Purpose of reviewChildhood obesity is a pandemic generating an enormous individual and socioeconomic burden worldwide. This narrative review summarizes recent evidence on successful and recommended prevention strategies according to age groups and different levels of interventions. Recent findingsEffective prevention of childhood obesity is feasible and most successful early in life up to preschool age, and it should include a multicomponent approach, integrating individuals, family and society. Trials that improve nutrition and/or enhance physical activity are the cornerstones of childhood obesity prevention on an individual level. However, their efficacy is determined by the combination of interventions for the target age group. Further, improving family support and sleep, as well as reducing screen time, lead to favourable results. Many research gaps remain, including a lack of effective interventions for high-risk groups.

Until recently, glucagon was considered a mere antagonist to insulin, protecting the body from hypoglycemia. This notion changed with the discovery of the liver-alpha cell axis (LACA) as a feedback loop. The LACA describes how glucagon secretion and pancreatic alpha cell proliferation are stimulated by circulating amino acids. Glucagon in turn leads to an upregulation of amino acid metabolism and ureagenesis in the liver. Several increasingly common diseases (e.g., non-alcoholic fatty liver disease, type 2 diabetes, obesity) disrupt this feedback loop. It is important for clinicians and researchers alike to understand the liver-alpha cell axis and the metabolic sequelae of these diseases. While most of previous studies have focused on fasting concentrations of glucagon and amino acids, there is limited knowledge of their dynamics after glucose administration. The authors of this systematic review applied PRISMA guidelines and conducted PubMed searches to provide results of 8078 articles (screened and if relevant, studied in full). This systematic review aims to provide better insight into the LACA and its mediators (amino acids and glucagon), focusing on the relationship between glucose and the LACA in adult and pediatric subjects.