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Gestational programming of offspring obesity/hypertension
Donald A Novak1, Mina Desai, Michael G Ross
1Department of Pediatrics, University of Florida College of Medicine, Gainesville, FL 32610, USA. novakda@peds.ufl.edu
Insights
Prenatal conditions influence postnatal health, linking fetal size at birth to adult obesity and hypertension. This review examines the mechanisms behind these developmental origins of disease.
Area of Science:
- Reproductive biology
- Developmental origins of health and disease
- Metabolic and cardiovascular health
Background:
- The intrauterine environment significantly affects fetal development and growth.
- Postnatal health and disease risk in adults are influenced by prenatal conditions.
- Fetal size at birth is associated with later-life disorders, including obesity and hypertension.
Purpose of the Study:
- To review current data on the association between fetal size and adult obesity/hypertension.
- To explore the pathophysiologic mechanisms linking prenatal conditions to postnatal disease.
- To synthesize findings from human and animal model studies.
Main Methods:
- Literature review of recent research on fetal programming.
- Analysis of human epidemiological data.
- Examination of animal models investigating developmental origins of disease.
Main Results:
- Strong evidence links smaller or larger fetal size to increased risk of adult obesity.
- Prenatal factors influencing fetal growth are also implicated in hypertension development.
- Shared pathophysiologic pathways may underlie these associations.
Conclusions:
- Prenatal environment plays a critical role in long-term metabolic and cardiovascular health.
- Understanding these developmental origins is key to preventing adult-onset obesity and hypertension.
- Further research into underlying mechanisms can inform targeted interventions.
Abstract:
The intrauterine milieu impacts fetal growth directly during gestation. It is now clear, however, that postnatal phenotype is also influenced by prenatal conditions. A variety of disorders in the adult have been linked to fetal size at birth; these include glucose intolerance, cardiovascular disease, and the subjects of this review, obesity and hypertension. We will review recent data regarding these associations and the pathophysiologic mechanisms underlying them in humans as well as in animal models.
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