Genetics, epigenetics and transgenerational transmission of obesity in children

Sedentary lifestyle and consumption of high-calorie foods have caused a relentless increase of overweight and obesity prevalence at all ages. Its presently epidemic proportion is disquieting due to the tight relationship of obesity with metabolic syndrome and several other comorbidities which do call for urgent workarounds. The usual ineffectiveness of present therapies and failure of prevention campaigns triggered overtime a number of research studies which have unveiled some relevant aspects of obesity genetic and epigenetic inheritable profiles. These findings are revealing extremely precious mainly to serve as a likely extra arrow to allow the clinician's bow to achieve still hitherto unmet preventive goals. Evidence now exists that maternal obesity/overnutrition during pregnancy and lactation convincingly appears associated with several disorders in the offspring independently of the transmission of a purely genetic predisposition. Even the pre-conception direct exposure of either father or mother gametes to environmental factors can reprogram the epigenetic architecture of cells. Such phenomena lie behind the transfer of the obesity susceptibility to future generations through a mechanism of epigenetic inheritance. Moreover, a growing number of studies suggests that several environmental factors such as maternal malnutrition, hypoxia, and exposure to excess hormones and endocrine disruptors during pregnancy and the early postnatal period may play critical roles in programming childhood adipose tissue and obesity. A deeper understanding of how inherited genetics and epigenetics may generate an obesogenic environment at pediatric age might strengthen our knowledge about pathogenetic mechanisms and improve the clinical management of patients. Therefore, in this narrative review, we attempt to provide a general overview of the contribution of heritable genetic and epigenetic patterns to the obesity susceptibility in children, placing a particular emphasis on the mother-child dyad

How painful is a heelprick or a venipuncture in a newborn?

Neonates undergo many painful procedures daily, in particular venipunctures and heelpricks. Our aim was to assess how painful these procedures actually are, and how effective are the common analgesic strategies to blunt this pain.Methods: We performed a MEDLINE/PubMed research from 1999 to 2013. We retrieved all papers in English language that evaluated pain during neonatal heelprick or venipuncture and that used as score the Premature Infant Pain Profile (PIPP), a widely used scale for evaluate acute pain in term and preterm babies.Results: Fifteen papers met the inclusion criteria, using different analgesic methods. Just in one case two studies used the same analgesic method. Most analgesic procedures show a relevant level of pain. We didnt find univocal difference between heelprick and venipuncture. Topic creams, systemic analgesics, posture and oral glucose 10% have scarce analgesic effectiveness. The most effective procedures are the use of oral sweet solutions (sucrose or glucose) at concentrations greater than 20%, multisensory stimulations and non-nutritive sucking used along with 10% glucose.Conclusions: A large amount of analgesic methods was used, making comparisons difficult. Nevertheless, in the absence of analgesic treatment, heelpricks and venipunctures are moderately-severely painful, and among the proposed analgesic procedures, few seem to be effective

Subcutaneous Fat Necrosis in a Newborn after Brief Therapeutic Hypothermia: Ultrasonographic Examination.

A 7-day-old infant developed erythematous indurated plaques on the back, left shoulder, and arm a few days after therapeutic hypothermia. Ultrasonographic study along with Doppler blood flow analysis of lesional skin areas revealed flogistic fat involvement and calcifications. On the basis of clinical appearance, patient history, and ultrasonographic study, a diagnosis of subcutaneous fat necrosis of the newborn was established

Subcutaneous Fat Necrosis in a Newborn after Brief Therapeutic Hypothermia: Ultrasonographic Examination.

8nonenoneTognetti L; Filippou G; Bertrando S; Picerno V; Buonocore G; Frediani B; Fimiani M; Rubegni PTognetti, L; Filippou, Georgios; Bertrando, S; Picerno, V; Buonocore, Giuseppe; Frediani, Bruno; Fimiani, Michele; Rubegni, P

The use of melatonin in hypoxic-ischemic brain damage: an experimental study

Objective: Oxidative stress (OS) plays a key role in perinatal brain damage. The aim of this study is to evaluate the effectiveness of melatonin as a neuroprotective drug by investigating the influence of melatonin on OS and inflammation biomarkers in an animal model of cerebral hypoxia-ischemia. Methods: Five minutes after hypoxic-ischemic (HI) injury melatonin was administered to 28 rats (HI-Mel group). At the same time, 28 hypoxic-ischemic rats were vehicle-treated (V-HI group). Five rats were used as sham operated controls (CTL). OS biomarkers: isoprostanes (IsoPs), neuroprostanes (NPs) and neurofurans (NFs), and microglial activation markers (glial fibrillary acidic protein [GFAP] and monoclonal antirat CD68 [ED1]) were measured in the cerebral cortex of the two lobes. Results: A significant increase of IsoPs on the left lobe was observed in V-HI after 1 hour (h) from HI injury (p < 0.001); a significant increase of NPs on both side (p < 0.05) and a significant increase of NFs on the left (p < 0.05) were also observed in V-HI after 24 h. A significant increase of IsoPs on the left (p < 0.05) and of NPs on both lobes (p < 0.05) were observed in HI-Mel after 48 h. The ED1 and GFAP expression was lower in the HI-Mel brain tissue. Conclusions: Melatonin reduces OS and inflammatory cells recruitment and glial cells activation in cerebral cortex after neonatal HI damage. These results lay the groundwork for future clinical studies in infants