Journal of Diabetes Investigation最新文献

{"title":"Uric acid to high-density lipoprotein cholesterol ratio is associated with the prevalence of diabetic kidney disease in euthyroid patients with type 1 diabetes mellitus in China: A multicenter cross-sectional study","authors":"Hui Zhao,&nbsp;Yu Wang,&nbsp;Yanli Liu,&nbsp;Zouxi Du,&nbsp;Limin Tian","doi":"10.1111/jdi.70107","DOIUrl":"10.1111/jdi.70107","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Globally, the inadequate diagnosis and treatment of diabetic kidney disease remains a significant challenge, impeding effective management. The uric acid to high-density lipoprotein cholesterol ratio (UHR) has been associated with type 2 diabetes; however, its role in euthyroid patients with type 1 diabetic kidney disease (T1DKD) remains unclear. The aim of this study was to assess the association between UHR and T1DKD in patients with euthyroidism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This cross-sectional study included 335 euthyroid patients with type 1 diabetes mellitus (T1DM) from 1,485 eligible participants. Sociodemographic and blood test data were collected from inpatients of the endocrinology departments of 18 hospitals in Gansu Province.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the 335 euthyroid patients with T1DM (mean age 35.5 years, 57.6% males), 49.6% had T1DKD. In the fully adjusted model, T1DKD was positively associated with UHR (odds ratio [OR] = 2.29; 95% confidence interval [CI]: 1.36–3.87; <i>P</i> = 0.002). A positive relationship between T1DKD and UHR was also observed (nonlinear, <i>P</i> = 0.575). Subgroup analysis showed that this independent association remained consistent regardless of sex, body mass index, nationality, and marital status. The predictive value of UHR was ~22% higher in adults than in individuals aged &lt;18 years.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>UHR is positively related to DKD in patients with euthyroid T1DM. Assessing the UHR might be a valuable part of follow-up visits for patients with T1DM.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1683-1691"},"PeriodicalIF":3.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144525726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles from adipose-derived mesenchymal stem cells prevent high glucose-induced retinal ganglion cell pyroptosis through a microRNA-26a-5p-dependent mechanism","authors":"Lei Tang,&nbsp;Jian Zhang,&nbsp;Jianping Gao","doi":"10.1111/jdi.70100","DOIUrl":"10.1111/jdi.70100","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Mesenchymal stromal/stem cells have neuroprotective effects that limit damage to the retina, which is predominantly mediated by the released extracellular vesicles (EVs). This study aims to investigate the protective effect of adipose-derived mesenchymal stem cell-derived EVs (ADSC-EVs) against pyroptosis of retinal ganglion cells (RGCs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>ADSC-EVs were isolated and then characterized. Mouse primary RGCs exposed to high glucose (HG) were applied for <i>in vitro</i> experiments. miR-26a-5p expression in RGCs after ADSC-EV treatment was determined by RT-qPCR. Target relation between miR-26a-5p and histone deacetylase 4 (HDAC4) was identified by luciferase reporter assay. miR-26a-5p blockad and HDAC4 ectopic expression experiments were conducted to clarify their functions in the pyroptosis of RGCs. The pyroptosis-associated protein GSDMD-N, inflammatory factors, and cell death were further evaluated by western blot, ELISA, and LDH assays, respectively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Exposure to HG reduced RGC viability and increased cell death, GSDMD-N protein level, and IL-1β and IL-18 levels, indicating pyroptosis induction. However, these HG-caused alterations could be reversed by ADSC-EVs. ADSC-EVs transferred miR-26a-5p into RGCs where miR-26a-5p targeted HDAC4 to limit its expression and enhance histone H3 lysine 27 acetylation (H3K27ac) modification at the nuclear factor erythroid 2-related factor 2 (Nrf2) promoter region. This effect contributed to increases in Nrf2 protein level and nuclear translocation. Importantly, decreased H3K27ac modification at the Nrf2 promoter region could partially abrogate the inhibiting effect of ADSC-EVs on HG-induced RGC pyroptosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, our findings reveal the beneficial effects of ADSC-EVs shuttling miR-26a-5p on HG-induced RGCs and determine a potential mechanism responsible for pyroptosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1597-1609"},"PeriodicalIF":3.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative disease burden of early-onset and late-onset type 2 diabetes in the U.S.: Evidence from NHANES 2003–2018","authors":"Shuoying Yue,&nbsp;Meng Su,&nbsp;Zihao Zhang,&nbsp;Zhiyi Hao,&nbsp;Man Li,&nbsp;Liang Zhang,&nbsp;Naijian Zhang,&nbsp;Zhilin Li,&nbsp;Qingcui Wu,&nbsp;Huijie Huang,&nbsp;Honglu Zhang,&nbsp;Yuanyuan Liu,&nbsp;Hui Wang,&nbsp;Jun Ma","doi":"10.1111/jdi.70096","DOIUrl":"10.1111/jdi.70096","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To estimate the disease burden of type 2 diabetes (T2D) in early-onset (age &lt; 40) and late-onset (age ≥ 40) in the U.S.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data obtained from the National Health and Nutrition Examination Survey 2003–2018. Prevalence, number, and disability-adjusted life years (DALYs) in early-onset and late-onset T2D were assessed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>There was a clear and steady upward trend in early-onset T2D, although the prevalence and number of late-onset T2D were higher than early-onset. The average loss of DALYs per capita (DALYs/per) in the early-onset T2D was higher than that in the late-onset. DALYs/per is higher in males than females in both early- and late-onset T2D groups. People living at or below the poverty line and those with education of high school and below had a higher DALYs/per of early-onset T2D. Among individuals with early-onset T2D, the DALYs/per loss was higher in the non-obesity group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>There was a clear upward trend in the prevalence of early-onset T2D, and the loss of DALYs/per in early-onset T2D was higher than that in late-onset T2D. The attribution risk factors, like sex, education levels, income levels, and body mass index, for the burden of early-onset T2D varied, and measures need to be taken to target different populations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1750-1757"},"PeriodicalIF":3.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70096","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144482720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory role of ATF2 in trophoblast ferroptosis via the PI3K/Akt/Nrf2 pathway in gestational diabetes mellitus","authors":"Dandan Xia,&nbsp;Yuhui Zhang,&nbsp;Chenying Zhang,&nbsp;Huiyan Wang","doi":"10.1111/jdi.70115","DOIUrl":"10.1111/jdi.70115","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>To investigate the expression of ATF2 in GDM patients and its impact on trophoblast viability and ferroptosis, as well as to explore the mechanism by which ATF2 regulates ferroptosis and affects trophoblast function in GDM.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>Placental tissues from pregnant women with normal glucose levels and those with GDM were collected. The expression of ATF2 was detected using immunohistochemistry and western blot analysis, and its correlation with clinical maternal and neonatal outcomes was analyzed. The trophoblast cell line HTR8/SVneo was infected with ATF2-overexpressing or interfering lentivirus and stimulated with high glucose to assess changes in cell viability and ferroptosis. Transcriptome sequencing and functional experiments were conducted to identify potential downstream pathways of ATF2.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found that ATF2 is highly expressed in GDM placental tissues and in trophoblast cells under high glucose conditions, and its overexpression is significantly positively correlated with increased levels of ferritin (<i>P</i> = 0.010), triglycerides (<i>P</i> = 0.039), and total cholesterol (<i>P</i> = 0.044) in GDM patients. Exogenous ATF2 expression further suppresses the proliferation of HTR8/SVneo cells under high glucose stimulation and promotes an increase in ferroptosis. Mechanistically, ATF2 targets the inhibition of the PI3K/Akt/Nrf2 pathway, reducing Nrf2 nuclear translocation and decreasing glutathione peroxidase 4 (GPX4) expression, thereby promoting ferroptosis in trophoblast cells and reducing their viability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>ATF2 regulates ferroptosis and impacts trophoblast function in GDM through the PI3K/Akt/Nrf2 pathway, serving as a significant biomarker and a potential target for prevention and treatment of GDM.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1720-1732"},"PeriodicalIF":3.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70115","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144493241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin resistance and exercise-induced insulin sensitization in skeletal muscle: Insights from personalized phosphoproteomics","authors":"Shun Masuda,&nbsp;Takashi Matsuzaka","doi":"10.1111/jdi.70113","DOIUrl":"10.1111/jdi.70113","url":null,"abstract":"<p>Insulin resistance in muscle mainly disrupts non-canonical insulin signaling pathways. Exercise-induced MINDY1 S441 phosphorylation improves insulin sensitivity, highlighting its potential role in mediating exercise benefits in metabolic disease.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1583-1585"},"PeriodicalIF":3.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70113","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lean body mass index and the risk of diabetes onset: A nationwide epidemiological cohort study","authors":"Kazuki Aoyama,&nbsp;Hidehiro Kaneko,&nbsp;Tatsuhiko Azegami,&nbsp;Akira Okada,&nbsp;Yuta Suzuki,&nbsp;Shu Meguro,&nbsp;Katsuhito Fujiu,&nbsp;Norifumi Takeda,&nbsp;Hiroyuki Morita,&nbsp;Norihiko Takeda,&nbsp;Hideo Yasunaga,&nbsp;Kaori Hayashi","doi":"10.1111/jdi.70102","DOIUrl":"10.1111/jdi.70102","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>Diabetes causes microvascular complications and cardiovascular diseases, and identifying its risk factors is a critical issue. Muscle is a primary target organ of insulin; however, previous studies on the relationship between lean body mass and the risk of developing diabetes have reported inconsistent findings. This study aimed to evaluate the association between the predicted lean body mass index (LBMI), which can be easily calculated in daily clinical practice, and the risk of developing diabetes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>This retrospective study analyzed a large scale real-world database to investigate the relationship between LBMI and diabetes risk in both men and women. The incidence of diabetes was determined using ICD-10 codes from an administrative claims database, and Cox regression and cubic spline models were employed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The median age (interquartile range) was 59 (45–67) years for men and 63 (50–68) for women. Among 581,176 men and 721,605 women, a lower LBMI was associated with an increased risk of diabetes onset in both men and women (hazard ratio [95% confidence interval] (Men): Q1, 1.27 [1.23–1.32]; Q2, 1.07 [1.04–1.10]; Q3, 1.02 [0.99–1.04]; Q4. 1 [reference value], HR [95% CI] (Women): Q1, 1.10 [1.06–1.15]; Q2, 1.00 [0.97–1.03]; Q3, 0.99 [0.96–1.02]; Q4. 1 [reference value]). The restricted cubic spline regression model revealed that the risk of diabetes onset increased as LBMI decreased in both men and women.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We demonstrated that a lower LBMI was associated with a higher risk of diabetes onset in both men and women.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1623-1630"},"PeriodicalIF":3.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship of the intensity of physical performance and sedentary time with uric acid in patients with type 2 diabetes","authors":"Jie Li,&nbsp;Ertao Zhang,&nbsp;Zhao Dong,&nbsp;Yan Liu","doi":"10.1111/jdi.70106","DOIUrl":"10.1111/jdi.70106","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>High uric acid (UA) facilitates diabetes progression and is responsible for developing other diseases, such as cardiovascular disease and renal disease. Lifestyle modifications could lower UA level, but relevant evidence is required in patients with type 2 diabetes. This study intended to explore the influence of different physical activities and sitting time on UA level in patients with type 2 diabetes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data on UA level, physical performance, and sitting time from 1892 patients with type 2 diabetes were retrospectively obtained from the Third People's Hospital of Datong, a subcenter of the Metabolic Management Center (MMC) Central database.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>There were 15.8%, 29.7%, 29.5%, and 25.0% of patients with inactive, mild, moderate, and vigorous intensity of physical activity. UA level presented a U-shaped distribution among patients with different intensities of physical activity, with the lowest in patients with mild intensity of physical activity and the highest in patients with vigorous intensity of physical activity (<i>P</i> = 0.007). There were 58.1% and 41.9% of patients with a sitting time of ≤30 h/week and &gt;30 h/week. UA level was lower in patients with sitting time ≤30 h/week than those with sitting time &gt; 30 h/week (<i>P</i> = 0.014). The above findings were confirmed by multivariate linear regression models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Mild intensity of physical activity and sitting time ≤ 30 h/week are recommended for reducing UA level in patients with type 2 diabetes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1733-1741"},"PeriodicalIF":3.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of insulin resistance on post-stroke depression and outcomes in diabetes","authors":"Lifei Tan,&nbsp;Yan Li,&nbsp;Ming Tan,&nbsp;Jing Gong,&nbsp;Jinbiao Zhang","doi":"10.1111/jdi.70097","DOIUrl":"10.1111/jdi.70097","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study aimed to examine the association between insulin resistance (IR) and post-stroke depression (PSD) occurrence in diabetic patients, providing novel insights for PSD prevention and treatment strategies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and methods</h3>\u0000 \u0000 <p>Clinical data from 124 patients with acute cerebral infarction and diabetes mellitus were retrospectively analyzed. Based on the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), participants were stratified into two groups: an IR group (HOMA-IR &gt; 2.69, <i>n</i> = 96) and a control group (HOMA-IR ≤ 2.69, <i>n</i> = 28). The occurrence of PSD was compared between the two groups by unadjusted analysis and inverse probability of treatment weighting (IPTW), and the correlation between HOMA-IR scores and PSD was analyzed by multivariate logistic regression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>At 3-month follow-up, the IR group exhibited significantly higher Hamilton Depression Scale (HAMD) scores (median 8 vs 6, <i>P</i> = 0.029) and a 3.28-fold increased PSD risk (OR = 3.28, 95% CI: 1.37–7.88, <i>P</i> = 0.006). After adjusting for baseline confounders using IPTW, the IR group maintained elevated PSD risk (adjusted OR = 2.64, <i>P</i> = 0.035). Multivariate analysis confirmed HOMA-IR as an independent PSD predictor (OR = 1.755, 95% CI: 1.360–2.263, <i>P</i> &lt; 0.001), with ROC analysis demonstrating moderate predictive accuracy (AUC = 0.76, 51.4% sensitivity, 94.2% specificity at cutoff 5.2).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Elevated HOMA-IR levels in diabetic patients with acute cerebral infarction are significantly associated with increased PSD incidence.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":"1704-1712"},"PeriodicalIF":3.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the Editor in response to “Predictive value of biliverdin reductase-A and homeostasis model assessment of insulin resistance on mild cognitive impairment in patients with type 2 diabetes”","authors":"Jie Chen,&nbsp;Li Zhou","doi":"10.1111/jdi.70104","DOIUrl":"10.1111/jdi.70104","url":null,"abstract":"&lt;p&gt;Dear Editor,&lt;/p&gt;&lt;p&gt;I read the recent article titled “Predictive value of biliverdin reductase-A and homeostasis model assessment of insulin resistance on mild cognitive impairment in patients with type 2 diabetes”&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; with great interest. This pioneering study elucidates the clinical association between biliverdin reductase-A (BVR-A) and mild cognitive impairment (MCI) in type 2 diabetes patients, integrating insulin resistance (HOMA-IR) to construct a predictive model. It fills a critical gap in understanding the role of BVR-A in diabetes-related cognitive impairment and provides a biomarker-based tool for early MCI screening, potentially enabling timely interventions to improve patient outcomes. However, several limitations warrant discussion to enhance the clinical applicability of the findings.&lt;/p&gt;&lt;p&gt;First, the study relies solely on the Montreal Cognitive Assessment (MoCA) for cognitive evaluation, which may overlook impairments in other domains (e.g., executive function, processing speed). Additionally, MoCA's education-level adjustments may inadequately balance assessment biases in low-education populations. Combining MoCA with tools like the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) and Mini-Mental State Examination (MMSE) would offer a more robust framework for assessing global cognitive function. Bayesian latent class modeling&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; could further address conditional dependencies and limitations of individual tests, improving sensitivity and specificity in detecting Alzheimer's disease (AD) and MCI. Future research should prioritize the combined use of these tools for multi-domain assessments to improve diagnostic accuracy.&lt;/p&gt;&lt;p&gt;Second, the laboratory methodology for measuring BVR-A lacks critical details. The use of ELISA is mentioned, but the study does not specify whether the assay underwent standardized validation or accounted for inter-batch variability, both of which could affect result reliability. Similarly, descriptions of biochemical and immunological assays (e.g., instrument brands, methodologies, and intra-/inter-assay coefficients of variation) are omitted, limiting data reproducibility. To strengthen validity, future work should standardize BVR-A detection protocols, include internal controls, and report technical specifications for all assays.&lt;/p&gt;&lt;p&gt;Lastly, the study does not incorporate neuroimaging evidence (e.g., MRI or PET-CT to assess hippocampal volume or amyloid deposition) to corroborate cognitive scores. Objective structural or functional brain markers would enhance the predictive model's robustness and provide mechanistic insights into MCI pathogenesis in diabetic patients.&lt;/p&gt;&lt;p&gt;Addressing these limitations could transform the proposed MCI prediction model into a more reliable clinical tool. The authors' work represents a significant step forward in identifying high-risk individuals, and further refinements may ultimately optimize preventive st","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 8","pages":"1568-1569"},"PeriodicalIF":3.0,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144281826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on “Concomitant use of metformin and proton pump inhibitors increases vitamin B12 deficiency risk in type 2 diabetes”","authors":"Kuan-Fu Liao,&nbsp;Shih-Wei Lai","doi":"10.1111/jdi.70103","DOIUrl":"10.1111/jdi.70103","url":null,"abstract":"&lt;p&gt;Dear Editor,&lt;/p&gt;&lt;p&gt;We read with great interest the article by Jung &lt;i&gt;et al&lt;/i&gt;. which reported that the concomitant use of metformin and proton pump inhibitor (PPI) is associated with an increased risk of vitamin B12 deficiency in patients with type 2 diabetes mellitus&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;. While the study benefits from a robust nationwide database and appropriate use of propensity score matching, we would like to offer several points for consideration.&lt;/p&gt;&lt;p&gt;First, the authors conclude that even short-term (≥2 weeks) concurrent use of metformin and a PPI in patients with type 2 diabetes mellitus is associated with an increased risk of vitamin B12 deficiency, recommending routine monitoring&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;. However, this conclusion appears inconsistent with the well-established physiology of vitamin B12 metabolism. Hepatic stores of vitamin B12 are typically sufficient to prevent deficiency for several years, even in the absence of dietary intake&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt;. Therefore, a 2-week exposure to a PPI is unlikely to significantly deplete these stores.&lt;/p&gt;&lt;p&gt;Second, based on the data presented, the incidence rate of vitamin B12 deficiency was 14.3 per 1,000 person-years in the metformin monotherapy group and 15.4 per 1,000 person-years in the metformin + PPI group&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;. This corresponds to an absolute risk increase (ARI) of 1.1 per 1,000 person-years and a number needed to harm (NNH) of 909. In practical terms, this means that 909 patients would need to be treated with both metformin and PPI for 1 year to result in one additional case of vitamin B12 deficiency. Given the sample size of 5,600 in the metformin + PPI group, this translates to approximately six additional cases per year—suggesting that the clinical significance of this association may be limited.&lt;/p&gt;&lt;p&gt;Third, while subgroup analyses by age and sex were conducted, the adjusted hazard ratios were not statistically significant, and no formal interaction tests were reported&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;. Without such analyses (e.g., interaction terms or &lt;i&gt;P&lt;/i&gt;-values for interaction), it is not possible to determine whether age or sex modifies the effect of PPI use on vitamin B12 deficiency. We respectfully suggest that the authors consider including formal interaction testing to enhance the interpretability of subgroup findings, as this would not require additional effort.&lt;/p&gt;&lt;p&gt;Finally, given that vitamin B12 deficiency typically develops over several years in the absence of dietary intake, routine screening for vitamin B12 deficiency in all type 2 diabetes mellitus patients using both metformin and PPI may not be necessary. Instead, targeted screening of those type 2 diabetes mellitus patients who use both metformin and PPI for extended durations (e.g., &gt;1 year) may be more appropriate. This approach could help reduce healthcare costs and avoid unnecessary testing, while still identifying patients at meaningful risk—potentially representing ","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"16 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}