Journal of Diabetes Research最新文献

Background: Deaf and hard of hearing (DHH) populations face higher rates of diabetes and systemic barriers accessing diabetes technology. Effective use of diabetes technology relies on sensory (e.g., visual and audible) input and interpretation by the user. This study evaluates the accessibility of continuous glucose monitoring systems (CGMs) and insulin pumps for DHH individuals.

Methods: A 2-h focus group was conducted to comprehensively evaluate the accessibility of two CGM and six insulin pumps in a sample of DHH individuals during an interactive, hands-on session. Participants used an investigator-developed 6-point Likert-like scale to score audible, haptic, and visual alarm features for each device and provided additional qualitative feedback that was captured. Observational field notes and team debriefing notes were analyzed using a thematic qualitative approach.

Results: Nine diverse DHH participants living with diabetes consistently scored all devices as poor across each alarm feature. Median scores for audible, haptic and visual alarms for CGM were 2, 2.6, and 1.2 and for insulin pumps were 0.5, 2, and 0.7, respectively. The overall qualitative theme was that the evaluated diabetes technology devices were not designed to be accessible for DHH individuals. Participants noted that CGM and insulin pump companies fell short in providing audible, haptic, and visual alarms and provided several important recommendations.

Conclusion: This study highlights the importance of diabetes technology companies including the creative and diverse perspectives of DHH people in diabetes technology design and testing to optimize accessibility. This inclusive approach fosters innovation by integrating universal design principles that can ultimately enhance the experience for all users.

Aims: Evidence suggests a bidirectional relationship between epilepsy and Type 1 diabetes mellitus (T1DM), but the underlying mechanisms and overall research landscape remain incompletely understood. This study is aimed at delineating research trends and sharing pathogenic pathways between epilepsy and T1DM through a comprehensive bibliometric analysis and genetic investigation.

Methods: We performed a systematic search of the Web of Science Core Collection database (from 1983 to 2024) to identify relevant publications on epilepsy and T1DM. Bibliometric tools (Bibliometrix and CiteSpace) were employed to analyze publication trends, major contributors, and research hotspots. Shared genes were identified via disease-gene association databases (GeneCards and OMIM), and differentially expressed genes (DEGs) were analyzed using GEO2R on GEO datasets.

Results: A total of 217 publications were included. Publication output demonstrated exponential growth over the study period (R ² = 0.6999). The United States, the United Kingdom, and China were the leading contributing countries, exhibiting varying collaboration patterns. Analysis of keywords and co-citations highlighted the central role of autoimmunity, particularly glutamic acid decarboxylase (GAD) antibodies, in linking the two diseases. Keyword and thematic analyses revealed that recent trends indicate growing attention to clinical management, particularly of severe hypoglycemia. Genetic analysis identified 44 overlapping genes between epilepsy and T1DM, which were significantly enriched for autoimmune-associated terms (p < 0.001). Notably, the translocator protein (TSPO) was the only DEG in both conditions, with upregulation observed in T1DM (log2FC = 0.504, p = 0.0319) and epilepsy (log2FC = 0.562, p < 0.001).

Conclusions: This study maps the evolving research landscape of epilepsy and T1DM, confirming autoimmunity as a key link. The identification of TSPO as a shared, upregulated gene provides novel molecular evidence for the connection between the two diseases and suggests TSPO as a potential target for future research and therapeutic strategies.

Background: In individuals with Type 1 diabetes mellitus (T1D) who maintain good glycemic control and are free of chronic complications, lipid profiles are generally within normal ranges. However, impaired renal function or albuminuria alters this profile, contributing to the progression of diabetic kidney disease (DKD). This study hypothesized that, in urinary sediment cells from T1D individuals (n = 87), the mRNA expression of genes related to free fatty acid (FFA) uptake (CD36, FABP1, SCL27A1, SLC27A2, and SLC27A4, which encode FATP1, FATP2, and FATP4, respectively), albumin uptake (LRP2 and CUBN), inflammation (IL1B and IL18), and fibrosis (TGFB1) would vary depending on the degree of renal function decline and of urinary albumin excretion (UAE) and correlate with each other and with plasma lipid concentrations.

Results: CD36 expression was higher in urinary sediment cells of individuals with relevant renal function decline compared to those without relevant decline. CD36, IL1B, TGFB1, and SLC27A4 (at the limit of statistical significance) expressions were higher in individuals with UAE > 11 mg/g versus UAE ≤ 11 mg/g creatinine (cohort median value). CD36 expression positively correlated with IL1B (r = 0.46) and TGFB1 (r = 0.45) expressions, and LRP2 expression positively correlated with IL18 (r = 0.44) and TGFB1 (r = 0.30). Expression of SLC27A genes also correlated with inflammatory and profibrotic genes. Plasma FFA concentrations positively correlated with CD36 (r = 0.27) and IL1B (r = 0.30) expressions, while plasma triglyceride (TG) concentrations positively correlated with CD36 (r = 0.22) and negatively correlated with FABP1 (r = -0.28) expressions. Urinary sediment gene expression was modulated by statin (IL18) and angiotensin II receptor blockers (LRP2, CUBN, and FABP1) use.

Conclusions: The expression of lipid metabolism-related genes in urinary sediment cells, correlated with proinflammatory and profibrotic genes, as well as with plasma FFA and TG, and associated with clinical indicators of renal function, provides indirect evidence for the involvement of lipids in the pathogenesis of DKD.

Background: Diabetic foot ulcers (DFUs) significantly contribute to disability and increased mortality rates among patients with diabetes. Researches on venous conditions of DFU are rather limited compared to other pathological factors. This study is aimed at investigating the correlation between venous dilation and various clinical and biochemical factors in patients with DFU.

Methods: We enrolled 100 patients with DFU and performed Doppler ultrasound examinations of the lower extremity vascular system by a senior ultrasonographer. Clinical and biochemical characteristics were collected, and their correlation with venous dilation was analyzed by Spearman's correlation and multiple linear regression.

Results: The diameters of the common femoral vein, femoral vein, great saphenous vein above knee and below knee (GSVa and GSVb), and the small saphenous vein (SSV) were larger on the affected side than those of the unaffected side of the ulcer, especially the superficial veins. Thus, the ratio of diameters of the superficial veins between affected and unaffected sides was calculated for correlation analysis. Fasting blood glucose levels were positively correlated to the ratio of GSVb, while plasma levels of procalcitonin and white blood cells, markers of inflammation, were found to be positively correlated with the ratio of SSV. However, after adjustment, male gender and duration of diabetes were the positive predictors for the changes in the ratio of GSVb, while systolic blood pressure (SBP) was an independent positive predictor for the changes in the ratio of SSV after adjustment. We did not identify a significant correlation between the severity of the ipsilateral dorsal pedis artery stenosis and the ratios of the GSV and SSV.

Conclusion: Our findings indicate that venous dilation in the affected lower limb is a common occurrence in patients with DFU. Male gender, duration of diabetes, and SBP, but not localized arterial stenosis or serum inflammatory markers, were independent predictors for venous dilation below the knee. Understanding these correlations could contribute to the broader understanding of diabetes-related venous complications.

Background: Diabetes is a complex, prevalent condition. Effective diabetes self-management requires knowledge, skills, and strategies to prevent or delay the onset of diabetes-related complications. This study evaluated the effectiveness of delivery methods, online versus in-person, for the 4-month-long Health Extension for Diabetes (HED) program, a self-management support program.

Methodology: A quasiexperimental comparative study design assessed whether online HED delivery was as effective as in-person delivery and whether group differences affected health outcomes. Multivariate analysis of covariance (MANCOVA) was conducted to assess changes in participants' weight, BMI, HbA1c, diabetes self-efficacy, knowledge, and self-management behaviors. This study included a total of 1018 participants (online = 613; in-person = 405). The online program was delivered synchronously via video or phone conferencing platforms, while in-person sessions occurred at a community location. Survey and biometric data were collected at baseline and upon program completion to evaluate pre- to postprogram changes.

Results: Online HED participants were mostly White non-Hispanic, significantly younger, more educated, and had higher income than in-person participants. Regardless of the delivery modality, positive changes pre- to postprogram were seen across all biometric and diabetes outcome measures. Significant differences between delivery modalities were observed for diabetes knowledge, with individuals in online groups demonstrating significantly higher knowledge scores at both assessment points. For weight and BMI, both modalities showed significant improvements.

Conclusion: Online and in-person HED modalities effectively improved diabetes self-management, reaching two different demographic groups. Demographic differences between groups underscore the importance of offering multiple participation modalities to ensure accessibility and engagement across diverse populations. The HED program model, using a community-clinical linkage through Cooperative Extension, is an effective model for improving health outcomes of participants enrolled in both online and in-person DSMS programs. Future research should focus on how different participant characteristics influence engagement and long-term diabetes outcomes across delivery modalities.

Background: Emerging evidence links visceral adiposity to arterial stiffness. However, the pathways underlying the association between an elevated visceral-to-subcutaneous fat ratio (V/S ratio) and brachial-ankle pulse wave velocity (baPWV), especially the mediating role of blood pressure, remain unclear in patients with diabetes. We aimed to assess the mediating effects of systolic blood pressure (SBP) and diastolic blood pressure (DBP) on the relationship between the V/S ratio and arterial stiffness in individuals with Type 2 diabetes mellitus (T2DM).

Methods: In this cross-sectional study, 1086 adults with T2DM were enrolled between 2022 and 2024. The visceral fat area (VFA) and subcutaneous fat area (SFA) were assessed using a dual bioelectrical impedance analyzer, and the V/S ratio was calculated as VFA/SFA. Arterial stiffness was evaluated via baPWV. Associations between V/S ratio, blood pressure, and baPWV were examined using multivariable regression. The potential mediating role of blood pressure was further investigated.

Results: After adjusting for confounders, a one-unit increase in the V/S ratio was statistically significantly associated with a 131.81 cm/s higher baPWV (95% CI: 25.67-237.96). The V/S ratio is positively associated with SBP (β = 7.76, 95% CI: 1.10-14.42) and DBP (β = 3.93, 95% CI: 0.31-7.56). Mediation analysis revealed that SBP and DBP accounted for 41.8% and 33.2% of the effect of the V/S ratio on baPWV, respectively.

Conclusions: An elevated V/S ratio is significantly associated with increased arterial stiffness among patients with T2DM. Moreover, this association may be partially mediated by SBP or DBP.

Ten male Sprague-Dawley rats were randomly assigned to serve as the negative control (NC) group, and 50 others were maintained on a high-fat diet (HFD). After 18 weeks of feeding, the HFD group received streptozotocin (STZ) intraperitoneally to establish a DKD model. HFD group rats (24-h urinary protein excretion rate ≥ 30 mg) were randomly divided into model (DKD), tiaolipiwei acupuncture (DKD + Acu, acupuncture for 30 min), AMD3100 (DKD + AMD3100, AMD3100 intraperitoneal injection) and tiaolipiwei acupuncture + AMD3100 group (DKD + Acu + AMD3100, AMD3100 intraperitoneal injection combined with tiaolipiwei acupuncture for 30 min) groups. The intervention lasted 4 weeks, and body weight and random blood glucose levels were recorded for each group before treatment each week. Postintervention (at 4 weeks), urine was collected to assess urinary protein-creatinine ratios, 24-h urinary protein contents and urinary podocyte injury-related enzyme levels. Renal cortex tissues from three to five rats in the control, DKD and DKD + Acu groups were sent for transcriptomic and proteomic analyses, and renal tissues were collected for analyses of pathological indicators and mechanisms. Twenty-four-hour Upro, 24-h urinary Spondin 2 (SPON2) levels, UACRs and random serum creatinine, urea nitrogen and blood glucose levels in the DKD + Acu group exhibited significantly reduced levels compared to the DKD group (#p < 0.05). According to the transcriptomic 2.2.2s and proteomic results, immunofluorescence or western blotting was used to assess podocyte-specific marker expression levels (nephrin, podocin and CD2AP), epithelial-mesenchymal transition (EMT) markers (desmin, Fsp1 and α-SMA) and DPP-4/SDF-1α/TGF-β/Smad signalling axis components; nephrin, podocin and CD2AP expression significantly elevated (#p < 0.05 or ##p < 0.01) and desmin, Fsp1 and α-SMA expression greatly decreased (#p < 0.05 or ##p < 0.01) in the DKD + Acu group. Tiaolipiwei acupuncture regulated the Dpp-4/SDF-1α/TGF-β/Smad signalling axis (#p < 0.05 or ##p < 0.01), but this effect was reduced by AMD3100 (@p < 0.05 or @@p < 0.01). Tiaolipiwei acupuncture modulates the DPP-4/SDF-1α/TGF-β/Smad signalling axis to inhibit podocyte EMT and alleviate podocyte and renal injury, ultimately ameliorating proteinuria in DKD model rats.

Background: Asia is experiencing the most significant and rapid increase in Type 2 diabetes mellitus (T2DM) globally. Previous studies have indicated a trend toward early onset of T2DM in this region. However, the burden of T2DM among young adults in Asia remains unclear. This study is aimed at exploring the burden of T2DM and its attributable risk factors in Asian adults aged 15-39 years from 1990 to 2021, which could generate insights into our further understanding and thus prevention and management of T2DM in this population.

Methods: Data from Global Burden of Disease 2021 was used to estimate the trends in age-standardized incidence, disability-adjusted life years (DALYs), and mortality of T2DM among young adults in Asia from 1990 to 2021. We analyzed the association between country development level and T2DM burden and investigated the attributable risk factors for T2DM in 2021.

Results: In 2021, total T2DM incidence, prevalence, DALYs, and deaths in Asian young adults were estimated to be 4.55, 59.69, 4.14 million, and 12,769, respectively. There was a consistent annual increase in age-standardized incidence (average annual percentage change [AAPC]: 2.39%) and DALYs (AAPC: 2.08%) and a fluctuating temporal trend in mortality (AAPC: 0.34%) between 1990 and 2021. Incidence and DALYs were higher in males than females in most age groups, although females under 20 years experienced higher DALYs compared to males. Mortality was higher in females before 2007 but lower thereafter. In both males and females, high body mass index was by far the primary attributable risk factor, accounting for 54.56% of T2DM DALYs overall.

Conclusion: The burden of T2DM has increased among young adults in Asia, particularly among females under 20 years. Prevention and treatment of obesity should be prioritized to reduce the burden of T2DM in this population in Asia.

Diabetic foot infections (DFIs) represent a significant and prevalent complication of diabetes, contributing to considerable morbidity, mortality, and healthcare costs globally. These infections, ranging from mild monomicrobial cases to severe polymicrobial infections, often require hospitalization and can result in limb amputation. The microbial etiology of DFIs is diverse, with common pathogens including Staphylococcus aureus (S. aureus), Escherichia coli, Pseudomonas aeruginosa, and various anaerobes. The pathogenic mechanisms of DFIs are complex, involving peripheral neuropathy, vascular insufficiency, and immune dysfunction, all exacerbated by a hyperglycemic state. Despite advances in treatment, the increasing prevalence of antimicrobial resistance, particularly among methicillin-resistant S. aureus (MRSA) strains, presents a major challenge to managing these infections effectively. This review systematically examines the pathogenesis, diagnostic techniques, microbial profiles, and treatment strategies for DFIs, with an emphasis on antibiotic resistance and new therapeutic approaches. Furthermore, the article highlights the need for a multidisciplinary approach, including early diagnosis, appropriate antibiotic therapy, advanced wound care, and patient education to mitigate the risk of severe complications. Given the rising global burden of diabetes, improved management of DFIs remains critical for reducing the incidence of amputations and minimizing the economic burden on healthcare systems.

Background: Hyperbaric oxygen treatment (HBOT) is clinically used to improve oxygen supply to hypoperfused tissues under certain conditions. HBOT can decrease the incidence of autoimmune diabetes in nonobese diabetic mice by reducing apoptosis and increasing β-cell proliferation. HBOT ameliorates glucose tolerance in Type 2 diabetes (T2D) mellitus patients, but the underlying mechanism needs further investigation. Methods: We used a diet-induced T2D mouse model and a genetic mouse model (ob/ob mice) to evaluate the effects of HBOT on serum glucose levels in mice. The body weights and blood glucose levels of the mice were measured weekly. An oral glucose tolerance test (OGTT) was performed 12 weeks after the start of the experiment. All the mice were euthanized, and the serum and liver tissues were collected to test the total cholesterol, triglycerides, alanine aminotransferase, aspartate aminotransferase, malondialdehyde, and antioxidant enzymes. Results: Our results demonstrated that HBOT can delay/attenuate the onset of diet-associated T2D in wild-type mice. However, HBOT had no significant effects on blood glucose or T2D incidence in ob/ob mice. Furthermore, we found that HBOT improved glucose tolerance and liver steatosis in diet-induced T2D model mice but not in ob/ob mice. Our results indicated that the effects of HBOT on T2D were dependent at least partly on the presence of leptin. Conclusion: Our study offers a rationale for using serum leptin as a predictor of clinical outcomes of HBOT and elucidates possible reasons why many patients may experience HBOT failure.