Maternal obesity induced metabolic disorders in offspring and myeloid reprogramming by epigenetic regulation
Maternal obesity and gestational diabetes are associated with childhood obesity and increased cardiovascular risk. In this review, we will discuss and summarize extensive clinical and experimental studies that metabolically imbalanced environment exposure in early life plays a critical role in influ...
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Published in | Frontiers in endocrinology (Lausanne) Vol. 14; p. 1256075 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
16.01.2024
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Subjects | |
Online Access | Get full text |
ISSN | 1664-2392 1664-2392 |
DOI | 10.3389/fendo.2023.1256075 |
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Summary: | Maternal obesity and gestational diabetes are associated with childhood obesity and increased cardiovascular risk. In this review, we will discuss and summarize extensive clinical and experimental studies that metabolically imbalanced environment exposure in early life plays a critical role in influencing later susceptibility to chronic inflammatory diseases and metabolic syndrome. The effect of maternal obesity and metabolic disorders, including gestational diabetes cause Large-for-gestational-age (LGA) children to link future development of adverse health issues such as obesity, atherosclerosis, hypertension, and non-alcoholic fatty liver disease by immune reprogramming to adverse micro-environment. This review also addresses intrauterine environment-driven myeloid reprogramming by epigenetic regulations and the epigenetic markers as an underlying mechanism. This will facilitate future investigations regarding maternal-to-fetal immune regulation and the epigenetic mechanisms of obesity and cardiovascular diseases. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Abhirami K. Iyer, Washington University in St. Louis, United States Edited by: Enrique Podaza, NewYork-Presbyterian, United States Reviewed by: Hyun Phil Shin, Kyung Hee University, Republic of Korea These authors have contributed equally to this work and share first authorship |
ISSN: | 1664-2392 1664-2392 |
DOI: | 10.3389/fendo.2023.1256075 |