Reviews: adipocytokines in normal and complicated pregnancies.
Human pregnancy is characterized by insulin resistance, traditionally attributed to the effects of placental hormones. Normal pregnancy-induced insulin resistance is further enhanced in pregnancy complications, associated with disturbed placental function, such as gestational diabetes mellitus, preeclampsia, and intrauterine growth restriction. Compelling evidence suggests that these pregnancy disorders are associated with future development of maternal metabolic syndrome. However, the pathogenetic mechanisms underlying the association between abnormal placental development, insulin resistance, and maternal metabolic syndrome are not fully understood. A large body of evidence has recently supported the role of adipose tissue 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 alpha, interleukin 6, as well as the newly discovered resistin, visfatin, and apelin, are also known to be produced within the intrauterine environment. However, data concerning the pattern of adipocytokines secretion in normal and complicated pregnancies are still limited and partially contradictory. Given the importance of adipose tissue and its hormones in terms of adequate metabolic control and energy homeostasis, we present a review of published data related to the role of adipocytokines in pregnancy, especially in relation to pregnancy complications. Focus will be placed on the functions and other potential roles of the novel adipocytokines resistin, visfatin, and apelin.
Briana
Despina D
DD
Neonatal Division, 2nd Department of Obstetrics and Gynecology, Athens University Medical School, Athens, Greece.
Malamitsi-Puchner
Ariadne
A
D054392:Adipokines / Q000378:metabolism*; D000818:Animals; D016640:Diabetes, Gestational / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D011225:Pre-Eclampsia / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D011247:Pregnancy; D011248:Pregnancy Complications / Q000175:diagnosis / Q000378:metabolism* / Q000517:prevention & control
D054392:Adipokines