Maternal obesity and offspring health: Adapting metabolic changes through autophagy and mitophagy

Area of Science:

• Reproductive Biology
• Metabolic Health
• Cellular Biology

Background:

• Maternal obesity is linked to obstetric complications and offspring metabolic anomalies.
• Developmental programming is a key factor in maternal obesity-associated chronic comorbidities.
• Cellular mechanisms like lipotoxicity, inflammation, oxidative stress, and defective autophagy/mitophagy contribute to these sequelae.

Purpose of the Study:

• To review metabolic disorders in fetal development and postnatal health caused by maternal obesity.
• To discuss the role of autophagy and mitophagy in these metabolic diseases.
• To explore potential therapeutic strategies targeting autophagy/mitophagy and metabolic disturbances.

Main Methods:

• Literature review of studies on maternal obesity, fetal development, and metabolic disorders.
• Analysis of the role of autophagy and mitophagy in cellular homeostasis and disease.
• Synthesis of current understanding and identification of therapeutic avenues.

Main Results:

• Defective autophagy/mitophagy is implicated in negative impacts on fetal development and postnatal health.
• Autophagy and mitophagy are crucial for clearing damaged cellular components and maintaining homeostasis.
• Maternal obesity and intrauterine overnutrition can disrupt these vital cellular processes.

Conclusions:

• Autophagy/mitophagy defects are significant contributors to metabolic disorders stemming from maternal obesity.
• Targeting autophagy/mitophagy presents a promising therapeutic strategy for mitigating metabolic disturbances.
• Further research is needed to fully elucidate the mechanisms and optimize interventions.