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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, USA.
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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