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Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents
Marie Josse1, Eve Rigal1, Nathalie Rosenblatt-Velin2
1Research Team of Physiopathologie et Epidémiologie Cérébro-Cardiovasculaires (PEC2, EA 7460), Faculté des Sciences de Santé, Université de Bourgogne-Franche Comté, 21000 Dijon, France.
Insights
Postnatal overfeeding (PNOF) in rodents permanently increases body weight and impairs cardiovascular function, leading to metabolic and cardiac abnormalities. However, caloric restriction and exercise show potential for therapeutic correction.
Area of Science:
- Cardiovascular Physiology
- Nutritional Science
- Developmental Biology
Background:
- Perinatal nutrition significantly impacts adult health and disease.
- Litter size reduction in rodents models postnatal overnutrition (PNOF), affecting long-term health.
- PNOF is linked to obesity, metabolic dysfunction, and cardiovascular alterations.
Purpose of the Study:
- To investigate the long-term cardiovascular and metabolic consequences of postnatal overfeeding (PNOF) in a rodent model.
- To explore the molecular and functional cardiac changes induced by PNOF.
- To assess the potential for interventions like caloric restriction and exercise.
Main Methods:
- Rodent model of postnatal overfeeding (litter size reduction).
- Assessment of body weight, adiposity, plasma biomarkers (insulin, leptin, lipids).
- Cardiovascular function tests (blood pressure, vascular responsiveness, cardiac function).
- Cardiac tissue analysis (hypertrophy, collagen, mitochondrial respiration, gene expression, epigenetics).
Main Results:
- PNOF led to sustained increased body weight and adiposity.
- Metabolic alterations included hyperinsulinemia, leptin resistance, and dyslipidemia.
- Cardiovascular effects comprised elevated blood pressure, altered vascular reactivity, cardiac hypertrophy, and impaired mitochondrial function.
- PNOF induced gene expression changes, epigenetic modifications, and reduced ventricular contractility, increasing susceptibility to ischemia-reperfusion injury.
Conclusions:
- Postnatal overfeeding (PNOF) causes persistent metabolic and cardiovascular dysfunction in rodents.
- Early nutritional programming has profound, long-lasting effects on cardiac health.
- Caloric restriction and physical exercise may offer therapeutic strategies to mitigate PNOF-induced damage.
Abstract:
Nutritional environment in the perinatal period has a great influence on health and diseases in adulthood. In rodents, litter size reduction reproduces the effects of postnatal overnutrition in infants and reveals that postnatal overfeeding (PNOF) not only permanently increases body weight but also affects the cardiovascular function in the short- and long-term. In addition to increased adiposity, the metabolic status of PNOF rodents is altered, with increased plasma insulin and leptin levels, associated with resistance to these hormones, changed profiles and levels of circulating lipids. PNOF animals present elevated arterial blood pressure with altered vascular responsiveness to vasoactive substances. The hearts of overfed rodents exhibit hypertrophy and elevated collagen content. PNOF also induces a disturbance of cardiac mitochondrial respiration and produces an imbalance between oxidants and antioxidants. A modification of the expression of crucial genes and epigenetic alterations is reported in hearts of PNOF animals. In vivo, a decreased ventricular contractile function is observed during adulthood in PNOF hearts. All these alterations ultimately lead to an increased sensitivity to cardiac pathologic challenges such as ischemia-reperfusion injury. Nevertheless, caloric restriction and physical exercise were shown to improve PNOF-induced cardiac dysfunction and metabolic abnormalities, drawing a path to the potential therapeutic correction of early nutritional programming.
