Preterm birth: A neuroinflammatory origin for metabolic diseases?

Preterm birth and its related complications have become more and more common as neonatal medicine advances. The concept of “developmental origins of health and disease” has raised awareness of adverse perinatal events in the development of diseases later in life. To explore this concept, we propose...

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Published inBrain, behavior, & immunity. Health Vol. 37; p. 100745
Main Authors Diao, Sihao, Chen, Chao, Benani, Alexandre, Magnan, Christophe, Van Steenwinckel, Juliette, Gressens, Pierre, Cruciani-Guglielmacci, Céline, Jacquens, Alice, Bokobza, Cindy
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.05.2024
Elsevier
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ISSN2666-3546
2666-3546
DOI10.1016/j.bbih.2024.100745

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Summary:Preterm birth and its related complications have become more and more common as neonatal medicine advances. The concept of “developmental origins of health and disease” has raised awareness of adverse perinatal events in the development of diseases later in life. To explore this concept, we propose that encephalopathy of prematurity (EoP) as a potential pro-inflammatory early life event becomes a novel risk factor for metabolic diseases in children/adolescents and adulthood. Here, we review epidemiological evidence that links preterm birth to metabolic diseases and discuss possible synergic roles of preterm birth and neuroinflammation from EoP in the development of metabolic diseases. In addition, we explore theoretical underlying mechanisms regarding developmental programming of the energy control system and HPA axis. [Display omitted] •Perinatal events play an essential role in the development of metabolic diseases.•Preterm birth contributes to an increased risk of metabolic diseases.•Encephalopathy of prematurity is a potential novel risk factor for metabolic diseases.•Possible underlying mechanisms might be related to energy imbalance and dysregulated HPA axis.
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PMCID: PMC10950814
Contributed equally.
ISSN:2666-3546
2666-3546
DOI:10.1016/j.bbih.2024.100745