Pediatric diabetes management remains challenging, as many young patients struggle to hit glycemic targets due to developmental factors and treatment burdens. Smart insulin pens are a game-changing "connected MDI" alternative, with "pump-like" features such as bolus calculators and automated Insulin-on-Board tracking for non-pump users. This review explores the clinical effectiveness, economic impact, and prospects of SIPs in pediatrics, including patient and caregiver insights and long-term effects on glycemic control. Caregivers and patients agree SIPs are accessible and easy to use due to user-friendly interfaces, data-driven approaches, and remote monitoring. Evidence shows SIPs improve safety and adherence, with a 31.4% reduction in daily hypoglycemia, a 24.4% decrease in nocturnal hypoglycemia, and a drop in Time Below Range Level 2 from 2.82% to 2.18%. By tracking insulin-on-board, SIPs prevent insulin stacking and enable safe correction doses; users correcting within three hours of a previous dose spend more time in range without increased hypoglycemia. SIPs also cut missed boluses by up to 43% in youth. Economically, SIPs save about SEK 124,270 per patient by delaying complications. However, adoption remains limited due to socioeconomic barriers, with 82% of clinics citing insurance issues and lower use among Medicaid beneficiaries. Barriers include the learning curve and device costs, which can be addressed through subsidies and training programs. Future AI developments, like hypoglycemia prediction, promise to further personalize pediatric care. Overall, SIPs benefit pediatric diabetes management, but more research, including clinical trials, is needed to confirm optimal outcomes.

Persistent hyperglycemia and uncontrolled type 2 diabetes contribute significantly to diabetes- related mortality by causing multiorgan and systemic injuries, particularly in vital organs such as the heart and kidneys, leading to both microvascular and macrovascular complications. The auto-oxidation of glucose increases oxidative stress, which in turn affects gene modulation and immune responses through the activation of four major pathways: (1) the polyol pathway, (2) the protein kinase C (PKC) pathway, (3) the advanced glycation end-product-receptor for advanced glycation end-product (AGE-RAGE) pathway, and (4) the hexosamine pathway. Oxidative stress and microRNAs (miRNAs) are closely related. These small non-coding RNAs bind to the 3' untranslated regions (3' UTRs) of target mRNAs, leading to mRNA degradation and translational repression. Although numerous studies have identified microRNAs (miRNAs) as important regulators of oxidative stress and diabetic complications, the available evidence remains fragmented. Therefore, this review aims to discuss the roles of miRNAs in oxidative stress-activated pathways and in the generation and detoxification of reactive oxygen species. It also highlights the potential of miRNAs as novel therapeutic targets in type 2 diabetes mellitus and outlines the challenges associated with their clinical application.

Diabetic foot ulcers (DFUs) are a serious diabetic complication leading to high rates of morbidity, amputation risks, and economic burdens on the treatment facilities. The present review continues our exploration of the novel paradigm of combining micronutrients with nanoparticles to address diabetes-related DFUs effectively. We performed a detailed examination of published studies to discuss our views on the ever-increasing utilization of essential micronutrients like zinc, selenium, and vitamins A, C, D, and E to modulate oxidative stress levels, stimulate the secretion of vascular endothelial growth factors, and aid in tissue repair mechanisms. This detailed scrutiny was carried out in parallel to analyze various nanoparticle-based systems to specifically address their bioavailability, stability, deliverability, and efficiency in carrying out wound repair in DFUs. Both micronutrients and nanoparticles have shown substantial activity to increase antioxidant mechanisms, boost the immunomodulatory system, and accelerate tissue repair mechanisms in DFUs. Both methods utilize advanced delivery mechanisms to precisely deliver drugs to the affected areas reliably. Novel delivery methods with micronutrients in DFUs showed a therapeutic integration approach to quicken the healing time to DFUs in faster re-epithelialization, decrease microbial counts, increase extracellular matrix remodeling, and improve healing rates in clinical settings. There is a need for further clinical development to stabilize formulations of combining micronutrients with delivering nanoparticles to serve clinical needs effectively in DFUs. There is a great potential influence in applying this novel multipurpose approach to treat DFUs effectively to increase healing rates and minimize risks of complications in diabetic clients.

Diabetes mellitus affects both the peripheral and central nervous systems, giving rise to a spectrum of neurological complications that extend far beyond the traditional focus on diabetic peripheral neuropathy (DPN). Chronic hyperglycemia disrupts cellular homeostasis through increased formation of advanced glycation end-products, activation of inflammatory pathways, mitochondrial dysfunction, oxidative stress, and impaired neurovascular regulation. These disturbances converge to drive axonal degeneration, demyelination, synaptic injury, and progressive cognitive decline. Emerging evidence also highlights a critical role for gut dysbiosis and intestinal barrier dysfunction, which facilitate microbial translocation and systemic inflammation, ultimately disrupting the blood-brain barrier and amplifying neuroimmune injury. This narrative review synthesizes current mechanistic, clinical, and translational insights into how metabolic, inflammatory, vascular, and microbial pathways interact to produce diabetes-associated neurodegeneration. We summarize key molecular drivers-including mitochondrial ROS overproduction, microglial and astrocytic activation, endothelial dysfunction, and insulin resistance-while also describing their contributions to DPN, autonomic neuropathy, and diabetes-related cognitive impairment. We further integrate evidence from emerging therapeutic domains, including mitochondrial stabilizers, anti-inflammatory strategies, gut-microbiome modulation, and neurovascular-targeted interventions. Despite advances in understanding, disease-modifying therapies remain limited, and diagnostic tools for early detection are underutilized. Bridging these gaps will require longitudinal human studies, improved biomarkers, and integrative therapeutic approaches that target multiple convergent pathways. A deeper understanding of cross-talk among metabolic, immune, vascular, and microbial systems may enable earlier intervention and more effective strategies to mitigate the neurological burden of diabetes.