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Childhood obesity is a worldwide health emergency. In many cases, it is directly linked to inappropriate eating habits and a sedentary lifestyle. During lockdown aimed at containing the coronavirus disease (COVID-19) spread, children have been forced to stay at home. The present study aimed at investigating the lifestyles of outpatients (aged 5–17 years) with complicated obesity enrolled in the day-hospital food education program at the Children’s Hospital Bambino Gesù in Rome. A survey was performed based on a structured questionnaire, investigating dietary habits and lifestyles. The questionnaire answers were rated as “yes/no/sometimes” or “often/never/sometimes”. Eighty-eight families correctly completed the questionnaire between March and May 2020. The results highlighted that 85.2% (N = 75) of the patients ate breakfast regularly, and 64.3% (N = 72) consumed fruit as an afternoon snack. However, 21.6% (N = 19) did just “often” home workouts, and 50.0% (N = 44) reported an increase of feeling hungry with “sometimes” frequency. There is a significant relationship of feeling hungry with gender (p < 0.0001) and age (p = 0.048) and, also, between gender with having breakfast (p = 0.020) and cooking (p = 0.006). Living a healthy lifestyle during lockdown was difficult for the outpatients, mainly due to the increase in a sedentary lifestyle and the increase in feeling hungry, but some healthy eating habits were maintained, as advised during the food education program provided before lockdown.

The autism spectrum disorder (ASD) is an etiologically heterogeneous disorder. Dysfunctions of the intermediate metabolism have been described in some patients. We speculate these metabolic abnormalities are associated with brain insulin resistance (IR), i.e., the reduced glucose metabolism at the level of the nervous central system. The Homeostasis model assessment of insulin resistance (HOMA-IR) is very often used in population studies as estimate of peripheral IR and it has been recently recognized as proxy of brain IR. We investigated HOMA-IR in 60 ASD patients aged 4–18 years and 240 healthy controls, also aged 4–18 years, but unmatched for age, sex, body weight, or body mass index (BMI). At multivariable linear regression model, the HOMA-IR was 0.31 unit higher in ASD individuals than in controls, after having adjusted for sex, age, BMI z-score category, and lipids that are factors known to influence HOMA-IR. Findings of this preliminary study suggest it is worth investigating brain glucose metabolism in larger population of patients with ASD by using gold standard technique. The recognition of a reduced glucose metabolism in some areas of the brain as marker of autism might have tremendous impact on our understanding of the pathogenic mechanisms of the disease and in terms of public health.

Aims Insulin resistance (IR) may develop very early in life being associated with occurrence of cardiometabolic risk factors (CMRFs). Aim of the present study was to identify in young Caucasians normative values of IR as estimated by the homeostasis model assessment (HOMA-IR) and cutoffs diagnostic of CMRFs. Methods Anthropometrics and biochemical parameters were assessed in 2753 Caucasians (age 2–17.8 years; 1204 F). Reference ranges of HOMA-IR were defined for the whole population and for samples of normal-weight and overweight/obese individuals. The receiver operator characteristic analysis was used to find cutoffs of HOMA-IR accurately identifying individuals with any CMRF among total cholesterol and/or triglycerides higher than the 95th percentile and/or HDL cholesterol lower than the 5th for age and sex, impaired glucose tolerance, and alanine aminotransferase levels ≥40 U/l. Results Overweight/obese individuals had higher HOMA-IR levels compared with normal-weight peers ( p  < 0.0001) at any age. HOMA-IR index rose progressively with age, plateaued between age 13 and 15 years and started decreasing afterward. HOMA-IR peaked at age 13 years in girls and at 15 years in boys. The 75th percentile of HOMA-IR in the whole population (3.02; AUROC = 0.73, 95 % CI = 0.70–0.75), in normal-weight (1.68; AUROC = 0.76, 95 % CI = 0.74–0.79), and obese (3.42; AUROC = 0.71, 95 % CI = 0.69–0.72) individuals identified the cutoffs best classifying individuals with any CMRF. Conclusions Percentiles of HOMA-IR varied significantly in young Caucasians depending on sex, age, and BMI category. The 75th percentile may represent an accurate cutoff point to suspect the occurrence of one or more CMRFs among high total cholesterol and triglycerides, low HDL cholesterol, and ALT ≥ 40 UI/l.

Childhood obesity is a growing global health concern, with established links to physical activity, nutrition, and, increasingly, to prenatal and perinatal factors. Emerging evidence highlights the significant role of maternal conditions such as obesity, comorbidities, nutrition, and environmental exposures in predisposing offspring to long-term metabolic and cardiovascular diseases. The “Developmental Origins of Health and Disease” (DOHaD) paradigm provides a framework for understanding how early life environmental exposures, particularly during the periconceptional, fetal, and neonatal periods, can program future health outcomes through epigenetic mechanisms. Epigenetic modifications alter gene expression without changing the DNA sequence and are increasingly recognized as key mediators in the development of obesity. This narrative review summarizes current findings on the early determinants of childhood obesity, emphasizing the molecular and epigenetic pathways involved. A comprehensive literature search was conducted across multiple databases and international sources, focusing on recent studies from the past decade. Both human and animal research were included to provide a broad perspective. This review aims to consolidate recent insights into early life influences on obesity, underscoring the need for preventive strategies starting as early as the preconception period.

The formation of reactive oxygen species (ROS) contributes to the pathogenesis and progression of several diseases. Polyphenols have been shown to be beneficial against ROS. The aim of this study was to evaluate the effects of a natural antioxidant ice cream on oxidative stress, vascular function, and physical performance. In this controlled, single-blind, crossover study, 14 healthy individuals were randomized to consume 100 g of either antioxidant ice cream containing dark cocoa powder and hazelnut and green tea extracts or milk chocolate ice cream (control ice cream). Participants were studied at baseline and 2 h after ingesting ice cream. Serum polyphenols, antioxidant status (ferric-reducing ability of plasma [FRAP]), nitric oxide (NOx) bioavailability, markers of oxidative stress (determination of reactive oxygen metabolites [d-ROMs] and hydrogen peroxide [H2O2]), endothelium function (flow-mediated dilation [FMD] and reactive hyperemia index [RHI]), and exercise tolerance (stress test) were assessed, and the double product was measured. Serum polyphenols (P < 0.001), NOx (P < 0.001), FRAP (P < 0.005), FMD (P < 0.001), and RHI (P < 0.05) increased significantly, oxidative stress decreased (d-Roms, P < 0.001; H2O2, P < 0.001), and the double product (P < 0.001) was improved only after antioxidant ice cream ingestion. No changes were found after control ice cream ingestion. To our knowledge, this is the first study to demonstrate that a natural ice cream rich in polyphenols acutely improved vascular function and physical performance in healthy individuals through a reduction in oxidative stress. •To our knowledge, this study is the first to evaluate the antioxidant effect of a natural ice cream.•We discussed new strategies for the primary prevention of cardiovascular diseases.•Antioxidant ice cream is a natural approach to improve vascular function and physical performance.

Non-alcoholic fatty-liver disease (NAFLD) is frequent in obese patients and represents a major risk factor for the development of diabetes and its complications. Bariatric surgery reverses the hepatic features of NAFLD. However, its mechanism of action remains elusive. We performed a comprehensive analysis of the mechanism leading to the improvement of NAFLD and insulin resistance in both obese rodents and humans following sleeve-gastrectomy (SG). SG improved insulin sensitivity and reduced hepatic and monocyte fat accumulation. Importantly, fat accumulation in monocytes was well comparable to that in hepatocytes, suggesting that Plin2 levels in monocytes might be a non-invasive marker for the diagnosis of NAFLD. Both in vitro and in vivo studies demonstrated an effective metabolic regeneration of liver function and insulin sensitivity. Specifically, SG improved NAFLD significantly by enhancing AMP-activated protein kinase (AMPK) phosphorylation and chaperone-mediated autophagy (CMA) that translate into the removal of Plin2 coating lipid droplets. This led to an increase in lipolysis and specific amelioration of hepatic insulin resistance. Elucidating the mechanism of impaired liver metabolism in obese subjects will help to design new strategies for the prevention and treatment of NAFLD.

Purpose The aim of the present review is to analyze dynamic interactions between nutrigenomics, environmental cues, and parental influence, which can all lead to children’s neophobic reactions and its persistence in time. Methods We reviewed studies available on electronic databases, conducted on children aged from birth to 18 years. We also considered official websites of Italian Institutions, providing advice on healthy eating during infancy. Results Modern day societies are faced with an eating paradox, which has severe and ever-growing implications for health. In face of a wider availability of healthy foods, individuals instead often choose processed foods high in fat, salt and sugar content. Economic reasons surely influence consumers’ access to foods. However, there is mounting evidence that food choices depend on the interplay between social learning and genetic predispositions (e.g., individual eating traits and food schemata). Neophobia, the behavioral avoidance of new foods, represents an interesting trait, which can significantly influence children’s food refusal. Early sensory experiences and negative cognitive schemata, in the context of primary caregiver–child interactions, importantly contribute to the priming of children’s food rejection. Conclusions As neophobia strongly affects consumption of healthy foods, it will be relevant to rule definitively out its role in the genesis of maladaptive food choices and weight status in longitudinal studies tracking to adulthood and, in meanwhile, implement early in life effective social learning strategies, to reduce long-term effects of neophobia on dietary patterns and weight status. Level of evidence Level II, controlled trials without randomization.

With the enormous effort that microbiologists are investing in trying to understand the contribution of gut microbiota to human health and disease, a pivotal role of the gut microbiota is emerging as an environmental cue which influences the developmental programming. Epidemiological findings have been supported by experimental evidences in germ-free (GF) mice (mice born and raised in a sterile environment and that are devoid of an enteric bacteria) which demonstrated that exposure to microbial pathogens during vulnerable periods result in behavioral abnormalities, including anxiety-like behavior, impaired cognitive function (Sullivan et al., 2006; Goehler et al., 2008), and more elevated home-cage activity counts than conventionalized animals (Bäckhed et al., 2007). The humans’ internal ecosystem (“human microbiome”) seems to intrude and modify significantly this bidirectional communication starting very early in the life so much to led some to suggest that the brain–gut axis may be more accurately termed “the brain–gut–microbiota axis” (Rhee et al., 2009). [...]the human microbiome may enrich and complicate the control system of energy balance which is already one of the most highly integrated and complex functions of the body; not surprisingly, given its importance. Administration of exogenous glucocorticoids (the equivalent of corticosterone in mice) is known to reduce synaptophysin expression in the fetal brain of non-human primates (Antonow-Schlorke et al., 2003). [...]excessive release of steroids during vulnerable periods of the life can be one of the mechanisms by which gut microbiota modulates HPA neuroplasticity and may, hence, enhance the risk to develop obesity later in adulthood.

Purpose Gestational obesity (GO) presents a multifaceted challenge to maternal and fetal health, with an escalating prevalence and far-reaching consequences extending beyond pregnancy. This perspective statement by the Italian Society of Obesity (SIO) provides current insights into the diagnosis, maternal and fetal impacts, and treatment strategies for managing this pressing condition. Methods This article provides a comprehensive review of the maternal and fetal effects of GO and provides suggestions on strategies for management. Comprehensive review was carried out using the MEDLINE/PubMed, CINAHL, EMBASE, and Cochrane Library databases. Results The diagnosis of GO primarily relies on pre-pregnancy body mass index (BMI), although standardized criteria remain contentious. Anthropometric measures and body composition assessments offer valuable insights into the metabolic implications of GO. Women with GO are predisposed to several health complications, which are attributed to mechanisms such as inflammation and insulin resistance. Offspring of women with GO face heightened risks of perinatal complications and long-term metabolic disorders, indicating intergenerational transmission of obesity-related effects. While nutritional interventions are a cornerstone of management, their efficacy in mitigating complications warrants further investigation. Additionally, while pharmacological interventions have been explored in other contexts, evidence on their safety and efficacy specifically for GO remains lacking, necessitating further investigation. Conclusion GO significantly impacts maternal and fetal health, contributing to both immediate and long-term complications. Effective management requires a multifaceted approach, including precise diagnostic criteria, personalized nutritional interventions, and potential pharmacological treatments. These findings underscore the need for individualized care strategies and further research to optimize outcomes for mothers and their offspring are needed. Enhanced understanding and management of GO can help mitigate its intergenerational effects, improving public health outcomes. Level of evidence : Level V narrative review.

OBJECTIVE:--The purpose of this study was to elucidate the mechanisms of diabetes reversibility after malabsorptive bariatric surgery. RESEARCH DESIGN AND METHODS--Peripheral insulin sensitivity and β-cell function after either intravenous (IVGTT) or oral glucose tolerance (OGTT) tests and minimal model analysis were assessed in nine obese, type 2 diabetic subjects before and 1 month after biliopancreatic diversion and compared with those in six normal-weight control subjects. Insulin-dependent whole-body glucose disposal was measured by the euglycemic clamp, and glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were also measured. RESULTS:--The first phase of insulin secretion after the IVGTT was fully normalized after the operation. The disposition index from OGTT data was increased about 10-fold and became similar to the values found in control subjects, and the disposition index from IVGTT data increased about 3.5-fold, similarly to what happened after the euglycemic clamp. The area under the curve (AUC) for GIP decreased about four times (from 3,000 ± 816 to 577 ± 155 pmol · l⁻¹ · min, P < 0.05). On the contrary, the AUC for GLP1 almost tripled (from 150.4 ± 24.4 to 424.4 ± 64.3 pmol · l⁻¹ · min, P < 0.001). No significant correlation was found between GIP or GLP1 percent changes and modification of the sensitivity indexes independently of the route of glucose administration. CONCLUSIONS:--Restoration of the first-phase insulin secretion and normalization of insulin sensitivity in type 2 diabetic subjects after malabsorptive bariatric surgery seem to be related to the reduction of the effect of some intestinal factor(s) resulting from intestinal bypass.