Mommy issues: how maternal diet shapes offspring mitochondrial physiology

Avika Gomez-Sharma1,2, Carrie E McCurdy1

  • 1Department of Human Physiology, University of Oregon, Eugene, OR 97403, United States.

Insights

Maternal high-calorie diets during pregnancy can negatively impact offspring mitochondrial function, increasing risks for obesity and type 2 diabetes. Early life interventions targeting mitochondrial health may prevent these long-term cardiometabolic diseases.

Area of Science:

  • Developmental biology
  • Mitochondrial biology
  • Nutritional science

Background:

  • Early life exposures, including maternal diet and obesity, are linked to increased cardiometabolic disease risk in offspring.
  • Mitochondria are central to energy metabolism and cellular stress, making them potential mediators of diet-induced developmental programming.
  • Understanding these early life effects is crucial for preventing childhood obesity and type 2 diabetes.

Purpose of the Study:

  • To review the impact of maternal high-calorie diets on offspring mitochondrial structure and function.
  • To explore how mitochondrial alterations influence metabolic health and disease risk.
  • To discuss mechanisms linking maternal diet to offspring mitochondrial dysfunction.

Main Methods:

  • Literature review of studies examining maternal diet effects on offspring mitochondria in animal models.
  • Analysis of data on mitochondrial content, architecture, and bioenergetics in skeletal and cardiac muscle.
  • Synthesis of findings on substrate utilization, oxidative capacity, and metabolic flexibility.

Main Results:

  • Maternal high-calorie diets alter offspring mitochondrial content, architecture, and bioenergetics.
  • These mitochondrial changes impair substrate dependence, oxidative capacity, and metabolic efficiency.
  • Reduced metabolic flexibility and increased cardiometabolic risk are observed in offspring.

Conclusions:

  • Maternal diet quality significantly impacts offspring mitochondrial physiology, contributing to long-term cardiometabolic disease risk.
  • Mechanisms include redox imbalance, disrupted mitochondrial-nuclear communication, and epigenetic changes.
  • Targeting mitochondrial health during development offers potential therapeutic strategies.

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