Purpose: The increasing prevalence of type 2 diabetes (T2D) among adolescents and young adults (AYAs) is a major public health concern worldwide. This pilot study evaluated the effectiveness of lifestyle education in managing T2D in obese AYAs using continuous glucose monitoring (CGM) and smartwatch-derived lifelog data. Methods: Seven obese AYAs and T2D aged 12–19 years were enrolled in this prospective interventional study. Patients continued to take their previously prescribed T2D medication. CGM data were collected for 10 days, followed by lifestyle education using CGM and smartwatch data. Outcomes, including anthropometrics, glycemic control, dietary intake, physical activity, and self-management skills, were reassessed after an additional 10 days. Results: The median time in range increased from 58.1% (53.2%–75%) to 72% (64%–88%) (p=0.043) and time above range (>250 mg/dL) decreased from 10% (2.9%–18.6%) to 3.0% (1.0%–11.0%) (p=0.028). Median peak total caloric intake decreased from 2,854 (2,465–3,040) kcal/day to 2,091 (1,751–2,283) kcal/day and walking calorie expenditure increased from 163.9 (116.7–321.3) kcal/day to 180.2 (165.3–492.4) kcal/day (p=0.018 for both). The Summary of Diabetes Self-Care Activities score improved from 0.29 (0.05–0.43) to 0.33 (0.32–0.68) (p=0.043). Conclusion This integrated approach combining CGM and smartwatch-based education exhibited short-term effects on glycemic control, dietary habits, physical activity, and self-management skills in obese AYAs and T2D. Further studies are needed to confirm the long-term effectiveness of this strategy in this challenging population.

Obesity is pervasive from infancy to adulthood and presents a major challenge to healthcare systems worldwide. In children and adolescents, the prevalence of overweight and obesity continues to increase, especially in classes II and III, and in younger toddlers and preschool-aged children. Childhood obesity may be associated with comorbidities in all organ systems and increased cardiovascular risk, as it tracks into adolescent and adult obesity. Although intensive health and behavior lifestyle treatments form the foundation of obesity treatment, there are limitations in the extent and maintenance of weight loss with lifestyle modifications alone. The offering of obesity pharmacotherapy in adjunct to intensive lifestyle treatment in children aged > 12 years may improve outcomes in pediatric obesity. In this review, we discuss currently approved medications for childhood and adolescent obesity, focusing on orlistat, phentermine monotherapy, glucagon-like peptide-1 receptor agonists (liraglutide and semaglutide injections), and phentermine/topiramate combination.

Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.

Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.

Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.

Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.

Purpose: Hypothalamic damage may increase the risk of adulthood obesity and cardiovascular disease in patients with craniopharyngioma. We evaluated the effects of hypothalamic involvement (HI) and growth hormone (GH) discontinuation on cardiovascular risk factors during the transition period in patients with childhood-onset craniopharyngioma. Methods: Thirty-three patients (17 males, 16 females) underwent retesting for adult GH deficiency (GHD) between 2005 and 2020 at Seoul National University Children's Hospital. Postoperative HI was graded by Puget's criteria and data regarding GH replacement were collected. At retesting, body mass index (BMI), fasting blood glucose, insulin, high-density lipoprotein cholesterol (HDL-C), triglycerides, and blood pressure were assessed. Results: The mean age of commencement and discontinuation of GH replacement for childhood GHD was 10.0±3.6 and 15.3±3.1 years, respectively. The mean age at retesting for adult GHD was 17.7±2.5 years. When patients were categorized by post-GH discontinuation duration, those with durations >6 months (n=27) showed lower HDL-C levels than those with <6 months (P=0.037). Patients with extensive HI (n=16) had higher BMI z-scores than did those with no HI or mild HI (P=0.020). Both the extent of HI and longer post-GH discontinuation duration were significantly predictive for decreased HDL-C levels (P<0.05, for both). Conclusion The extent of HI and GH discontinuation duration during the transition period can increase cardiovascular risks in patients with childhood-onset craniopharyngioma.

BACKGROUND: AND PURPOSE: The aim of this study was to determine the diagnostic performance and safety of a new ¹⁸F-labeled amyloid tracer, ¹⁸F-FC119S. METHODS: This study prospectively recruited 105 participants, comprising 53 with Alzheimer's disease (AD) patients, 16 patients with dementia other than AD (non-AD), and 36 healthy controls (HCs). In the first screening visit, the Seoul Neuropsychological Screening Battery cognitive function test was given to the dementia group, while HC subjects completed the Korean version of the Mini Mental State Examination. Individuals underwent ¹⁸F-FC119S PET, ¹⁸F-fluorodeoxyglucose (FDG) PET, and brain MRI. The diagnostic performance of ¹⁸F-FC119S PET for AD was compared to a historical control (comprising previously reported and currently used amyloid-beta PET agents), ¹⁸F-FDG PET, and MRI. The standardized uptake value (SUV) ratio (ratio of the cerebral cortical SUV to the cerebellar SUV) was measured for each PET data set to provide semiquantitative analysis. All adverse effects during the clinical trial periods were monitored. RESULTS: Visual assessments of the ¹⁸F-FC119S PET data revealed a sensitivity of 92% and a specificity of 84% in detecting AD. ¹⁸F-FC119S PET demonstrated equivalent or better diagnostic performance for AD detection than the historical control, ¹⁸F-FDG PET (sensitivity of 80.0% and specificity of 76.0%), and MRI (sensitivity of 98.0% and specificity of 50.0%). The SUV ratios differed significantly between AD patients and the other groups, at 1.44±0.17 (mean±SD) for AD, 1.24±0.09 for non-AD, and 1.21±0.08 for HC. No clinically significant adverse effects occurred during the trial periods. CONCLUSIONS ¹⁸F-FC119S PET provides high sensitivity and specificity in detecting AD and therefore may be considered a useful diagnostic tool for AD.

Purpose: To determine the metabolic influence of the traditional Korean diet (K-diet), which has been regarded as a healthy diet, we investigated the profile of urine organic acids that are intermediates of various types of metabolism including energy metabolism. Methods: Ten women aged 50–60 years were recruited and randomly divided into 2 diet groups, K-diet and control diet, the latter of which is a Westernized Korean diet that is commonly consumed by Koreans nowadays. Before and after the 2-week intervention, 46 urine organic acids were determined using LC/MS/MS, along with clinical parameters. Results: The average concentrations of succinate (4.14 ± 0.84 μg/mg creatinine vs. 1.49 ± 0.11, p = 0.0346) and hydroxymethylglutarate (3.67 ± 0.36 μg/mg creatinine vs. 2.97 ± 0.29, p = 0.0466), both of which are intermediates of energy metabolism, decreased in the K-diet group after the 2-week intervention, but these were not observed in the control diet group. In particular, the average concentration of succinate in the K-diet group was lower than that in the control group (3.33 ± 0.56 μg/mg creatinine vs. 1.49 ± 0.11, p = 0.0284) after 2 weeks. The concentrations of two tryptophan metabolites, 5-hydroxyindolacetate (3.72 ± 0.22 μg/mg creatinine vs. 3.14 ± 0.21, p = 0.0183) and indican (76.99 ± 8.35 μg/mg creatinine vs. 37.89 ± 10.06, p = 0.0205) also decreased only in the K-diet group. After the 2-week intervention, the concentration of kynurenate, another tryptophan metabolite, was lower in the K-diet group than that in the control diet group (3.96 ± 0.51 μg/mg creatinine vs. 2.90 ± 0.22, p = 0.0356). Interestingly, the urine level of kynurenate was positively correlated with BMI (r = 0.61424, p = 0.0003) and total cholesterol (r = 0.46979, p = 0.0088), which decreased only in the K-diet group (239.40 ± 15.14 mg/dL vs. 198.20 ± 13.25, p = 0.0163). Conclusion The K-diet alters the urinary excretion of organic acids involved in energy metabolism and tryptophan metabolism, suggesting the influence of the K-diet on these types of metabolism. Urine organic acids changed by the K-diet may serve as biomarkers in future studies.

Over the last decades, the onset of puberty in girls has occurred earlier, but the tempo of pubertal progression has been relatively slower, resulting in a younger age at puberty onset without a change in age at menarche. Sufficient energy availability and adiposity contribute to early pubertal development, and environmental factors, such as endocrine-disrupting chemicals (EDCs), may affect not only the control of energy balance, but also puberty and reproduction. EDCs are hormonally active substances that can perturb puberty by acting both peripherally on target organs, such as adipose tissue or adrenal glands, and/or centrally on the hypothalamic-pituitary-gonadal (HPG) axis. Depending on whether the exposure takes place earlier during fetal and neonatal life or later during early childhood, EDCs can lead to different outcomes through different mechanisms. Evidence of associations between exposures to EDCs and altered pubertal timing makes it reasonable to support their relationship. However, human epidemiologic data are limited or inconsistent and cannot provide sufficient evidence for a causal relationship between EDC exposure and changes in pubertal timing. Further investigation is warranted to determine the overall or different effects of EDCs exposure during prenatal or childhood windows on pubertal milestones and to reveal the underlying mechanisms, including epigenetic marks, whereby early-life exposure to EDCs affect the HPG-peripheral tissue axis.
Adipose Tissue ; Adiposity ; Adolescent ; Adrenal Glands ; Endocrine Disruptors ; Epigenomics ; Female ; Humans ; Menarche ; Puberty ; Reproduction