Author(s): Briana DD, MalamitsiPuchner A
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Abstract Cumulative evidence suggests that the origins of obesity may occur during fetal development. In this respect, the concept of "developmental programming" was introduced and supported by experimental and epidemiological data. This concept supports the idea that the nutritional and hormonal status during pregnancy could irreversibly interfere in metabolism control. The mechanisms responsible for this developmental programming remain poorly documented. However, recent research indicates that adipocytokines may play a critical role in this process. Thus, leptin, adiponectin, and the recently identified resistin, visfatin, and apelin, all exert effects on fat, muscle, and liver cells early in life. The aforementioned adipocytokines are secreted by adipocytes and human placenta during fetal life and may play a major role in the etiopathogenesis of the metabolic syndrome. This review will focus on the intrauterine expression of adipocytokines, their contribution to the hormonal control of fetal growth, and their role in restricted and exaggerated intrauterine growth. © 2010 New York Academy of Sciences.
This article was published in Ann N Y Acad Sci
and referenced in Journal of Diabetes & Metabolism