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Early-life cardiovascular programming by maternal protein restriction: Electrophysiological, structural, and
Luísa C Gomes1, Matheus N Fioretto1, Lucas S Lemos1
1Department of Cellular and Molecular Biology, Institute of Biosciences, Sao Paulo State University, Botucatu, SP, Brazil.
Insights
Maternal protein restriction in rats leads to early heart changes in female offspring, including altered electrical activity and extracellular matrix remodeling. These findings highlight the impact of maternal nutrition on offspring cardiovascular health.
Area of Science:
- Developmental Biology
- Cardiovascular Physiology
- Nutritional Science
Background:
- Maternal malnutrition is a significant risk factor for adverse offspring health outcomes, particularly cardiovascular disorders.
- The Developmental Origins of Health and Disease (DOHaD) concept posits that early life exposures can lead to long-term health consequences.
- Maternal protein restriction (MPR) is a known experimental model linked to cardiovascular and hypertensive phenotypes in offspring.
Purpose of the Study:
- To investigate the effects of maternal protein restriction (MPR) on the cardiovascular morphophysiology of female offspring at postnatal day 21 (PND21).
Main Methods:
- Pregnant rats were assigned to a control (normoprotein) or gestational and lactational low-protein (GLLP) diet.
- Female offspring were assessed at PND21 for electrocardiography, morphology, molecular changes, and oxidative stress.
- Analyses included heart weight, electrocardiogram (ECG) parameters, cardiomyocyte structure, extracellular matrix components, gene expression, and redox status.
Main Results:
- GLLP offspring showed reduced body weight and length but increased relative heart weight, indicating disproportionate growth.
- Electrocardiographic analysis revealed a shortened P-R interval and decreased heart rate in GLLP offspring.
- Morphological analysis showed increased collagen and elastin deposition, suggesting early extracellular matrix remodeling.
- Molecular analysis indicated reduced PRDX3 expression and altered antioxidant homeostasis (decreased CAT activity, GSH levels, and TBARS).
Conclusions:
- Maternal protein restriction induces early structural, molecular, oxidative, and electrophysiological alterations in the hearts of female offspring.
- These adaptations may represent developmental programming events that increase susceptibility to cardiovascular dysfunction later in life.
- The study underscores the critical role of maternal nutrition in programming long-term cardiovascular health across generations.
Abstract:
Maternal malnutrition is a major risk factor for adverse health outcomes in offspring, including cardiovascular disorders. According to the Developmental Origins of Health and Disease (DOHaD) concept, adverse conditions during critical developmental windows can induce long-lasting physiological adaptations that increase disease susceptibility later in life. Among the experimental models used to investigate these mechanisms, maternal protein restriction (MPR) has been associated with metabolic, cardiovascular, and hypertensive phenotypes in offspring, some of which emerge early in life. Therefore, this study evaluated the effects of MPR on the cardiovascular morphophysiology of female offspring at postnatal day 21 (PND21). Pregnant rats were allocated to either a Control group (CTR), receiving a normoprotein diet (17% protein), or a Gestational and Lactational Low-Protein group (GLLP), receiving a low-protein diet (6% protein) throughout gestation and lactation. At PND21, female offspring underwent electrocardiographic assessment and were subsequently euthanized for morphological, molecular, and oxidative stress analyses. Female offspring from the GLLP group exhibited reduced body weight and body length, whereas absolute heart weight was preserved, resulting in increased relative heart weight and suggesting disproportionate somatic growth. Electrocardiographic analysis revealed a shortened P-R interval and decreased heart rate, indicating early alterations in cardiac electrical activity. Morphologically, cardiomyocyte architecture was preserved; however, reduced nuclear width and increased collagen and elastin deposition were observed, indicating early extracellular matrix remodeling without significant changes in reticular fibers. At the molecular level, GLLP offspring exhibited reduced PRDX3 expression, accompanied by decreased catalase (CAT) activity, reduced glutathione (GSH) levels, and lower lipid peroxidation (TBARS), suggesting alterations in redox regulation and antioxidant homeostasis during early cardiac development. Collectively, these findings demonstrate that MPR induces early structural, molecular, oxidative, and electrophysiological alterations in the hearts of female offspring. These adaptations may represent early programming events that increase susceptibility to cardiovascular dysfunction later in life, reinforcing the importance of maternal nutrition in shaping cardiovascular health across generations.
