Maternal obesity induced metabolic disorders in offspring and myeloid reprogramming by epigenetic regulation

Area of Science:

• Reproductive biology
• Developmental biology
• Immunology

Background:

• Maternal obesity and gestational diabetes are linked to adverse childhood health outcomes.
• Early life exposure to a metabolically imbalanced environment influences chronic disease susceptibility.
• Large-for-gestational-age (LGA) children born to mothers with metabolic disorders face increased risks.

Purpose of the Study:

• To review clinical and experimental studies on early life metabolic environment exposure.
• To summarize the role of maternal obesity and gestational diabetes in childhood obesity and cardiovascular risk.
• To explore intrauterine environment-driven myeloid reprogramming and epigenetic mechanisms.

Main Methods:

• Comprehensive review of existing clinical and experimental studies.
• Analysis of data linking maternal metabolic status to offspring health.
• Examination of epigenetic regulations and markers involved in immune reprogramming.

Main Results:

• Exposure to maternal obesity and gestational diabetes can lead to LGA children.
• Adverse intrauterine environments reprogram fetal immune systems, increasing susceptibility to obesity, atherosclerosis, hypertension, and NAFLD.
• Epigenetic mechanisms play a crucial role in intrauterine environment-driven myeloid reprogramming.

Conclusions:

• Early life immune reprogramming by adverse intrauterine environments contributes to chronic inflammatory diseases and metabolic syndrome.
• Epigenetic modifications are key underlying mechanisms linking maternal metabolic disorders to offspring's long-term health.
• Further research into maternal-fetal immune regulation and epigenetic mechanisms is warranted for obesity and cardiovascular disease prevention.