Journal
INTERNATIONAL JOURNAL OF OBESITY
Volume 36, Issue 10, Pages 1270-1277Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ijo.2012.54
Keywords
non-alcoholic fatty liver disease (NAFLD); type 2 diabetes; cardiometabolic disease; programming; intrauterine growth retardation (IUGR)
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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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