Diabetes is one of the most common endocrine diseases in children worldwide.¹ For many years, childhood diabetes generally constituted type 1 diabetes (T1D). Recently, the global epidemic of childhood obesity has led to an increasing prevalence of type 2 diabetes (T2D) in children.^1-3 The main underlying factors are obesity and poor lifestyle (eg, sedentary living), and most affected children have a parental history of T2D.^3-6 Obesity, the most prominent risk factor for T2D, requires lifestyle modifications (eg, nutrition and exercise) beginning in childhood.^3,6 The increasing incidence of T2D has not influenced the incidence of T1D, which steadily increases during childhood and adolescence; it is currently 22.9 new cases per 100 000 people younger than 15 years of age per year.⁷ Children with T1D require specialized pediatric diabetes treatment and constant medical care. The increasing incidence of diabetes in children leads to prolonged exposure to hyperglycemia and other metabolic abnormalities; early diabetes onset carries an elevated risk of cardiovascular complications.^8,9 These disease dynamics, which constitute a heavy burden on patients and their families, have become global public health problems.

Aims: We conducted a systematic review and meta-analysis to assess various antidiabetic agents’ association with mortality in patients with type 2 diabetes (T2DM) who have coronavirus disease 2019 (COVID-19).Methods: We performed comprehensive literature retrieval from the date of inception until February 2, 2021, in medical databases (PubMed, Web of Science, Embase, and Cochrane Library), regarding mortality outcomes in patients with T2DM who have COVID-19. Pooled OR and 95% CI data were used to assess relationships between antidiabetic agents and mortality.Results: Eighteen studies with 17,338 patients were included in the meta-analysis. Metformin (pooled OR, 0.69; P=0.001) and sulfonylurea (pooled OR, 0.80; P=0.016) were associated with lower mortality risk in patients with T2DM who had COVID-19. However, patients with T2DM who had COVID-19 and received insulin exhibited greater mortality (pooled OR, 2.20; P=0.002). Mortality did not significantly differ (pooled OR, 0.72; P=0.057) between DPP-4 inhibitor users and non-users.Conclusions: Metformin and sulfonylurea could be associated with reduced mortality risk in patients with T2DM who have COVID-19. Furthermore, insulin use could be associated with greater mortality, while DPP-4 inhibitor use could not be. The effects of antidiabetic agents in patients with T2DM who have COVID-19 require further exploration.Systematic Review Registration: PROSPERO (identifier, CRD42021242898).

We have entered an era of population aging, and many public health problems associated with aging are becoming more serious. Older adults have earlier onset of chronic diseases and suffer more disability. Therefore, it is extremely important to promote active aging and enhance health literacy. These involves full consideration of the need for education and the provision of solutions to problems associated with aging. The development of OAE is an important measure for implementing the strategy of active aging, and curriculum construction is a fundamental component of achieving OAE. Various subjective and objective factors have limited the development of OAE. To overcome these difficulties and ensure both active and healthy aging, the requirements for active aging should be implemented, the limitations of current OAE should be addressed, system integration should be increased, and the curriculum system should be improved. These approaches will help to achieve the goal of active aging. This paper discusses OAE from the perspective of active aging, based on the promotion of health literacy and provides suggestions to protect physical and mental health among older adults, while promoting their social participation. The provision of various social guarantees for normal life in older adults is a new educational concept.

Abdominal aortic aneurysms (AAAs) are typically asymptomatic, and there is a high mortality rate associated with aneurysm rupture. AAA pathogenesis involves extracellular matrix degradation, vascular smooth muscle cell phenotype switching, inflammation, and oxidative stress. There is increasing evidence of excessive adipocyte accumulation in ruptured AAA walls. These excessive numbers of adipocytes in the vascular wall have been closely linked with AAA progression. Perivascular adipose tissue (PVAT), a unique type of adipose tissue, can be involved in adipocyte accumulation in the AAA wall. PVAT produces various chemokines and adipocytokines around vessels to maintain vascular homeostasis through paracrine and autocrine mechanisms in normal physiological conditions. Nevertheless, PVAT loses its normal function and promotes the progression of vascular diseases in pathological conditions. There is evidence of significantly reduced AAA diameter in vessel walls of removed PVAT. There is a need to highlight the critical roles of cytokines, cells, and microRNA derived from PVAT in the regulation of AAA development. PVAT may constitute an important therapeutic target for the prevention and treatment of AAAs. In this review, we discuss the relationship between PVAT and AAA development; we also highlight the potential for PVAT-derived factors to serve as a therapeutic target in the treatment of AAAs.

Background: Compared with typical visceral fat deposits in obesity and metabolic syndrome, perirenal adipose tissue (PRAT) dysfunction is more closely linked to obesity-related chronic kidney disease (OB-CKD). The myokine irisin reportedly promotes positive outcomes in metabolic disease. This study investigated whether irisin could reduce urinary albumin excretion and demonstrate renoprotective effects through the regulation of PRAT function in obese mice. Methods: C57BL/6 J mice received a high-fat diet (HFD) with or without concurrent administration of irisin. Glucose tolerance, plasma levels of free fatty acids, and urinary albumin excretion were assessed, along with renal morphology. The vascular endothelial growth factor and nitric oxide in glomeruli were also analyzed, in addition to PRAT function-associated proteins. Results: Irisin administration significantly reduced the final body weight, fat mass, and free fatty acids, without reducing PRAT mass, in HFD mice. Furthermore, irisin decreased urinary albumin excretion and attenuated both renal fibrosis and lipid accumulation. Irisin administration led to increases in PRAT function-associated proteins, including sirtuin1, uncoupling protein-1, and heme-oxygenase-1. Ex vivo treatment of PRAT and glomeruli with irisin also restored PRAT function. Finally, irisin treatment restored the vascular endothelial growth factor–nitric oxide axis. Conclusions: Irisin attenuated metabolic disorders and protected against OB-CKD by normalizing the PRAT–kidney axis. These results suggest that agents targeting PRAT activation might be useful for treatment of OB-CKD.