Search

Background: Fasting levels of glucagon are known to be elevated in youth and adults with type 2 diabetes mellitus (T2D). Children and adolescents with obesity were previously reported to show increasing fasting and post-glucose-challenge hyperglucagonemia across the spectrum of glucose tolerance, while no data are available in those with impaired fasting glucose (IFG). Materials and methods: Individuals from the Beta-JUDO study population (Uppsala and Salzburg 2010-2016) (n=101, age 13.3 ± 2.8, m/f=50/51) were included (90 with overweight or obesity, 11 with normal weight). Standardized OGTT were performed and plasma glucose, glucagon and insulin concentrations assessed at baseline, 5, 10, 15, 30, 60, 90 and 120 minutes. Patients were grouped according to their glycemic state in six groups with normal glucose metabolism (NGM) and normal weight (NG-NW), NGM with obesity or overweight (NG-O), impaired glucose tolerance (IGT), impaired fasting glucose (IFG), IGT+IFG and T2D, and in two groups with NGM and impaired glucose metabolism (IGM), for statistical analysis. Results and conclusion: Glucagon concentrations were elevated in young normoglycemic individuals with overweight or obesity (NG-O) compared to normoglycemic individuals with normal weight. Glucagon levels, fasting and dynamic, increased with progressing glycemic deterioration, except in IFG, where levels were comparable to those in NG-O. All glycemic groups showed an overall suppression of glucagon during OGTT. An initial increase of glucagon could be observed in T2D. In T2D, glucagon showed a strong direct linear correlation with plasma glucose levels during OGTT. Glucagon in adolescents, as in adults, may play a role in the disease progression of T2D. [ABSTRACT FROM AUTHOR]

Summary: Background: Relationships between movement‐related behaviours and metabolic health remain underexplored in adolescents with obesity. Objectives: To compare profiles of sedentary time (more sedentary, SED+ vs. less sedentary, SED−), moderate to vigorous physical activity (MVPA) time (more active, MVPA+ vs. less active, MVPA−) and combinations of behaviours (SED−/MVPA+, SED−/MVPA−, SED+/MVPA+, SED+/MVPA−) in regard to metabolic health. Methods: One hundred and thirty‐four subjects (mean age 13.4 ± 2.2 yrs, mean body mass index [BMI] 98.9 ± 0.7 percentile, 48.5% females) underwent 24 h/7 day accelerometry, anthropometric, body composition, blood pressure (BP), lipid profile and insulin resistance (IR) assessments. Results: Metabolic health was better in SED− [lower fat mass (FM) percentage (p < 0.05), blood pressure (BP) (p < 0.05), homeostasis model assessment of insulin resistance (HOMA‐IR) (p < 0.001) and metabolic syndrome risk score (MetScore) (p < 0.001), higher high‐density lipoprotein‐cholesterol (HDL‐c) (p = 0.001)] vs. SED+ group and in MVPA+ [lower triglyceridemia (TG), (p < 0.05), HOMA‐IR (p < 0.01) and MetScore (p < 0.001), higher HDL‐c (p < 0.01)] vs. MVPA− group after adjustment with age, gender, maturation and BMI. SED−/MVPA+ group had the best metabolic health. While sedentary (p < 0.001) but also MVPA times (p < 0.001) were lower in SED−/MVPA− vs. SED+/MVPA+, SED−/MVPA− had lower FM percentage (p < 0.05), HOMA‐IR (p < 0.01) and MetScore (p < 0.05) and higher HDL‐c (p < 0.05), independently of BMI. Sedentary time was positively correlated with HOMA‐IR and Metscore and negatively correlated with HDL‐c after adjustment with MVPA (p < 0.05). MVPA was negatively correlated with HOMA‐IR, BP and MetScore and positively correlated with HDL‐c after adjustment with sedentary time (p < 0.05). Conclusion: Lower sedentary time is associated with a better metabolic health independently of MVPA and might be a first step in the management of pediatric obesity when increasing MVPA is not possible. [ABSTRACT FROM AUTHOR]

Background: Nonalcoholic fatty liver disease (NAFLD) is the leading hepatic disease in children, ranging from steatosis to steatohepatitis and fibrosis. Age, sex, hormonal levels, pubertal stages, genetic risk- and epigenetic factors are among the many influencing factors. Appearing predominantly in children with obesity, but not exclusively, it is the liver's manifestation of the metabolic syndrome but can also exist as an isolated entity. Summary: Pediatric NAFLD differs from the adult phenotype. This narrative review on NAFLD in children with obesity provides an overview of the current knowledge on risk factors, screening, and diagnostic methods, as well state-of-the-art treatment. The recent discussion on the proposition of a new nomenclature – Metabolic [Dysfunction-] Associated Liver Disease – is featured, and current gaps of knowledge are discussed. Key Messages: Currently, there is no international consensus on screening and monitoring of pediatric NAFLD. With lifestyle interventions being the cornerstone of treatment, no registered pharmacological treatment for pediatric NAFLD is available. Development and validation of additional noninvasive biomarkers, scores and imaging tools suitable to subcategorize, screen and monitor pediatric patients are necessary. With a variety of upcoming and promising agents, clear recommendations for pediatric nonalcoholic steatohepatitis trials are urgently needed. [ABSTRACT FROM AUTHOR]