In pregnant women without a history of thyroid dysfunction, lower concentrations of fT4 and a higher conversion of fT4 to fT3, as inferred by changes in the fT3-to-fT4 ratio, were found to be associated with a less favorable metabolic phenotype and with more placental growth.

Objective: The fat mass and obesity-associated gene (FTO) participates in the control of postnatal weight gain. We assessed whether FTO is expressed in human placenta and whether such expression relates to prenatal weight gain and to the rs9939609 single nucleotide polymorphism (SNP) in FTO. Design and subjects: In a birth cohort study, placentas from women (n ¼ 147) with an uncomplicated, singleton, term pregnancy were weighed at delivery. Real-time PCR was used to study, in placental tissue, the expression of FTO and of housekeeping genes (TATA box binding protein and succinate dehydrogenase complex, subunit A) and to genotype the rs9939609 SNP in FTO. Weights and lengths of the newborns were measured; circulating insulin and insulin-like growth factor-I (IGF-I) were quantified in cord blood. Results: FTO was highly expressed in placenta and was associated with increased fetal weight and length (Po0.001 to Po0.0001). Maternal parity showed an interaction (Po0.001) in the association between placental FTO expression and placental weight. Placental FTO mRNA expression was associated with increased fetal-to-placental weight ratio (Po0.005) in infants from primiparous women, and was associated with increased fetal weight and length and placental weight (Po0.001 to Po0.0001) in infants from nonprimiparous women. These associations were not explained by either cord insulin or IGF-I. Placental FTO expression was unrelated to placental FTO rs9939609 SNP Conclusion: FTO is expressed in the human placenta. In a maternal parity-dependent manner, placental FTO may participate either in the control of fetal weight gain or in the partitioning between placental and fetal growth.

Omentin‐1 is a recently recognized adipokine primarily originating in visceral adipose tissue. We posited that circulating omentin‐1 could be an early marker of metabolic dysfunction. To this end, we examined the associations between circulating omentin‐1, body fat (bioelectric impedance), an endocrine‐metabolic profile (homeostasis model assessment for insulin resistance (HOMAIR), serum lipids, high‐molecular‐weight (HMW) adiponectin and blood pressure (BP)) and family history of obesity and diabetes in asymptomatic prepubertal children (n = 161; 77 boys and 84 girls; age 7 ± 1 year) with a normal distribution of height and weight. Increased circulating omentin‐1 was associated with a poorer metabolic profile, with relatively higher HOMAIR, fasting triacylglycerol, BP and familial prevalence of diabetes (all P < 0.005 to P < 0.0001), and relatively lower fraction of HMW adiponectin (P < 0.005), whereas no relationship was found with body weight or fat or with family history of obesity. All these associations were independent of age, gender and fat mass. In conclusion, circulating omentin‐1 may become a marker of metabolic dysfunction integrating insulin sensitivity, markers of adipose‐tissue metabolism and BP as early as in prepubertal childhood.

SFRP5 and WNT5A comprise a balanced duo that may regulate metabolic homeostasis in prepubertal children.

By age 7, common variations in FTO, TMEM18 and NRXN3 influence the vulnerability to metabolic complications of sleep deprivation. Further genetic studies are warranted to replicate these findings in other populations.