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Updated: May 22, 2026

Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
Published on: June 29, 2013
Effect of intrauterine growth retardation on liver and long-term metabolic risk
S Cianfarani1, C Agostoni, G Bedogni
1Molecular Endocrinology Unit-DPUO, Bambino Gesù Children's Hospital - 'Rina Balducci' Center of Pediatric Endocrinology, Tor Vergata University, Rome, Italy. stefano.cianfarani@uniroma2.it
Abstract:
Intrauterine growth retardation predisposes toward long-term morbidity from type 2 diabetes and cardiovascular disease. To explain this association, the concept of programming was introduced to indicate a process whereby a stimulus or insult at a critical period of development has lasting or lifelong consequences on key endocrine and metabolic pathways. Subtle changes in cell composition of tissues, induced by suboptimal conditions in utero, can influence postnatal physiological functions. There is increasing evidence, suggesting that liver may represent one of the candidate organs targeted by programming, undergoing structural, functional and epigenetic changes following exposure to an unfavorable intrauterine environment. The aim of this review is to provide insights into the molecular mechanisms underlying liver programming that contribute to increase the cardiometabolic risk in subjects with intrauterine growth restriction.
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