The secretion pattern of ApN in normal and complicated pregnancies strongly suggests an involvement of ApN in insulin resistance during gestation, while resistin seems to have a minor role. Moreover, the detection of high levels of resistin and ApN in cord blood during gestation is consistent with a regulatory action of these adipokines on tissue differentiation and foetal growth.

The relationship between in utero fetal growth and fetal leptin concentrations was investigated between 19 and 41 wk in 40 normal (appropriate for gestational age, AGA) fetuses, in 25 intrauterine growth-restricted (IUGR) fetuses, and in 18 fetuses from gestational diabetic mothers (GDM), representing different intrauterine growth patterns. Umbilical venous plasma leptin concentrations were determined at the time of either in utero fetal blood sampling or delivery. Plasma leptin was measurable as early as 19 wk of gestation. A significant difference was observed between umbilical venous and arterial plasma leptin concentrations (0.6 Ϯ 0.6 ng/mL; p Ͻ 0.01). In AGA and in IUGR fetuses, significant positive relationships were found between fetal leptin concentrations and both gestational age (p Ͻ 0.001) and fetal weight (p Ͻ 0.001). Leptin concentrations were significantly higher in AGA than IUGR only after 34 wk (p Ͻ 0.05), but leptin per kilogram fetal weight (leptin/kg) was not significantly different. In IUGR with abnormal umbilical arterial Doppler velocimetry and fetal heart rate, leptin/kg significantly higher than in IUGR with normal biophysical and biochemical parameters was found (p Ͻ 0.05). Both circulating plasma leptin and leptin/kg were significantly higher in GDM than in normal fetuses (p Ͻ 0.001) and correlated with abdominal fat mass measured by ultrasound. No gender differences were observed in any group of fetuses. These findings indicate a clear relationship between fetal leptin concentrations and fetal fat mass. Data in severe IUGR suggest the presence of increased leptin concentrations associated with in utero signs of fetal distress. Abbreviations AGA, appropriate for gestational age IUGR, intrauterine growth restricted LGA, large for gestational age GDM, gestational diabetes mellitus PI, pulsatility index FHR, fetal heart rate FBS, fetal blood sampling Leptin is a circulating polypeptide hormone expressed abundantly in the adipose tissue (1) that regulates body weight and energy expenditure through a negative feedback signal between the adipose tissue and the hypothalamic centers of satiety (2). In humans, there is a positive correlation between leptin and body fat content or body mass index (BMI), with a sexual dimorphism in its regulation at the same level of fatness or BMI, and significantly higher concentrations in females than in males (3, 4). Moreover, leptin deficiency is accompanied by reduced fertility in ob/ob female mice and leptin treatment restored fertility along with decreased dietary intake, body weight, and fat mass (5). Recently, these data have been confirmed in a 9-y-old girl with congenital leptin deficiency treated with recombinant leptin that lead to a sustained reduction in body weight and percent body fat, which was associated with an increase in gonadotropin concentrations and pulsatility (6).Leptin concentrations have been measured in cord blood of newborn infants and a significant relationship has been reported with fetal weight (7-11). Both fetal and placental pr...

Introduction Sexual dysfunction is reported in diabetic women (female sexual dysfunction [FSD]). Aim To examine the frequency of FSD in diabetic women, and its clinical or metabolic correlates, through meta-analysis of available studies. Methods We searched in MEDLINE, EMBASE, Cochrane Library, and in reference lists of articles and systematic reviews; we considered human clinical studies published as full articles reporting on FSD in diabetic and control women. In total, we considered 26 studies, including 3,168 diabetic and 2,823 control women. Main Outcome Measures Frequency of FSD and score of Female Sexual Function Index (FSFI) as a function of study size, patient details (age, body mass index [BMI], duration of diabetes, metabolic control [HbA1c], chronic complications, Beck Depression Inventory [BDI] score). Results Frequency of FSD was higher in type 1 (OR [95%CI] 2.27 [1.23, 4.16]), in type 2 diabetes (2.49 [1.55, 3.99]), and in “any diabetes” (type 1 and 2) women (2.02 [1.49, 2.72]) than in controls for any duration of diabetes. FSFI was lower in type 1 (−0.27 [−0.41, −0.12]), in type 2 diabetes (−0.65 [−0.75, −0.54]), and in “any diabetes” women (−0.80 [−0.88, −0.71]) than in controls. Depression was significantly more frequent in diabetic than in control women. At meta-regression only BMI was significantly associated with effect size (P = 0.005). At weighed regression, the only significant association was found between age and FSFI (P = 0.059). The limitations were as follows: only studies of observational nature were available, and heterogeneity was seen among studies. Conclusions FSD is more frequent in diabetic than in control women, but it is still poorly understood; low FSFI is associated with high BMI. Further studies are necessary to better understand risk factors for FSD in diabetic women.