A 49-year-old woman developed new-onset type 1 diabetes after initiating Wegovy (semaglutide) via an online clinic, without prior screening. She experienced rapid weight loss and hyperglycemia symptoms. Blood tests indicated high GAD65 and low C-peptide. The case underscores the need for biochemical screening and follow-up in digital obesity care.

The development of Type 1 diabetes (T1D) is shaped by genetic predisposition and epigenetic regulation. Human leukocyte antigen (HLA) risk alleles are major genetic determinants, but the epigenetic landscape in relation to disease onset remains unclear. Early-life epigenetic modifications may reveal how environmental and epigenetic factors interact in T1D pathogenesis.

We investigated epigenetic differences in cord blood DNA from individuals with different HLA risk alleles who later developed T1D using epigenome-wide association studies.

High-risk HLA carriers showed differentially methylated genes (DMGs) mainly involved in immune and autoimmune processes, resembling patterns in other autoimmune diseases. In contrast, low-to-neutral risk carriers exhibited DMGs linked to signaling cascades, metabolic pathways, and Type 2 diabetes-related mechanisms such as beta cell function and insulin signaling.

These findings indicate that heterogeneity in T1D pathogenetic mechanisms based on HLA background may influence disease development.

Remote patient monitoring (RPM) has demonstrated potential to improve glycemic control in type 2 diabetes mellitus (T2DM), yet evidence from middle-income public health systems remains limited. This study evaluated the clinical impact of structured telemonitoring in insulin-treated T2DM patients at a public hospital in Ecuador.

A prospective, controlled cohort study was conducted over a six-month period. Adults with insulin-treated T2DM and baseline HbA1c >8% were assigned to structured telemonitoring or standard care. The intervention included Bluetooth-enabled glucometers linked to the mySugr app, automated data uploads, and weekly clinical review. The primary outcome was the change in HbA1c; secondary outcomes included emergency visits and hospitalizations. Repeated measures ANOVA assessed HbA1c trajectories. Emergency visits were analyzed using Fisher's Exact Test and Firth's logistic regression.

Among 100 patients (50 per group), mean HbA1c decreased by 2.67% in the intervention group compared to 1.38% in the control group (p = 0.006). Emergency visits occurred in eight control patients and none in the intervention group (p = 0.006). Firth's regression showed a non-significant odds ratio. No hospitalizations were reported. Direct cost savings totaled USD 9,660 over six months for the studied population and USD 174,000 annually, based on a 10% adoption rate (450 patients) over one year, using 2024 data from HGDC.

Structured telemonitoring was associated with improved glycemic control and reduced utilization of acute care services. These findings support RPM feasibility in middle-income public health settings.

Chronic kidney disease (CKD) is a public health issue often accompanied by anemia from its early stages. Identifying associated factors is essential, especially given the limited data on the Brazilian population and the outcomes of anemia among individuals with CKD.

To investigate the factors associated with anemia in individuals with CKD in the Brazilian population.

A cross-sectional study was conducted using the 2013 National Health Survey (PNS) laboratory database. Socioeconomic, demographic, and clinical variables (sex, age, education, race/color, nutritional status, arterial hypertension (AH), diabetes mellitus (DM), hypercholesterolemia, cardiovascular disease (CVD), smoking, and excessive alcohol consumption) were evaluated. Associations between anemia and the stages of CKD were examined using multivariable logistic regression models.

8,952 individuals were evaluated. The prevalence of anemia in the total population was 10.1%, and in the population with CKD, it was 15.1%. Anemia was found to be more prevalent among women, older adults, individuals with lower educational, and those of mixed and black race/color. In the fully adjusted model, women (OR 1.59; CI, 1.35-1.88), black individuals (OR 1.76; CI, 1.36-2.26), and those with AH (OR 1.26; CI, 1.04-1.52) or DM (OR 1.30; CI, 1.00-1.69) exhibited a higher likelihood of anemia. Conversely, individuals with higher educational levels (OR 0.65; CI, 0.49-0.87), smokers (OR 0.71; CI, 0.56-0.91) those with a eutrophic body status (OR 0.66; CI, 0.49-0.90), and obese individuals (OR 0.49; CI, 0.36-0.67) had lower likelihood of anemia compared to underweight individuals. Individuals with advanced stages of CKD had a higher likelihood of anemia compared with those in early stages, and this association remained significant after adjustment for sociodemographic and clinical variables, with the highest odds observed in stages 4 and 5.

This study made it possible to identify the variables related to the presence of anemia in the different stages of CKD, such as AH, DM, sex, education, race/color, and nutritional status.

Diabetes, particularly type 2 diabetes, poses a significant public health challenge globally, with an especially pronounced impact in China. The prevalence of diabetes in China has surged from 2.5% in 1994 to 13.0% in 2021, with projections indicating a continued upward trend. This review provides a comprehensive overview of the diabetes burden in China and underscores the urgent need for effective prevention and control measures. We examine the epidemiology of diabetes, highlighting the rising prevalence of prediabetes, type 1 and type 2 diabetes, youth-onset diabetes, and gestational diabetes mellitus, as well as diabetes-related complications, including both macrovascular and microvascular complications, and emerging conditions like cancer, infectious disease, fatty liver disease, and dementia. Key risk factors, including genetic susceptibility, obesity, dietary factors, and physical activity, are discussed, with particular attention to how these factors manifest differently in Chinese versus western populations. The review highlights advancements in national prevention efforts, innovative diabetes management models, and emerging technological innovations. The review also addresses advancements in pharmacological therapies, including the introduction of novel glucose-lowering agents such as GLP-1 receptor agonists, and SGLT2 inhibitors, which offer both metabolic and cardio-renal benefits. However, significant challenges remain, including the underrepresentation of the Chinese population in current research, persistent regional disparities, gaps in primary healthcare capacity, and the need for better integration of new technologies into clinical practice.

Type 1 Diabetes (T1D) is a high-incidence chronic autoimmune disease, with patients requiring lifelong insulin therapy. In the most severe cases, pancreas transplantation (PTA) arises as the first choice of treatment for these patients in the hope of achieving insulin independence. However, the long-term success of PTA is hindered by ischemia-reperfusion injury (IRI) and immune rejection, both of which limit graft survival. To address these challenges, we have developed multifunctional theranostic nanoparticles (t-PLGA NPs) co-encapsulating Fe₃O₄ and MnO NPs, along with cyclosporine A, an immunosuppressive drug. These immunomodulating NPs serve as dual contrast agent for MRI, while generating oxygen to combat hypoxia during IRI. The t-PLGA NPs exhibit efficient drug encapsulation and sustained release, enhancing immunosuppression while minimizing systemic toxicity. In vitro studies also demonstrated the NPs' ability to suppress the immune system, validating the NPs' potential to prevent graft rejection. The combination of imaging and therapeutic properties makes this platform highly promising for improving PTA outcomes in T1D patients.

High dietary sugar intake has emerged as a key modulator of systemic inflammation and metabolic dysregulation, both of which are associated with an increased risk of several chronic diseases, including cancer. Although bladder cancer is primarily driven by factors such as smoking and occupational exposures, metabolic dysregulation may also play a contributory role. Experimental studies indicate that elevated glucose levels promote proliferation, epithelial-mesenchymal transition, increase invasion, and reduce autophagy in bladder cancer cells. Epidemiological evidence suggests associations of high dietary glycaemic index/load and high sugar consumption with bladder cancer risk, although findings for these dietary factors remain heterogeneous. Furthermore, epidemiological data consistently demonstrate a positive association between diabetes mellitus and increased bladder cancer incidence and adverse clinical outcomes. Mechanistically, hyperglycaemia and accumulation of advanced glycation end products (AGEs) can activate inflammatory signalling pathways, including NF-κB, MAPK, and the NLRP3 inflammasome, leading to increased cytokine production, immune dysregulation, and oxidative stress. High dietary sugar intake has also been shown to alter gut microbiota composition, typically reducing short-chain fatty acid (SCFA)-producing bacteria and promoting intestinal permeability, endotoxaemia, and sustained immune activation through TLR4-dependent pathways. Within the bladder tumour microenvironment, systemic inflammatory disturbances enhance oncogenic signalling cascades such as COX-2, JAK/STAT3, and NF-κB, thereby fostering epithelial-mesenchymal transition, angiogenesis, and potential resistance to therapy. Evidence suggests that maintaining well-regulated blood sugar levels may help lower the risk of bladder cancer. Adopting lifestyle habits such as whole-food, fibre-rich diets, probiotics, and regular physical activity supports metabolic and microbial homeostasis, SCFA-mediated immune regulation, and inflammation reduction, thereby serving as a preventive strategy. This review aims to synthesise current evidence on the complex interplay between dietary sugar intake, gut microbiota dysregulation, systemic inflammation, and bladder cancer, and to highlight potential preventive dietary interventions.

Adherence to treatment with sodium-glucose co-transporter protein type 2 inhibitors (SGLT2i) is essential for the successful treatment of type 2 diabetes. As SGLT2i induce glucosuria, the main study objective was to assess the potential relationship between glucosuria level and adherence to SGLT2i.

The study used electronic health records of patients aged ≥45 years old that had urinalysis data. Glucosuria was classified as absent/normal (0 mg/dL), intermediate (1-1000 mg/dL), and evident (>1000 mg/dL). Renal function, expressed by estimated glomerular filtration rate and stage of chronic kidney disease (CKD), was also assessed. Adherence to SGLT2i was measured with the proportion of days covered in 6 months.

Only 9.2% of samples showed evident glucosuria; of these, 87.5% belonged to patients treated with SGLT2i. Among these patients, glucosuria was mostly evident (78.9%). Absent glucosuria was more common in patients with CKD and in advanced KDIGO stages; therefore, in these patients glucosuria as adherence marker should be interpreted with caution.In patients treated with SGLT2i, absent glucosuria was detected in 4.5% of samples from patients with good adherence, 18.5% of samples from patients with intermediate adherence, and up to 38.5% of samples from patients with poor adherence (p <0.01). Absent glucosuria was also associated with higher blood uric acid level and lower hemoglobin and hematocrit. Absent glucosuria was more common in women and older patients.

Absent glucosuria could be an easy biomarker of poor adherence in patients treated with SGLT2i in clinical practice.

In type 1 diabetes (T1D), partial remission (PR) is a pivotal phase with preserved β-cell function, better glycemic stability, and reduced disease burden, and is as such a potential target for disease-modifying interventions. Identifying robust biomarkers of PR is critical for designing targeted therapies. This systematic review synthesizes current evidence from observational studies of biomarkers associated with PR in pediatric T1D.

We searched the literature in PubMed, Scopus, and Embase (2009-2025), using strategies based on PICOS criteria. Investigated biomarkers covered multiple domains: anthropometric and clinical factors, continuous glucose monitoring metrics, HLA genotyping, immune cell and cytokine profiles, hormones, proteomics, and microRNAs. Eligible studies included observational cohorts of children and adolescents with newly diagnosed T1D. PR was defined as IDAA1c ≤9, HbA1c <7% with insulin requirement <0.5 IU/kg BW/day, or stimulated C-peptide ≥ 300pmol/L. Studies were selected according to PRISMA guidelines, and risk of bias was appraised using the Joanna Briggs Institute checklist.

Of 353 records, 39 studies including 9,368 patients met the inclusion criteria. Study populations ranged from 16 to 3,657 participants, with mean age of disease onset ranging from 7.0 to 13.8 years. Most studies (n=32) defined PR using IDAA1c. Routine clinical parameters and CGM-derived indices consistently distinguished remitters from non-remitters. Biological markers like immune signatures or proteomic profiles provided mechanistic insights into PR pathways. The methodological quality was moderate to high, though control of confounders and follow-up were incomplete.

Standard-of-care biomarkers appear sufficient to identify PR and monitor its impact on glycemic outcomes. Emerging biological markers offer promising insights into the underlying mechanisms of PR. Well-powered studies are needed to clarify PR determinants and their therapeutic potential.

Diabetic foot ulcers (DFUs) are one of the most serious and intractable complications of diabetes, caused by oxidative stress due to hyperglycemia, chronic inflammation, and repeated infections. Conventional treatments such as insulin therapy do not improve the pathological wound microenvironment, resulting in slow healing and a high rate of recurrence. Nanozymes, with superior catalytic stability, tuneable enzyme-like activities, and multifunctional synergy, have emerged as a promising therapeutic strategy. Nanozymes that imitate natural enzymes such as glucose oxidase, peroxidase, catalase, and superoxide dismutase can actively remodel the DFUs microenvironment via glucose depletion, dynamic regulation of reactive oxygen species, disruption of biofilm, suppression of inflammation, and oxygen generation. These integrated functions can help wounds heal faster, and they can promote angiogenesis and tissue regeneration. This review discusses recent advances in catalytic mechanisms and therapeutic applications of nanozymes for DFUs management, with special attention paid to the microenvironment-responsive systems, hydrogel-based composites, and synergistic photothermal or drug delivery platforms. Lastly, the current issues of biosafety, catalytic efficiency, and target accuracy are mentioned, followed by future directions for clinical application.