and cytokine presence, epigenetic alterations regulating key gene expression for control of metabolism, and accumulated cellular stress limiting cell proliferation and plasticity. Recent relaxation in the legislated oversight of recreational drugs presents an unknown paradigm of risk to the offspring in addition to other maternal lifestyle choices, nutrition, inherited genetic and epigenetic risk, and environmental stressors such as poverty and poor air or water quality. Understanding the extent of environmental impact on tissue plasticity and the potential for when and how this might be reversed is essential to preventing future metabolic diseases.
Environmental stressors, major tissues affected during development and future impact for metabolic diseases.
Stressors: Environmental pollutants, Socio-economic stress, Maternal lifestyle choices, Nutrition
Tissues: Placenta, Endocrine pancreas, Cardiovascular system and endothelial health, Liver, Adipose tissue, Kidney, Brain
Ontology of development: Maternal pre-pregnancy, Pregnancy, Postnatal life, Childhood
Potential mechanisms: Epigenetic modifications, stem cell populations, cellular stress, cellular aging, altered endocrinology, tissue inflammation, placental function and intrauterine hypoxia, pre- and postnatal nutrition
Combination of review articles and original papers.
Diverse environmental factors influence future metabolic health starting with the pre-pregnancy health of the mother, the in utero environment, and early childhood development. Some of these windows of risk are critical with limited opportunity for subsequent recovery and an amplified risk of adult diabetes and associated chronic diseases. Risk factors are diverse including maternal stress, nutrition, environmental pollutants, air quality and lifestyle choices such as recreational drugs and alcohol. Target tissues of these stressors are diverse and include the developing pancreas, liver, kidneys, skeletal muscle, adipose tissue, cardiovascular system and brain. The placenta is a key mediator between maternal metabolic stress and offspring development during pregnancy and can both contribute and protect against future metabolic disorders. Substantial gaps exist in our mechanistic understanding of how individual organs and tissues are modified in both form and function by early life stressors, how limitations in tissue plasticity combine to build risk of adult disease, and where might there be opportunities for metabolic rescue before or after birth.
The goals of this Topic are to illustrate key structural and functional developmental changes to organs that arise in response to sub-optimal environmental conditions before and during pregnancy and during childhood development and how these can mutually build risk for adult metabolic diseases. The mechanisms by which different environmental stressors contribute and accumulate to result in altered embryonic, fetal, neonatal and child development resulting in adult onset of diabetes and metabolic syndrome are poorly understood. These are likely to involve lineage changes to tissue-specific stem cell populations, altered hormone, growth factor and cytokine presence, epigenetic alterations regulating key gene expression for control of metabolism, and accumulated cellular stress limiting cell proliferation and plasticity. Recent relaxation in the legislated oversight of recreational drugs presents an unknown paradigm of risk to the offspring in addition to other maternal lifestyle choices, nutrition, inherited genetic and epigenetic risk, and environmental stressors such as poverty and poor air or water quality. Understanding the extent of environmental impact on tissue plasticity and the potential for when and how this might be reversed is essential to preventing future metabolic diseases.
Environmental stressors, major tissues affected during development and future impact for metabolic diseases.
Stressors: Environmental pollutants, Socio-economic stress, Maternal lifestyle choices, Nutrition
Tissues: Placenta, Endocrine pancreas, Cardiovascular system and endothelial health, Liver, Adipose tissue, Kidney, Brain
Ontology of development: Maternal pre-pregnancy, Pregnancy, Postnatal life, Childhood
Potential mechanisms: Epigenetic modifications, stem cell populations, cellular stress, cellular aging, altered endocrinology, tissue inflammation, placental function and intrauterine hypoxia, pre- and postnatal nutrition
Combination of review articles and original papers.
