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Hypopituitarism is defined as one or more partial or complete pituitary hormone deficiencies, which are related to the anterior and/or posterior gland and can have an onset in childhood or adulthood. The most common aetiology is a sellar or suprasellar lesion, often an adenoma, which causes hypopituitarism due to tumour mass effects, or the effects of surgery and/or radiation therapy. However, other clinical conditions, such as traumatic brain injury, and autoimmune and inflammatory diseases, can result in hypopituitarism, and there are also genetic causes of hypopituitarism. Furthermore, the use of immune checkpoint inhibitors to treat cancer is increasing the risk of hypopituitarism, with a pattern of hormone defects that is different from the classic patterns and depends on mechanisms that are specific for each drug. Moreover, autoantibody production against the pituitary and hypothalamus has been demonstrated in studies investigating the development or worsening of some cases of hypopituitarism. Finally, evidence suggests that posterior pituitary damage can affect oxytocin secretion. The aim of this Review is to summarize current knowledge on non-classic and emerging causes of hypopituitarism, so as to help clinicians improve early identification, avoid life-threatening events and improve the clinical care and quality of life of patients at risk of hypopituitarism.This Review summarizes current knowledge on non-classic and less common causes of hypopituitarism, such as traumatic brain injury, genetic causes, use of immune checkpoint inhibitors, autoimmune diseases and inflammatory diseases. Furthermore, emerging evidence that posterior pituitary damage can affect oxytocin secretion is highlighted.

Growth hormone (GH) and insulin-like growth factor-1 (IGF-I) are pleiotropic hormones with important roles in lifespan. They promote growth, anabolic actions, and body maintenance, and in conditions of energy deprivation, favor catabolic feedback mechanisms switching from carbohydrate oxidation to lipolysis, with the aim to preserve protein storages and survival. IGF-I/insulin signaling was also the first one identified in the regulation of lifespan in relation to the nutrient-sensing. Indeed, nutrients are crucial modifiers of the GH/IGF-I axis, and these hormones also regulate the complex orchestration of utilization of nutrients in cell and tissues. The aim of this review is to summarize current knowledge on the reciprocal feedback among the GH/IGF-I axis, macro and micronutrients, and dietary regimens, including caloric restriction. Expanding the depth of information on this topic could open perspectives in nutrition management, prevention, and treatment of GH/IGF-I deficiency or excess during life.

Breakfast skipping increases with age, and an association with a high risk of being overweight (OW) and of obesity (OB), cardiometabolic risk, and unhealthy diet regimen has been demonstrated in observational studies with children and adults. Short-term intervention trials in adults reported conflicting results. The purpose of this systematic review was to summarize the association of breakfast skipping with body weight, metabolic features, and nutrition quality in the groups of young people that underwent randomized controlled (RCT) or intervention longitudinal trials lasting more than two months. We searched relevant databases (2000–2021) and identified 584 articles, of which 16 were suitable for inclusion. Overall, 50,066 children and adolescents were included. No studies analyzed cardiometabolic features. Interventions were efficacious in reducing breakfast skipping prevalence when multi-level approaches were used. Two longitudinal studies reported a high prevalence of OW/OB in breakfast skippers, whereas RCTs had negligible effects. Ten studies reported a lower-quality dietary intake in breakfast skippers. This review provides insight into the fact that breakfast skipping is a modifiable marker of the risk of OW/OB and unhealthy nutritional habits in children and adolescents. Further long-term multi-level intervention studies are needed to investigate the relationship between breakfast, nutrition quality, chronotypes, and cardiometabolic risk in youths.

The incidence of traumatic brain injury (TBI) has increased over the last years with an important impact on public health. Many preclinical and clinical studies identified multiple and heterogeneous TBI-related pathophysiological mechanisms that are responsible for functional, cognitive, and behavioral alterations. Recent evidence has suggested that post-TBI neuroinflammation is responsible for several long-term clinical consequences, including hypopituitarism. This review aims to summarize current evidence on TBI-induced neuroinflammation and its potential role in determining hypothalamic-pituitary dysfunctions.

The purposes of this study were to evaluate the differences in Mediterranean diet and its components among primary and secondary school children and adolescents living in northern Italy, and the associations with the weight status. Adherence was assessed by the KIDMED (Mediterranean Diet Quality Index) questionnaire on 669 subjects (6–16 years) attending five schools of Novara. The adherence was poor in 16.7%, average in 63.7%, and high in 19.6% of the students. Poor adherence was more frequent in primary than in secondary schools (20.7% vs. 13.7%, p < 0.04). Some unhealthy behaviors were more prevalent in younger children. Children of other ethnic origins had a mixed behavior, choosing both traditional healthy and unhealthy foods. Besides male gender and primary school, in Italian children, the risk of overweight was directly associated with eating at fast-food restaurants (OR: 1.890, CI 95% 1.002–3.563), and inversely with consumption of vegetables more than once a day (OR: 0.588, CI 95% 0.349–0.991), and olive oil at home (OR: 0.382, CI 95% 0.176–0.826). In children of other ethnic origins, this risk was associated with skipping breakfast (OR: 16.046, CI 95% 1.933–133.266), or consuming commercial baked good or pastries for breakfast (OR: 10.255, CI 95% 1.052–99.927). The overall KIDMED score correlated with height (β: 0.108; p < 0.005). Poor food quality is replacing the Mediterranean dietary pattern in children and adolescents, in particular among younger children. Because the risk of overweight was associated with different components of the Mediterranean diet depending on ethnic origins, tailored nutritional programs remain a need.

The objective of this study was to identify clinical and/or metabolic predictive factors of genetic obesity. Subjects aged ≤ 18 years with obesity (BMI ≥ 97 th percentile) followed-up at the Paediatric Endocrinology Clinic of Maggiore Hospital in Novara, Italy were screened for genes associated with obesity by next-generation sequencing. Anamnestic, anthropometric, and biochemical data were collected, and parents completed two questionnaires, to screen for hyperphagia and daytime sleepiness, respectively. The study included 50 patients. Six genetic variants (6/50 patients,12%) were classified as pathogenic/likely pathogenic, three (3/50 patients,6%) as polygenic, and 16 (13/50 patients,26%) as variants of uncertain clinical significance (VUS). Eight patients carried > 1 variant. All pathogenic mutations were in genes implicated in the hypothalamic melanocortin pathway or responsible for syndromic obesity. All subjects with definitive genetic diagnosis developed obesity before five years of age. There were no statistically significant differences in auxological nor metabolic parameters between the three genetic patterns of absent genetic mutations, VUS, and pathogenic/likely pathogenic mutations. Finally, a Genetic Obesity Risk Score was developed using logistic regression analysis, selecting Hyperphagia Questionnaire score, age of onset of obesity, and family history as variables. Genetic screening of our cohort of children and adolescents with severe obesity revealed pathogenic/polygenic variants in 18% of cases, with PCSK1 the most frequently mutated gene and with a definitive genetic diagnosis in 3 patients. Identifying clinical, behavioral, and metabolic features predictive of genetic obesity would facilitate early diagnosis and tailored management.

Vitamin D plays a pivotal role in the regulation of calcium-phosphorus metabolism, particularly during pediatric age when nutritional rickets and impaired bone mass acquisition may occur. Besides its historical skeletal functions, in the last years it has been demonstrated that vitamin D directly or indirectly regulates up to 1250 genes, playing so-called extraskeletal actions. Indeed, recent data suggest a possible role of vitamin D in the pathogenesis of several pathological conditions, including infectious, allergic and autoimmune diseases. Thus, vitamin D deficiency may affect not only musculoskeletal health but also a potentially wide range of acute and chronic conditions. At present, the prevalence of vitamin D deficiency is high in Italian children and adolescents, and national recommendations on vitamin D supplementation during pediatric age are lacking. An expert panel of the Italian Society of Preventive and Social Pediatrics reviewed available literature focusing on randomized controlled trials of vitamin D supplementation to provide a practical approach to vitamin D supplementation for infants, children and adolescents.

Cachexia is a wasting syndrome associated with cancer, AIDS, multiple sclerosis, and several other disease states. It is characterized by weight loss, fatigue, loss of appetite, and skeletal muscle atrophy and is associated with poor patient prognosis, making it an important treatment target. Ghrelin is a peptide hormone that stimulates growth hormone (GH) release and positive energy balance through binding to the receptor GHSR-1a. Only acylated ghrelin (AG), but not the unacylated form (UnAG), can bind GHSR-1a; however, UnAG and AG share several GHSR-1a-independent biological activities. Here we investigated whether UnAG and AG could protect against skeletal muscle atrophy in a GHSR-1a-independent manner. We found that both AG and UnAG inhibited dexamethasone-induced skeletal muscle atrophy and atrogene expression through PI3Kβ-, mTORC2-, and p38-mediated pathways in myotubes. Upregulation of circulating UnAG in mice impaired skeletal muscle atrophy induced by either fasting or denervation without stimulating muscle hypertrophy and GHSR-1a-mediated activation of the GH/IGF-1 axis. In Ghsr-deficient mice, both AG and UnAG induced phosphorylation of Akt in skeletal muscle and impaired fasting-induced atrophy. These results demonstrate that AG and UnAG act on a common, unidentified receptor to block skeletal muscle atrophy in a GH-independent manner.

Ghrelin gene products—the peptides ghrelin, unacylated ghrelin, and obestatin—have several actions on the immune system, opening new perspectives within neuroendocrinology, metabolism and inflammation. The aim of this review is to summarize the available evidence regarding the less known role of these peptides in the machinery of inflammation and autoimmunity, outlining some of their most promising therapeutic applications.