Research Topic

Endocrine-Disrupting and Inflammatory Effects of Environmental Chemicals on Animal Metabolism

About this Research Topic

The incidence of metabolic diseases has become highly prevalent globally. Individuals with a susceptible genetic background are especially predisposed toward the development of these diseases. Moreover, physical inactivity and the consumption of calorie-dense diets are major contributing risk factors. However, not all these factors are able to account for the high prevalence of the diseases. Therefore, additional efforts to characterize the disease pathogenesis are critical.

Recent research focuses have turned to other potential risk factors that could disrupt energy homeostasis. The role of environmental chemical contaminants has drawn significant attention as a contributor, independent of diet and physical activity. These chemicals come from diverse chemical classes, mostly ubiquitous, and are dispersed in the air, water, soil, and hence contaminate food and water supplies. Humans are exposed to these chemicals at different routes including inhalation, ingestion, and dermal contact, leading to an accumulation of hundreds of various chemical contaminants. More importantly, the transfer of these chemicals across placenta and during lactation suggest risk of fetal exposure. Consequently, a direct interaction of chemical contaminants with functional macromolecules in our body system would follow.

Most environmental chemical contaminants are known as endocrine-disrupting chemicals (EDCs) since their molecular structures are similar to endogenous hormones. Generally, EDCs can affect gene expression and cell signaling via direct interactions with nuclear receptors (NRs) to modulate downstream pathways. For example, studies have demonstrated the involvement of estrogen receptors, androgen receptors, retinoid X receptors, peroxisome proliferator-activated receptors, constitutive androstane receptor, pregnane X receptors, glucocorticoid receptors, and thyroid hormone receptors in EDC actions. Moreover, different EDCs share common receptor targets and interfere with various NRs at different affinities and intensities. Therefore, EDC-elicited effects can result from perturbations at multiple tissue levels through cross-talking among different endocrine pathways. In addition to the receptor-mediated actions, oxidative effects of EDCs on tissue inflammation were seen to cause chronic effects on exposed animals. Collectively EDC's can act on different biological components via a diverse mechanism of actions. A challenge ahead is to decipher the underlying mechanistic actions to provide a link to translate environmental stress to pathological mechanisms.

This Research Topic aims to collect original research and reviews unraveling the impact of environmental pollution on disease susceptibility. In particular, to define the causal relationship between EDC exposure and an increased susceptibility of metabolic diseases. An understanding of the underlying mechanisms will shed light on solutions of real environmental importance to safeguard the health of present and future generations. We are especially interested in work related to the following:

• Experimental studies using relevant animal and cell models to identify the underlying mechanistic actions of EDCs
• Epidemiological/clinical studies on the disease correlation


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

The incidence of metabolic diseases has become highly prevalent globally. Individuals with a susceptible genetic background are especially predisposed toward the development of these diseases. Moreover, physical inactivity and the consumption of calorie-dense diets are major contributing risk factors. However, not all these factors are able to account for the high prevalence of the diseases. Therefore, additional efforts to characterize the disease pathogenesis are critical.

Recent research focuses have turned to other potential risk factors that could disrupt energy homeostasis. The role of environmental chemical contaminants has drawn significant attention as a contributor, independent of diet and physical activity. These chemicals come from diverse chemical classes, mostly ubiquitous, and are dispersed in the air, water, soil, and hence contaminate food and water supplies. Humans are exposed to these chemicals at different routes including inhalation, ingestion, and dermal contact, leading to an accumulation of hundreds of various chemical contaminants. More importantly, the transfer of these chemicals across placenta and during lactation suggest risk of fetal exposure. Consequently, a direct interaction of chemical contaminants with functional macromolecules in our body system would follow.

Most environmental chemical contaminants are known as endocrine-disrupting chemicals (EDCs) since their molecular structures are similar to endogenous hormones. Generally, EDCs can affect gene expression and cell signaling via direct interactions with nuclear receptors (NRs) to modulate downstream pathways. For example, studies have demonstrated the involvement of estrogen receptors, androgen receptors, retinoid X receptors, peroxisome proliferator-activated receptors, constitutive androstane receptor, pregnane X receptors, glucocorticoid receptors, and thyroid hormone receptors in EDC actions. Moreover, different EDCs share common receptor targets and interfere with various NRs at different affinities and intensities. Therefore, EDC-elicited effects can result from perturbations at multiple tissue levels through cross-talking among different endocrine pathways. In addition to the receptor-mediated actions, oxidative effects of EDCs on tissue inflammation were seen to cause chronic effects on exposed animals. Collectively EDC's can act on different biological components via a diverse mechanism of actions. A challenge ahead is to decipher the underlying mechanistic actions to provide a link to translate environmental stress to pathological mechanisms.

This Research Topic aims to collect original research and reviews unraveling the impact of environmental pollution on disease susceptibility. In particular, to define the causal relationship between EDC exposure and an increased susceptibility of metabolic diseases. An understanding of the underlying mechanisms will shed light on solutions of real environmental importance to safeguard the health of present and future generations. We are especially interested in work related to the following:

• Experimental studies using relevant animal and cell models to identify the underlying mechanistic actions of EDCs
• Epidemiological/clinical studies on the disease correlation


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

16 June 2020 Abstract
21 September 2020 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

16 June 2020 Abstract
21 September 2020 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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