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.

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Intrauterine growth restriction (IUGR) is the failure of the fetus to achieve his/her intrinsic growth potential, due to anatomical and/or functional disorders and diseases in the feto-placental-maternal unit. IUGR results in significant perinatal and long-term complications, including the development of insulin resistance/metabolic syndrome in adulthood.The thrifty phenotype hypothesis holds that intrauterine malnutrition leads to an adaptive response that alters the fetal metabolic and hormonal milieu designed for intrauterine survival. This fetal programming predisposes to an increased susceptibility for chronic diseases. Although the mechanisms controlling intrauterine growth are poorly understood, adipose tissue may play an important role in linking poor fetal growth to the subsequent development of adult diseases. Adipose tissue secretes a number of hormones, called adipocytokines, important in modulating metabolism and recently involved in intrauterine growth.This review aims to summarize reported findings concerning the role of adipocytokines (leptin, adiponectin, ghrelin, tumor necrosis factor (TNF), interleukin-6 (IL6), visfatin, resistin, apelin) in early life, while attempting to speculate mechanisms through which differential regulation of adipocytokines in IUGR may influence the risk for development of chronic diseases in later life.

The term intrauterine growth restriction (IUGR) is assigned to newborns with a birth weight and/or birth length below the 10th percentile for their gestational age and whose abdominal circumference is below the 2.5th percentile with pathologic restriction of fetal growth. IUGR is usually due to maternal, fetal, or placental factors. However, many IUGR cases have unknown underlying cause. Recent studies focus on new factors that can influence fetal development and birth outcome like the timing and the type of fetal nutrition, maternal psychosocial stress and personality variables, 11beta-hydroxysteroid dehydrogenase type 2 placental activity, the activity of the neuroendocrine system that mediates the effects of psychosocial stress, and the role of proinflammatory cytokines and of oxidative stress. Data have shown that IUGR is associated with a late life increased prevalence of metabolic syndrome, a condition associating obesity with hypertension, type 2 diabetes mellitus (DM2), and cardiovascular disease. Recent data demonstrated that the diabetes-associated mortality appears to be disproportionately concentrated among individuals of abnormal birth weight.

Pathologic conditions in pregnancy that lead to intrauterine growth restriction could be responsible for elevated maternal visfatin levels. Higher visfatin levels in neonates with intrauterine growth restriction may serve as an early marker with prognostic value for later development of insulin resistance or type 2 diabetes, whereas lower insulin levels may indicate reduced beta-cell mass and/or impaired beta-cell function.

Objective: Leptin and adiponectin are two adipocytokines that play a critical role in the control of energy balance and metabolism as well as in conditions, such as insulin resistance, inflammation, and the development of the metabolic syndrome in adult life. Leptin has been associated with asymmetric intrauterine growth restriction (IUGR). The aim of this study was to investigate the perinatal implication of leptin and adiponectin in IUGR. Design: Leptin and adiponectin were measured in the plasma of 40 mothers, in the umbilical cord (UC) blood of their 20 appropriate for gestational age (AGA) and 20 IUGR singleton, full-term fetuses, and neonates on day 1 (d1) and day 4 (d4) of life postnatally. Methods: Serum leptin and adiponectin levels were measured by RIA. Serum cortisol levels were measured with an electrochemiluminescence immunoassay. Results: Leptin and adiponectin serum levels were higher and lower respectively in IUGR (meanGS.E.M., 32.5G3.8 and 5.4G0.9 mg/l respectively) compared with AGA (20.4G2.1 and 11.8G1.3 mg/l respectively) mothers (P!0.05), although body mass index did not differ between these two groups. Leptin levels positively correlated with adiponectin levels in the AGA (rZ0.547, P!0.05) but not in the IUGR mothers. UC, d1, and d4 leptin and adiponectin levels did not differ between IUGR and AGA groups. UC were significantly higher than d1 leptin levels (P!0.05) in the IUGR group but not in the AGA group. Conclusions: The increased UC leptin levels compared with d1 in IUGR fetuses might be directly and/or indirectly related to the subsequent development of insulin resistance in these neonates. This pathologic situation seems to be related to a specific profile of increased leptin and decreased adiponectin levels in IUGR mothers indicating a genetic predisposition for the development of insulin resistance.European Journal of Endocrinology 158 343-348

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.

The role of maternal colostrum to infant development has been extensively studied and presented. Among the main factors which contribute to breast milk composition are maternal diet, age and body mass index, parity, duration of pregnancy and stage of lactation. This study aims to investigate the potential impact of several factors including demographic (i.e. maternal age and nationality) on the colostrum fatty acid profile. Colostrum was collected the third day postpartum in a Greek maternity hospital. Certain lipid quality indices and fatty acid ratios were estimated and results were statistically processed. The main identified fatty acids were palmitic (C16:0), oleic (C18:1ω-9), and linoleic (C18:2ω-6) acids. Among fatty acids, saturated fatty acids predominated (47.61%), followed by monounsaturated fatty acids (39.26%), while polyunsaturated fatty acids had the lowest proportion (13.13%). Values of lipid quality indices were within the reported in the literature ranges. Maternal body mass index, nationality, age, mode of delivery, gender and fetal weight percentile were studied in respect to their potential influence on the fatty acid profile of colostrum fat. Results suggest that colostrum fatty acid profile was mainly dependent on maternal nationality and age rather than mode of delivery and maternal BMI. Regarding the effect of maternal nationality, significant differences were found for saturated and monounsaturated fatty acids. Of the most interesting findings is that colostrum fat from older (≥35 years) mothers had less saturated fat and more appropriate LQIs values. Finally, a reversed correlation was observed between the customized centile of the infants and the colostrum fat content.