Laura Perrone

The Italian Consensus Position Statement on Diagnosis, Treatment and Prevention of Obesity in Children and Adolescents integrates and updates the previous guidelines to deliver an evidence based approach to the disease. The following areas were reviewed: (1) obesity definition and causes of secondary obesity; (2) physical and psychosocial comorbidities; (3) treatment and care settings; (4) prevention. The main novelties deriving from the Italian experience lie in the definition, screening of the cardiometabolic and hepatic risk factors and the endorsement of a staged approach to treatment. The evidence based efficacy of behavioral intervention versus pharmacological or surgical treatments is reported. Lastly, the prevention by promoting healthful diet, physical activity, sleep pattern, and environment is strongly recommended since the intrauterine phase.

A1 Preterm and low birth weight nutrition in the first month life: implications for the outcome Massimo Agosti A2 Behind human milk and breastfeeding: not only food, not only growth Carlo Agostoni A3 To prevent obesity: importance and issues of cultural adaptation from weaning to 3 years of age Serge Chalons A4 Diet before and during pregnancy and child health: lessons from animal models Pascale Chavatte-Palmer A5 Infant nutrition: an opportunity to optimize future health José Manuel Moreno Villares A6 Complementary feeding strategies to facilitate acceptance of fruits and vegetables Sophie Nicklaus A7 Diet of young children in the Mediterranean region Luís Pereira-da-Silva A8 Proposal of 10 good practices to help prevent obesity in the first 1,000 days Angelo Pietrobelli, the MeNu Group A9 Macronutrient intakes in early life and subsequent risk of obesity Marie Françoise Rolland-Cachera A10 The burden of childhood obesity in Italy and the results of Nutrintake study Gian Vincenzo Zuccotti A11 Growth body composition and growth hormone therapy: linear growth Marco Cappa A12 Early nutrition pattern and late metabolic consequences Manuela Caruso-Nicoletti A13 Nutrition and Insulin-like Growth Factor (IGF) System Elena Inzaghi, Stefano Cianfarani A14 Nutrition of preterm infants Mario De Curtis A15 Early nutrition patterns and later metabolic outcomes- I part: Genetic and metabolic mechanisms Laura Guazzarotti A16 Diagnosis of metabolic disease by imaging techniques Lorenzo Iughetti A17 Nutrition, growth and cardiovascular diseases Francesco Chiarelli, Laura Comegna, Simone Franchini A18 Body fat mass and gender Laura Perrone, Giuseppina Rosaria Umano A19 Lifestyle interventions for an appropriate birth weight Elisabetta Petrella, Raffaele Bruno, Valentina Bertarini, Giulia Pedrielli, Isabella Neri, Fabio Facchinetti A20 Nutrition, growth and body composition Flavia Prodam A21 Nation-specific reference growth charts in the daily practice Alessandro Sartorio, John M. H. Buckler, Nicoletta Marazzi A22 Growth patterns in inflammatory bowel diseases (IBD) and in cystic fibrosis (CF) Maria E. Street, Viviana D. Patianna, Paola Accorsi, Sara Lo Scocco, Sergio Amarri A23 Newborn in the digital era and their body feeling: physical exercise to counteract hyperphagia Alberto Pellai A24 Nutrition, young athletes and effects of exercise. Practical suggestions Giampiero Merati A25 Physical exercise as a way to prevent criminality in minors and teenagers Isabella Merzagora A26 The measurement of daily energy expenditure in children. Evaluation of a new wrist portable device vs breath-by-breath metabolimeter Susanna Rampichini, Arsenio Veicsteinas A27 Probiotic and inflammasomes Mario Clerici A28 Probiotics and newborns Paolo Manzoni, Elena Tavella, Elena Boano, Daniele Farina A29 Relationship between gut microbiota and obesity Fabio Pace

Obesity and iron deficiency (ID) are two of the most common nutritional disorders in the world. In children both conditions deserve particular attention. Several studies revealed an association between obesity and iron deficiency in children and, in some cases, a reduced response to oral supplementation. The connecting mechanism, however, is not completely known. This review is focused on: (1) iron deficiency in obese children and the role of hepcidin in the connection between body fat and poor iron status; (2) iron status and consequences on health, in particular on cognitive function; (3) cognitive function and obesity; (4) suggestion of a possible link between cognitive dysfunction and ID in pediatric obesity; and implications for therapy and future research.

The mycotoxin zearalenone exhibits estrogenic and anabolic properties in several animal species, humans included. Food contamination by zearalenone is caused either by direct contamination of grains, fruits, and their based-products or by “carry-over” of mycotoxins in animal tissues, milk, and eggs after intake of contaminated feedstuff. Now, a survey on zearalenone contamination in breast milk of healthy primiparous women living in the Naples countryside was conducted. From 47 healthy primiparous women, breast milk samples were collected within the first six weeks after delivery as well as clinical data of mother–newborn pairs. Breast milk analyses were performed with both competitive indirect enzyme-linked immunosorbent assay and high-performance liquid chromatography with fluorescence detection. At 36.9 ± 2.6 days after vaginal delivery, the mean zearalenone contents of the breast milk samples were 1.13 ± 0.34 µg/L. The zearalenone levels correlated with both mother weights before pregnancy (r = −0.506; P < 0.001) and at delivery (r = −0.351; P < 0.05). The present results indicate that breast milk may be contaminated with zearalenone.

Central precocious puberty (CPP) is often familial but its genetic cause is largely unknown. Very recently, the makorin RING finger protein 3 (MKRN3) gene, located on chromosome 15 in the Prader-Willi syndrome (PWS)-associated region (15q11-q13), has been found mutated in 5 families with familial precocious puberty. The MKRN3 is a maternal imprinted gene and the phenotype is expressed only when the MKRN3 mutations are localized on the allele inherited from the father. The function of this gene is not completely known and the phenotype caused by its defect is not yet fully elucidated. We report a new MKRN3 mutation (Pro160Cysfs*14) causing familial CPP. The index case is a 7 years old girl showing Tanner stage 3 and pubic hair stage 1. Her bone age evaluated by TW2 method was 10.3 years. Her hormonal data confirmed the diagnosis of central precocious puberty. Familial medical history revealed precocious puberty in a cousin on paternal side. Paternal grandmother had menarche at the age of 9 years and 6 months and premature menopause when she was 36 years old. Genetic analysis revealed a new mutation (c477_485del; Pro160Cysfs*14) in the maternally imprinted MKRN3. Puberty onset was at 5 years in the other affected female family member. Precocious puberty was well controlled by pharmacological therapy. We expand the number of the MKRN3 mutations associated with CPP and highlight the importance of an accurate family medical history to disclose the peculiar pattern of inheritance of this gene.

Context: Studies examining vitamin D levels in association with childhood obesity usually do not consider the effect of insulin on vitamin D-binding protein and do not calculate the unbound, bioavailable vitamin D. Objective: To evaluate in a group of children i) the concentrations of both total 25-hydroxyvitamin D and bioavailable fraction ii) the potential role of insulin resistance in modulating the concentrations of bioavailable vitamin D. Design: Cross-sectional study. Setting: University Pediatric Department. Patients or Other Participants: Sixty-three obese children and 21 lean controls were enrolled. Main Outcome Measures: Total 25-hydroxyvitamin D and vitamin D-binding protein were measured, two SNPs in the coding region of the vitamin D-binding protein (rs4588 and rs7041) were studied and the vitamin D bioavailable fraction was calculated. Results: Obese children showed total 25-hydroxyvitamin D levels lower compared to not-obese children (21.3 ±- 6.7 ng/ml vs. 29.6 ±- 11.7 ng/ml; p: 0.0004). Bi...

Objectives: Studies of adults and children with celiac disease have reported an increased risk of overweight during gluten‐free diet (GFD). The fat mass and obesity‐associated gene (FTO) variant rs9939609 has been associated with increased risk of developing obesity in children and adults.Methods: In our study, we analyzed the effect of this variant on weight gain in a cohort of 280 children with celiac disease on GFD.Results: We found that after a mean follow‐up time of 3.0 years on GFD, FTO polymorphism influenced significantly the mean change in body mass index z score (P = 0.01).Conclusions: We conclude that the FTO gene contributes to determine weight changes in children with celiac disease on GFD.

The prevalence of obesity is increasing among children/adolescents. Subtle cardiovascular abnormalities, responsible for a higher mortality later in life, have been reported in obese children/adolescents. The aims of the study were to evaluate cardiovascular autonomic regulation, by means of spectrum analysis of R-R interval variability, and myocardial function, by means of standard and tissue Doppler echocardiography, in a group of non-hypertensive asymptomatic obese children and adolescents; furthermore, the influence of insulin resistance was tested. R-R interval variability was analyzed during both the 70° head-up tilt and 24-hour electrocardiographic holter monitoring. Spectrum analysis of R-R interval variability provided the indices of sympathetic (low frequency [LF_RR]) and vagal (high frequency [HF_RR]) modulation of the sinoatrial node. Homeostasis model assessment of insulin resistance (HOMA-IR) was used to classify obese children/adolescents (n=72) as insulin resistant (n=37) and non-insulin resistant (n=35). In obese subjects: a) left ventricular mass was significantly (pRR was lower, and the LF_RR/HF_RR ratio was higher; c) during tilting, magnitude of tilt-induced inhibition of HF_RR was lower; d) during 24-hour electrocardiographic holter monitoring, LF_RR and the LF_RR/HF_RR ratio were higher, whereas HF_RR was lower; e) HOMA-IR inversely correlated with both the e'/a' ratio (r=-0.655; pRR/HF_RR ratio (r=-0.933; pRR/HF_RR ratio (r=0.501; pRR at rest, magnitude of tilt-induced HF_RR reduction, and the e'/a' ratio in insulin resistant obese children/adolescents were markedly lower when compared with the remaining subjects. Subclinical abnormalities of myocardial function and of cardiac autonomic regulation were closely associated in obese children/adolescents and both correlated with the degree of insulin resistance.

Summary: Background: The Glu167Lys (E167K) transmembrane 6 superfamily member 2 (TM6SF2) variant has been associated with liver steatosis, high alanine transaminase (ALT) levels and reduced plasma levels of liver‐derived triglyceride‐rich lipoproteins.Objectives: The objectives of this study were to investigate in a group of obese children the association among the 167K allele of TM6SF2 gene and ALT, cholesterol and triglycerides levels, and hepatic steatosis, and to evaluate the potential interaction between this variant and the I148M patatin like phospholipase 3 gene (PNPLA3) polymorphism on liver enzymes.Methods: We genotyped 1010 obese children for TM6SF2 E167K and PNPLA3 I148M polymorphisms. Anthropometrical and biochemical data were collected. Ultrasound imaging of the liver was performed.Results: The 167K allele showed an association with steatosis (P < 0.0001), higher ALT levels (P < 0.001) and lower total cholesterol (P < 0.00001), low‐density lipoprotein cholesterol (P < 0.0001), triglycerides (P = 0.02) and non‐high‐density lipoprotein cholesterol levels (P < 0.000001). The subjects homozygous for the PNPLA3 148M allele carrying the rare variant of TM6SF2 showed an odds ratio of 12.2 (confidence interval 3.8–39.6, P = 0.000001) to present hypertransaminasaemia compared with the remaining patients.Conclusion: Although the TMS6SF2 E167K variant predisposes the obese children to non‐alcoholic fatty liver disease, there is an association between this variant and lower levels of cardiovascular risk factors. Overall, the data suggest differential effects of TMS6SF2 E167K variant on liver and heart health.