Surgical treatment of craniopharyngioma often leads to a rapid and dramatic weight gain, leading to hypothalamic obesity. Treatment focused on the diet, physical activity, and different types of drugs have very often provided unsatisfactory results. To date, no data have been reported on hypothalamic obesity (HO) regarding the use of semaglutide, a novel type 1 receptor glucagon-like peptide-1 agonist, to limit body weight gain after surgical removal of a neoplasm, despite its already documented efficacy in obesity treatment. In this case report, we tested semaglutide in an 18-year-old patient with HO induced by a surgical intervention for craniopharyngioma. A very favorable treatment response was found in terms of body weight reduction and improvement in metabolic parameters. Our patient lost more than than 30 kg after only 6 months of therapy, which has never been reported before in the literature on HO.

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.

Endometrial cancer (EC) is the most prevalent gynecological cancer in high‐income countries. Its incidence is skyrocketing due to the increase in risk factors such as obesity, which represents a true pandemic. This study aimed to evaluate microRNA (miRNA) expression in obesity‐related EC to identify potential associations between this specific cancer type and obesity. miRNA levels were analyzed in 84 EC patients stratified based on body mass index (BMI; ≥30 or <30) and nine noncancer women with obesity. The data were further tested in The Cancer Genome Atlas (TCGA) cohort, including 384 EC patients, 235 with BMI ≥30 and 149 with BMI <30. Prediction of miRNA targets and analysis of their expression were also performed to identify the potential epigenetic networks involved in obesity modulation. In the EC cohort, BMI ≥30 was significantly associated with 11 deregulated miRNAs. The topmost deregulated miRNAs were first analyzed in 84 EC samples by single miRNA assay and then tested in the TCGA dataset. This independent validation provided further confirmation about the significant difference of three miRNAs (miR‐199a‐5p, miR‐449a, miR‐449b‐5p) in normal‐weight EC patients versus EC patients with obesity, resulting significantly higher expressed in the latter. Moreover, the three miRNAs were significantly correlated with grade, histological type, and overall survival. Analysis of their target genes revealed that these miRNAs may regulate obesity‐related pathways. In conclusion, we identified specific miRNAs associated with BMI that are potentially involved in modulating obesity‐related pathways and that may provide novel implications for the clinical management of obese EC patients.