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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Perinatal exposure to maternal obesity: Lasting cardiometabolic impact on offspring
Sezen Kislal1, Lydia L Shook2, Andrea G Edlow1,2
1Vincent Center for Reproductive Biology, Massachusetts General Hospital Research Institute, Massachusetts General Hospital, Boston, Massachusetts, USA.
Insights
Maternal obesity and high-fat diets during pregnancy and lactation increase offspring cardiometabolic risks, including obesity and metabolic syndrome. Offspring sex may influence these adverse outcomes.
Area of Science:
- Reproductive biology
- Developmental biology
- Metabolic syndrome
Background:
- Maternal obesity and high-fat diet (HFD) consumption during critical developmental windows are linked to adverse cardiometabolic outcomes in offspring.
- These outcomes include increased risk for obesity, metabolic syndrome features (hypertension, hyperglycemia, insulin resistance, hyperlipidemia, adiposity), and non-alcoholic fatty liver disease.
- Fetal and offspring sex may act as a significant modifier of these effects.
Purpose of the Study:
- To synthesize human and animal data on the impact of maternal obesity and HFD on offspring cardiometabolic health.
- To review the underlying mechanisms contributing to cardiometabolic morbidity in offspring exposed to maternal obesity.
Main Methods:
- This review synthesizes evidence from epidemiological, clinical, and animal model studies.
- It examines data linking maternal diet and obesity during pregnancy and lactation to offspring health outcomes.
- Key molecular and physiological mechanisms are explored.
Main Results:
- Maternal obesity and HFD are consistently associated with increased cardiometabolic risks in offspring.
- Specific adverse outcomes include obesity, metabolic syndrome, and non-alcoholic fatty liver disease.
- Sex-specific effects and alterations in skeletal muscle, adipose tissue, pancreas, liver, and brain reward pathways are implicated.
Conclusions:
- Prenatal and lactational exposure to maternal obesity and HFD significantly contributes to offspring cardiometabolic morbidity.
- Understanding these programming mechanisms is crucial for developing targeted interventions.
- Further research into sex-specific effects is warranted to refine preventative strategies.
Abstract:
Evidence from epidemiological, clinical, and animal model studies clearly demonstrates that prenatal and lactational maternal obesity and high-fat diet consumption are associated with cardiometabolic morbidity in offspring. Fetal and offspring sex may be an important effect modifier. Adverse offspring cardiometabolic outcomes observed in the setting of maternal obesity include an increased risk for obesity, features of metabolic syndrome (hypertension, hyperglycemia and insulin resistance, hyperlipidemia, increased adiposity), and non-alcoholic fatty liver disease. This review article synthesizes human and animal data linking maternal obesity and high-fat diet consumption in pregnancy and lactation to adverse cardiometabolic outcomes in offspring. We review key mechanisms underlying skeletal muscle, adipose tissue, pancreatic, liver, and central brain reward programming in obesity-exposed offspring, and how such malprogramming contributes to offspring cardiometabolic morbidity.
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