Canverenler Emre, Buke Baris, Akkaya Hatice, Akarsu Suleyman and Isk Ahmet Zeki
Human pregnancy is affected by placental hormones which cause insulin resistance. In normal pregnancy, insulin resistance may lead to some problems associated with disturbed placental function, such as gestational diabetes mellitus, preeclampsia, and intrauterine growth restriction. These pregnancy conditions may result in the future development of metabolic syndrome. The pathogenetic mechanisms underlying the association between abnormal placental development, insulin resistanc and maternal metabolic syndrome are not fully understood. Adipose tissue may have an important role in the regulation of insulin resistance in both nonpregnant and pregnant participants. In this respect, adipocytokines, which are adipocyte derived hormones, have been implicated in the regulation of maternal metabolism and gestational insulin resistance. Adipocytokines, including leptin, adiponectin, tumor necrosis factor a, interleukin 6, as well as the recently ascertained resistin, visfatin, and apelin, are also known to be produced within the intrauterine environment. Release of adipocytokines in normal and abnormal pregnancy is still not clear and partially conflicting. This review aims to summarize reported findings concerning the role of adipocytokines (leptin, adiponectin, ghrelin, tumor necrosis factor [TNF], interleukin-6 [IL-6], visfatin, resistin, apelin). In early life, while attempting to speculate mechanisms through which differential regulation of adipocytokines in pregnancy complications may influence the risk for development of chronic diseases in later life.
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