Melatonin, the hormone of circadian rhythm regulation, is involved in the modulation of mitochondrial activity through its antioxidant and anti-inflammatory properties. Alteration of circadian rhythms such as sleep is related to obesity and metabolic pathogenesis in adulthood, but studies during childhood are scarce. The present study investigated the association of melatonin with metabolic and inflammatory markers in children with (n = 113) and without obesity (n = 117). Melatonin was measured in saliva four and two hours before bedtime, and after one hour of sleep. Cardiometabolic factors, high sensitivity C-reactive protein, immune markers (monocyte chemoattractant protein-1, plasminogen activator inhibitor-1, tumor necrosis α and interferon-γ), leptin and ghrelin were determined. Sleep duration was recorded by a questionnaire. The melatonin level at 1 h after sleep was found to be increased more than twofold in children with obesity (90.16 (57.16–129.16) pg/mL) compared to controls (29.82 (19.05–61.54) pg/mL, p < 0.001) and was related to fat mass (rho = 0.294, p < 0.001); melatonin levels at 1 h after sleep were inversely correlated with high-density lipoprotein cholesterol. Positive correlation was found with apolipoprotein B, adipokines, high sensitivity C-reactive protein, plasminogen activator inhibitor-1 and tumor necrosis factor-α. Shorter sleep duration and earlier waking times were recorded in children with obesity. In conclusion, melatonin in children with obesity appears to be involved in the global metabolic and inflammatory alteration of this condition.

Obesity is a multifactorial disease whose onset and development are shaped by the individual genetic background. The melanocortin 4 receptor gene (MC4R) is involved in the regulation of food intake and energy expenditure. Some of the single nucleotide polymorphisms (SNPs) of this gene are related to obesity and metabolic risk factors. The present study was undertaken to assess the relationship between three polymorphism SNPs, namely, rs17782313, rs17773430 and rs34114122, and obesity and metabolic risk factors. One hundred seventy-eight children with obesity aged between 7 and 16 years were studied to determine anthropometric variables and biochemical and inflammatory parameters. Our results highlight that metabolic risk factors, especially alterations in carbohydrate metabolism, were related to rs17782313. The presence of the minor C allele in the three variants (C–C–C) was significantly associated with anthropometric measures indicative of obesity, such as the body mass and fat mass indexes, and increased the values of insulinemia to 21.91 µIU/mL with respect to the wild type values. Our study suggests that the C–C–C haplotype of the SNPs rs17782313, rs17773430 and rs34114122 of the MC4R gene potentiates metabolic risk factors at early ages in children with obesity.

Despite the rising incidence of osteoporosis (the most common bone disorder) as life expectancy increases worldwide, the genetic and metabolic factors contributing to this multifactorial disease are still poorly understood. This study investigated the role of arginine metabolism in bone formation and its potential for preventing bone loss in postmenopausal osteoporosis. The osteogenic effects of arginine were evaluated in vitro by determining calcium mineral deposition and the expression of marker genes in the human osteoblastic cell line Saos-2. In vivo analyses were conducted in ovariectomized mice treated with arginine, focusing on femoral bone microarchitecture, marker gene expression and serum metabolite profiles. Arginine treatment enhanced calcium deposition and osteoblastic differentiation in vitro. In contrast, however, this treatment had a deleterious effect in vivo, exacerbating trabecular bone loss. These results are particularly relevant given the wide availability of arginine as a dietary supplement, and our findings underscore the necessity of verifying the safety of nutritional supplements in different populations and in the presence of disease.

Prader-Willi syndrome (PWS) is a rare genetic disorder characterized by severe obesity and associated with increased oxidative stress. This phenomenon is partly attributed to elevated levels of reactive oxygen species (ROS), which promote inflammation and metabolic dysfunction, contributing to significant metabolic complications. Growth hormone (GH) treatment is widely used in children with PWS due to its well-documented benefits, including improvements in body composition, motor development, and cognitive function. In this study, we assessed the oxidative stress profile in children with PWS treated with GH. Since obesity and inflammation are well-established contributors to oxidative stress, values obtained from non-syndromic obese patients were included as a reference, allowing the findings to be contextualized within the framework of oxidative stress. The study included 12 GH-treated PWS children with a mean age of 15 years and 11 non-syndromic obese patients with a mean age of 14 years. Flow cytometry was employed as the primary method to analyse markers of oxidative stress, inflammation, and mitochondrial function in both groups. Additionally, this technique enabled the identification of immune cell populations associated with chronic inflammation, acute inflammation, and immune response, providing a comprehensive understanding of the underlying mechanisms. Despite PWS children having 4- to 6-fold lower glutathione (GSH) levels, PWS children demonstrated 2- to 3.5-fold higher mitochondrial activity, increasing their antioxidant capacity and reducing lipid peroxidation and protein carbonylation by up to 2-fold compared to non-syndromic obese children. GH-treated PWS children also showed lower mitochondrial dysfunction under oxidative conditions, higher cell viability, and elevated inflammatory biomarkers, suggesting a link to senescence and premature ageing. GH-treated PWS children, despite being non-obese, exhibited higher systemic inflammation compared to the non-syndromic obese group, alongside significant differences in oxidative stress and inflammatory markers. These findings suggest that mitochondrial pathways may play a role in antioxidant responses in PWS, highlighting the complexity of oxidative stress and its potential contribution to premature ageing in this condition. Understanding these mechanisms and the role of GH treatment could inform the development of targeted therapies to better manage oxidative stress and inflammation, ultimately improving the quality of life for PWS children.

La apendicitis aguda, es una emergencia quirúrgica en pediatría. Un diagnóstico preciso, apoyado en nuevos biomarcadores podría disminuir las complicaciones asociadas. Objetivo: Valorar la utilidad de biomarcadores en sangre y orina en el diagnóstico de apendicitis aguda en pediatría. Pacientes y Método: Estudio observacional analítico prospectivo de casos y controles, realizado en un centro entre 2019-2022. La población estudiada estuvo compuesta por 160 niños de entre 0 y 15 años, divididos en dos grupos (80 niños con apendicitis aguda y 80 sin apendicitis aguda), que consultaron por dolor abdominal sugestivo de abdomen agudo, evaluados con analítica y ecografía para su diagnóstico. Se evaluaron marcadores en sangre (proteína C reactiva (PCR), índice neutrófilo linfocito (INL), proadrenomedulina (PADM), pentraxina 3 (PTX3), factor de necrosis tumoral alfa (TNF-alfa), interleucina 6 (IL6) y orina (alfa-2-glicoproteina rica en leucina (A2GRL). Se estimaron modelos de regresión logística binaria simple para estudiar su asociación con variables analizadas, estimación de un modelo múltiple con método de entrada paso a paso y consiguiente obtención de OR ajustados y construcción de curvas ROC. Consideramos como significativo un p < 0,05. Resultados: Comparado con controles, el recuento de leucocitos (AUC 0.829), neutrófilos (AUC 0.836) e INL (AUC 0,797) fueron significativamente superiores en el grupo apendicitis (p < 0,001), mientras que la elevación TNF-alfa (AUC 0,959) redujo la predicción de apendicitis, sin diferencias en los otros biomarcadores analizados. Conclusiones: Los valores de leucocitos, neutrófilos, INL y TNF-alfa son los que mejor discriminan apendicitis aguda de otras causas de dolor abdominal.