Inflammatory Signatures of Maternal Obesity as Risk Factors for Neurodevelopmental Disorders: Role of Maternal Microbiota and Nutritional Intervention Strategies.
Francesca CirulliRoberta De SimoneChiara MusilloMaria Antonietta Ajmone-CatAlessandra BerryPublished in: Nutrients (2022)
Obesity is a main risk factor for the onset and the precipitation of many non-communicable diseases. This condition, which is associated with low-grade chronic systemic inflammation, is of main concern during pregnancy leading to very serious consequences for the new generations. In addition to the prominent role played by the adipose tissue, dysbiosis of the maternal gut may also sustain the obesity-related inflammatory milieu contributing to create an overall suboptimal intrauterine environment. Such a condition here generically defined as "inflamed womb" may hold long-term detrimental effects on fetal brain development, increasing the vulnerability to mental disorders. In this review, we will examine the hypothesis that maternal obesity-related gut dysbiosis and the associated inflammation might specifically target fetal brain microglia, the resident brain immune macrophages, altering neurodevelopmental trajectories in a sex-dependent fashion. We will also review some of the most promising nutritional strategies capable to prevent or counteract the effects of maternal obesity through the modulation of inflammation and oxidative stress or by targeting the maternal microbiota.
Keyphrases
- birth weight
- oxidative stress
- insulin resistance
- weight gain
- weight loss
- metabolic syndrome
- adipose tissue
- type diabetes
- high fat diet induced
- pregnancy outcomes
- low grade
- white matter
- high fat diet
- resting state
- body mass index
- skeletal muscle
- randomized controlled trial
- gestational age
- high grade
- ischemia reperfusion injury
- pregnant women
- inflammatory response
- climate change
- depressive symptoms
- induced apoptosis
- diabetic rats
- physical activity
- cerebral ischemia
- brain injury
- functional connectivity
- endoplasmic reticulum stress
- preterm birth