Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming
Abstract Prenatal ethanol exposure (PEE) (mainly through maternal alcohol consumption) has become widespread. However, studies suggest that it can cause intrauterine growth retardation (IUGR) and multi-organ developmental toxicity in offspring, and susceptibility to various chronic diseases (such as...
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| Format: | Article |
| Language: | English |
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BMC
2023-11-01
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| Series: | Biological Research |
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| Online Access: | https://doi.org/10.1186/s40659-023-00473-y |
| _version_ | 1797577993436004352 |
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| author | Liang Liu Yinxian Wen Qubo Ni Liaobin Chen Hui Wang |
| author_facet | Liang Liu Yinxian Wen Qubo Ni Liaobin Chen Hui Wang |
| author_sort | Liang Liu |
| collection | DOAJ |
| description | Abstract Prenatal ethanol exposure (PEE) (mainly through maternal alcohol consumption) has become widespread. However, studies suggest that it can cause intrauterine growth retardation (IUGR) and multi-organ developmental toxicity in offspring, and susceptibility to various chronic diseases (such as neuropsychiatric diseases, metabolic syndrome, and related diseases) in adults. Through ethanol’s direct effects and its indirect effects mediated by maternal-derived glucocorticoids, PEE alters epigenetic modifications and organ developmental programming during fetal development, which damages the offspring health and increases susceptibility to various chronic diseases after birth. Ethanol directly leads to the developmental toxicity of multiple tissues and organs in many ways. Regarding maternal-derived glucocorticoid-mediated IUGR, developmental programming, and susceptibility to multiple conditions after birth, ethanol induces programmed changes in the neuroendocrine axes of offspring, such as the hypothalamus-pituitary-adrenal (HPA) and glucocorticoid-insulin-like growth factor 1 (GC-IGF1) axes. In addition, the differences in ethanol metabolic enzymes, placental glucocorticoid barrier function, and the sensitivity to glucocorticoids in various tissues and organs mediate the severity and sex differences in the developmental toxicity of ethanol exposure during pregnancy. Offspring exposed to ethanol during pregnancy have a “thrifty phenotype” in the fetal period, and show “catch-up growth” in the case of abundant nutrition after birth; when encountering adverse environments, these offspring are more likely to develop diseases. Here, we review the developmental toxicity, functional alterations in multiple organs, and neuroendocrine metabolic programming mechanisms induced by PEE based on our research and that of other investigators. This should provide new perspectives for the effective prevention and treatment of ethanol developmental toxicity and the early prevention of related fetal-originated diseases. |
| first_indexed | 2024-03-10T22:15:59Z |
| format | Article |
| id | doaj.art-03569df450c94f8585f0f48e32e79f70 |
| institution | Directory Open Access Journal |
| issn | 0717-6287 |
| language | English |
| last_indexed | 2024-03-10T22:15:59Z |
| publishDate | 2023-11-01 |
| publisher | BMC |
| record_format | Article |
| series | Biological Research |
| spelling | doaj.art-03569df450c94f8585f0f48e32e79f702023-11-19T12:25:45ZengBMCBiological Research0717-62872023-11-0156111910.1186/s40659-023-00473-yPrenatal ethanol exposure and changes in fetal neuroendocrine metabolic programmingLiang Liu0Yinxian Wen1Qubo Ni2Liaobin Chen3Hui Wang4Department of Orthopedic Surgery, Joint Disease Research Center of Wuhan University, Zhongnan Hospital of Wuhan UniversityDepartment of Orthopedic Surgery, Joint Disease Research Center of Wuhan University, Zhongnan Hospital of Wuhan UniversityDepartment of Orthopedic Surgery, Joint Disease Research Center of Wuhan University, Zhongnan Hospital of Wuhan UniversityDepartment of Orthopedic Surgery, Joint Disease Research Center of Wuhan University, Zhongnan Hospital of Wuhan UniversityHubei Provincial Key Laboratory of Developmentally Originated DiseaseAbstract Prenatal ethanol exposure (PEE) (mainly through maternal alcohol consumption) has become widespread. However, studies suggest that it can cause intrauterine growth retardation (IUGR) and multi-organ developmental toxicity in offspring, and susceptibility to various chronic diseases (such as neuropsychiatric diseases, metabolic syndrome, and related diseases) in adults. Through ethanol’s direct effects and its indirect effects mediated by maternal-derived glucocorticoids, PEE alters epigenetic modifications and organ developmental programming during fetal development, which damages the offspring health and increases susceptibility to various chronic diseases after birth. Ethanol directly leads to the developmental toxicity of multiple tissues and organs in many ways. Regarding maternal-derived glucocorticoid-mediated IUGR, developmental programming, and susceptibility to multiple conditions after birth, ethanol induces programmed changes in the neuroendocrine axes of offspring, such as the hypothalamus-pituitary-adrenal (HPA) and glucocorticoid-insulin-like growth factor 1 (GC-IGF1) axes. In addition, the differences in ethanol metabolic enzymes, placental glucocorticoid barrier function, and the sensitivity to glucocorticoids in various tissues and organs mediate the severity and sex differences in the developmental toxicity of ethanol exposure during pregnancy. Offspring exposed to ethanol during pregnancy have a “thrifty phenotype” in the fetal period, and show “catch-up growth” in the case of abundant nutrition after birth; when encountering adverse environments, these offspring are more likely to develop diseases. Here, we review the developmental toxicity, functional alterations in multiple organs, and neuroendocrine metabolic programming mechanisms induced by PEE based on our research and that of other investigators. This should provide new perspectives for the effective prevention and treatment of ethanol developmental toxicity and the early prevention of related fetal-originated diseases.https://doi.org/10.1186/s40659-023-00473-yIntrauterine programmingNeuroendocrine metabolismPrenatal ethanol exposureGlucocorticoidDevelopmental origins of Health and Disease (DOHaD) |
| spellingShingle | Liang Liu Yinxian Wen Qubo Ni Liaobin Chen Hui Wang Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming Biological Research Intrauterine programming Neuroendocrine metabolism Prenatal ethanol exposure Glucocorticoid Developmental origins of Health and Disease (DOHaD) |
| title | Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming |
| title_full | Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming |
| title_fullStr | Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming |
| title_full_unstemmed | Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming |
| title_short | Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming |
| title_sort | prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming |
| topic | Intrauterine programming Neuroendocrine metabolism Prenatal ethanol exposure Glucocorticoid Developmental origins of Health and Disease (DOHaD) |
| url | https://doi.org/10.1186/s40659-023-00473-y |
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