While treatment for diabetic polyneuropathy (DPN) is still developing, progress has stagnated. The alignment between pathological neurodegeneration in DPN and patients' subjective symptoms is often low, yet these symptoms are frequently used for diagnosis. This reliance has hindered the development of effective drugs to prevent neurodegeneration. This study aims to establish an objective electrophysiological diagnostic method that could support future treatment development and validate its accuracy.
Materials and Methods
This retrospective multicenter cohort study involved hospitalized diabetic patients. A total of 314 patients underwent nerve conduction studies using standard electromyography and a simplified nerve conduction testing device (NC-stat/DPNCheck™), along with electrocardiogram-based coefficient of variation of R-R intervals (CVR-R). Patients with a severity classification of Stage 2 or higher based on electromyography were defined as having DPN. Logistic regression analysis was used to identify significant factors explaining DPN presence, followed by ROC analysis to determine optimal cutoff values for diagnosis.
Results
Significant factors included resting CVR-R, sural nerve conduction velocity (SNCV), and amplitude of sensory nerve action potential (SNAP). SNCV had the highest area under the curve (AUC = 0.823). The optimal cutoff values were 1.62% for CVR-R, 46.5 m/s for SNCV, and 10.5 μV for SNAP. Diagnosing DPN based on abnormalities in two or more of these three conditions yielded an accuracy of 79.3%.
Conclusions
The established diagnostic criteria of DPN demonstrate high performance and are expected to be applicable in clinical settings.
{"title":"Electrophysiological diagnosis using the coefficient of variation of R-R intervals and a point-of-care nerve conduction device is highly correlated to the diagnosis of diabetic polyneuropathy using conventional electromyographs","authors":"Tatsuhito Himeno, Hideki Kamiya, Yuka Shibata, Masato Kase, Hiromi Nakai-Shimoda, Dai Yamagami, Masahiro Saito, Teruo Jojima, Aiko Arimura, Kenta Murotani, Chieko Suzuki, Hiroki Mizukami, Takahisa Deguchi, Yoshimasa Aso, Jiro Nakamura","doi":"10.1111/jdi.70190","DOIUrl":"10.1111/jdi.70190","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>While treatment for diabetic polyneuropathy (DPN) is still developing, progress has stagnated. The alignment between pathological neurodegeneration in DPN and patients' subjective symptoms is often low, yet these symptoms are frequently used for diagnosis. This reliance has hindered the development of effective drugs to prevent neurodegeneration. This study aims to establish an objective electrophysiological diagnostic method that could support future treatment development and validate its accuracy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>This retrospective multicenter cohort study involved hospitalized diabetic patients. A total of 314 patients underwent nerve conduction studies using standard electromyography and a simplified nerve conduction testing device (NC-stat/DPNCheck™), along with electrocardiogram-based coefficient of variation of R-R intervals (CV<sub>R-R</sub>). Patients with a severity classification of Stage 2 or higher based on electromyography were defined as having DPN. Logistic regression analysis was used to identify significant factors explaining DPN presence, followed by ROC analysis to determine optimal cutoff values for diagnosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Significant factors included resting CV<sub>R-R</sub>, sural nerve conduction velocity (SNCV), and amplitude of sensory nerve action potential (SNAP). SNCV had the highest area under the curve (AUC = 0.823). The optimal cutoff values were 1.62% for CV<sub>R-R</sub>, 46.5 m/s for SNCV, and 10.5 μV for SNAP. Diagnosing DPN based on abnormalities in two or more of these three conditions yielded an accuracy of 79.3%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The established diagnostic criteria of DPN demonstrate high performance and are expected to be applicable in clinical settings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 2","pages":"280-290"},"PeriodicalIF":3.0,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12863008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627222","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}
A 48-year-old man was referred to our hospital due to hyperglycemia. His casual plasma glucose and glycated hemoglobin A1c were 25.2 mmol/L and 8.7%, respectively. He had undergone bilateral cataract surgery in his 30s. He exhibited a bird-like face contour, gray hair, alopecia, and bilateral calcifications of the Achilles' tendons, suggestive of Werner syndrome (WS). Genetic analysis revealed compound heterozygous mutations in the WRN gene (mutation c. 3139-1G>C, mutation c. 1105C>T), leading to the diagnosis of WS. Adequate glycemic control was not achieved by the treatment with pioglitazone and metformin. Additional administration of dapagliflozin, a sodium-glucose cotransporter 2 inhibitor, ameliorated insulin resistance and resulted in an improvement in glycemic control without adverse events. Dapagliflozin may potentially be a choice in treating diabetes associated with WS with an amelioration of insulin resistance.
{"title":"Efficacy and safety of SGLT2 inhibitor on insulin resistance and hyperglycemia in Werner syndrome—A case report","authors":"Takashi Yagi, Daisuke Aotani, Chie Hasegawa, Yuki Shimizu, Hiroyuki Koyama, Yoshiro Maezawa, Koutaro Yokote, Tomohiro Tanaka","doi":"10.1111/jdi.70203","DOIUrl":"10.1111/jdi.70203","url":null,"abstract":"<p>A 48-year-old man was referred to our hospital due to hyperglycemia. His casual plasma glucose and glycated hemoglobin A1c were 25.2 mmol/L and 8.7%, respectively. He had undergone bilateral cataract surgery in his 30s. He exhibited a bird-like face contour, gray hair, alopecia, and bilateral calcifications of the Achilles' tendons, suggestive of Werner syndrome (WS). Genetic analysis revealed compound heterozygous mutations in the <i>WRN</i> gene (mutation c. 3139-1G>C, mutation c. 1105C>T), leading to the diagnosis of WS. Adequate glycemic control was not achieved by the treatment with pioglitazone and metformin. Additional administration of dapagliflozin, a sodium-glucose cotransporter 2 inhibitor, ameliorated insulin resistance and resulted in an improvement in glycemic control without adverse events. Dapagliflozin may potentially be a choice in treating diabetes associated with WS with an amelioration of insulin resistance.</p>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 2","pages":"366-370"},"PeriodicalIF":3.0,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12862991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627286","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}
Mean platelet volume (MPV), which reflects platelet size and activity, is known to be elevated in patients with type 2 diabetes mellitus. Although increased MPV has been linked to poor glycemic control and diabetic vascular complications, evidence regarding its association with hard kidney outcomes remains limited. We aimed to investigate the relationship between MPV and kidney events in patients with type 2 diabetes mellitus.
Materials and Methods
We retrospectively analyzed longitudinal data from 1,076 Japanese patients with type 2 diabetes mellitus enrolled in the Fukushima Cohort Study. Participants were categorized into quartiles based on baseline MPV levels. The primary endpoint was kidney events, defined as a ≥50% decline in estimated glomerular filtration rate (eGFR) from baseline or progression to end-stage kidney disease requiring kidney replacement therapy. The secondary endpoint was new-onset cardiovascular events.
Results
During a median follow-up of 5.3 years, 97 patients experienced kidney events. The second quartile (Q2) had the lowest incidence of kidney events. Compared with Q2 as the reference, patients in the highest quartile (Q4) had a significantly increased risk of kidney events (adjusted hazard ratio 2.05, 95% confidence interval 1.13–3.72). Higher MPV levels were also significantly associated with an increased risk of cardiovascular events.
Conclusion
Elevated MPV was independently associated with both kidney and cardiovascular events in Japanese patients with type 2 diabetes mellitus. MPV may serve as a simple and useful biomarker for predicting kidney disease progression in this high-risk population.
{"title":"Association between mean platelet volume and kidney events in patients with type 2 diabetes mellitus","authors":"Syuhei Watanabe, Kenichi Tanaka, Hiroshi Kimura, Hirotaka Saito, Michio Shimabukuro, Koichi Asahi, Tsuyoshi Watanabe, Junichiro James Kazama","doi":"10.1111/jdi.70206","DOIUrl":"10.1111/jdi.70206","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Mean platelet volume (MPV), which reflects platelet size and activity, is known to be elevated in patients with type 2 diabetes mellitus. Although increased MPV has been linked to poor glycemic control and diabetic vascular complications, evidence regarding its association with hard kidney outcomes remains limited. We aimed to investigate the relationship between MPV and kidney events in patients with type 2 diabetes mellitus.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We retrospectively analyzed longitudinal data from 1,076 Japanese patients with type 2 diabetes mellitus enrolled in the Fukushima Cohort Study. Participants were categorized into quartiles based on baseline MPV levels. The primary endpoint was kidney events, defined as a ≥50% decline in estimated glomerular filtration rate (eGFR) from baseline or progression to end-stage kidney disease requiring kidney replacement therapy. The secondary endpoint was new-onset cardiovascular events.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>During a median follow-up of 5.3 years, 97 patients experienced kidney events. The second quartile (Q2) had the lowest incidence of kidney events. Compared with Q2 as the reference, patients in the highest quartile (Q4) had a significantly increased risk of kidney events (adjusted hazard ratio 2.05, 95% confidence interval 1.13–3.72). Higher MPV levels were also significantly associated with an increased risk of cardiovascular events.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Elevated MPV was independently associated with both kidney and cardiovascular events in Japanese patients with type 2 diabetes mellitus. MPV may serve as a simple and useful biomarker for predicting kidney disease progression in this high-risk population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 1","pages":"51-59"},"PeriodicalIF":3.0,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70206","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627013","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}
We aimed to explore the association of the triglyceride-glucose (TyG) index and homeostasis model assessment of insulin resistance (HOMA-IR) with subclinical left ventricular function in the general population.
Materials and Methods
A total of 2,850 participants with left ventricular ejection fraction ≥50% were recruited from 2017 to 2019 in Danyang. Speckle-tracking echocardiography (Philips CX50) was used to measure global longitudinal strain (GLS). Subclinical left ventricular systolic dysfunction (LVSD) was defined as GLS < 18%.
Results
In univariate analyses, higher TyG index and HOMA--IR were significantly associated with reduced GLS, lower E/A ratio and e', and higher E/e' ratio (P < 0.001). After adjustment for confounders, HOMA-IR remained significantly associated with lower GLS (P = 0.002), whereas the TyG index showed stronger correlations with E/e' ratio (P < 0.01). The inclusion of log-transformed HOMA-IR significantly improved model fit in analyses incorporating GLS and TyG index (P = 0.004) but not in those with E/e' ratio and TyG index (P = 0.65). Conversely, the TyG index enhanced model performance for the E/e'–HOMA-IR association (P < 0.001) but not for GLS–HOMA-IR relationships (P = 1). In addition, participants in the highest versus lowest HOMA-IR quartile demonstrated significantly increased odds ratio of subclinical LVSD (OR = 2.22, 95% CI: 1.26–3.92; P = 0.006), while the TyG index showed no significant association with its prevalence (P = 0.98).
Conclusions
In a community-based population, elevated HOMA-IR demonstrated a robust association with subclinical LVSD, whereas the TyG index exhibited a more pronounced correlation with early diastolic dysfunction.
{"title":"Comparison of the correlation between triglyceride-glucose index and homeostasis model assessment of insulin resistance with subclinical left ventricular dysfunction","authors":"Tianna Zhou, Xinyue Wang, Xiwu Yan, Weina Guo, Zhicong Pi, Junya Liang, Yun Gao, Siqi Zhang, Mulian Hua, Chao Chen, Xixuan Zhao, Ming Liu","doi":"10.1111/jdi.70201","DOIUrl":"10.1111/jdi.70201","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>We aimed to explore the association of the triglyceride-glucose (TyG) index and homeostasis model assessment of insulin resistance (HOMA-IR) with subclinical left ventricular function in the general population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>A total of 2,850 participants with left ventricular ejection fraction ≥50% were recruited from 2017 to 2019 in Danyang. Speckle-tracking echocardiography (Philips CX50) was used to measure global longitudinal strain (GLS). Subclinical left ventricular systolic dysfunction (LVSD) was defined as GLS < 18%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In univariate analyses, higher TyG index and HOMA--IR were significantly associated with reduced GLS, lower E/A ratio and e', and higher E/e' ratio (<i>P</i> < 0.001). After adjustment for confounders, HOMA-IR remained significantly associated with lower GLS (<i>P</i> = 0.002), whereas the TyG index showed stronger correlations with E/e' ratio (<i>P</i> < 0.01). The inclusion of log-transformed HOMA-IR significantly improved model fit in analyses incorporating GLS and TyG index (<i>P</i> = 0.004) but not in those with E/e' ratio and TyG index (<i>P</i> = 0.65). Conversely, the TyG index enhanced model performance for the E/e'–HOMA-IR association (<i>P</i> < 0.001) but not for GLS–HOMA-IR relationships (<i>P</i> = 1). In addition, participants in the highest versus lowest HOMA-IR quartile demonstrated significantly increased odds ratio of subclinical LVSD (OR = 2.22, 95% CI: 1.26–3.92; <i>P</i> = 0.006), while the TyG index showed no significant association with its prevalence (<i>P</i> = 0.98).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In a community-based population, elevated HOMA-IR demonstrated a robust association with subclinical LVSD, whereas the TyG index exhibited a more pronounced correlation with early diastolic dysfunction.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 1","pages":"60-72"},"PeriodicalIF":3.0,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627043","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}
Meng-Han Li, Jun-Wei Wang, Man-Rong Xu, Ya-Wen Zhang, Lian-Xi Li
Background
The association between estradiol/testosterone (E2/T) ratio and metabolic dysfunction-associated steatotic liver disease (MASLD) remains controversial. Moreover, few studies have explored their relationship in men with type 2 diabetes mellitus. We aimed to investigate the association of the E2/T ratio with MASLD in type 2 diabetes mellitus male patients.
Methods
This real-world observational study was performed in 1441 male type 2 diabetes mellitus patients. MASLD was determined by abdominal ultrasonography. The clinical characteristics and prevalence of MASLD were compared across the E2/T ratio quartiles. The association of the E2/T ratio and quartiles with MASLD was also evaluated using binary logistic regression.
Results
After adjusting for age and diabetes duration (DD), MASLD prevalence significantly increased across the E2/T ratio quartiles (37.7%, 42.6%, 53.1%, and 69.3%, respectively, P < 0.001 for trend). Fully adjusted logistic regression showed that both the E2/T ratio (OR: 2.201, 95% CI: 1.380–3.511, P = 0.001) and quartiles (P = 0.001) were positively associated with MASLD in males with type 2 diabetes mellitus. Furthermore, C-reactive protein (CRP) levels were significantly higher in patients with MASLD compared with those without (P < 0.001), and obviously increased across the E2/T ratio quartiles after controlling for age and DD (P = 0.016 for trend).
Conclusions
The E2/T ratio was independently and positively associated with the increased risk of MASLD in male type 2 diabetes mellitus patients, which may be attributed to the close association between the E2/T ratio and inflammation. The E2/T ratio may serve as a simple and practical indicator to assess the risk of MASLD in male type 2 diabetes mellitus patients.
{"title":"High estradiol/testosterone ratio increased the risk of metabolic dysfunction-associated steatotic liver disease in men with type 2 diabetes mellitus","authors":"Meng-Han Li, Jun-Wei Wang, Man-Rong Xu, Ya-Wen Zhang, Lian-Xi Li","doi":"10.1111/jdi.70202","DOIUrl":"10.1111/jdi.70202","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The association between estradiol/testosterone (E2/T) ratio and metabolic dysfunction-associated steatotic liver disease (MASLD) remains controversial. Moreover, few studies have explored their relationship in men with type 2 diabetes mellitus. We aimed to investigate the association of the E2/T ratio with MASLD in type 2 diabetes mellitus male patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This real-world observational study was performed in 1441 male type 2 diabetes mellitus patients. MASLD was determined by abdominal ultrasonography. The clinical characteristics and prevalence of MASLD were compared across the E2/T ratio quartiles. The association of the E2/T ratio and quartiles with MASLD was also evaluated using binary logistic regression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After adjusting for age and diabetes duration (DD), MASLD prevalence significantly increased across the E2/T ratio quartiles (37.7%, 42.6%, 53.1%, and 69.3%, respectively, <i>P</i> < 0.001 for trend). Fully adjusted logistic regression showed that both the E2/T ratio (OR: 2.201, 95% CI: 1.380–3.511, <i>P</i> = 0.001) and quartiles (<i>P</i> = 0.001) were positively associated with MASLD in males with type 2 diabetes mellitus. Furthermore, C-reactive protein (CRP) levels were significantly higher in patients with MASLD compared with those without (<i>P</i> < 0.001), and obviously increased across the E2/T ratio quartiles after controlling for age and DD (<i>P</i> = 0.016 for trend).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The E2/T ratio was independently and positively associated with the increased risk of MASLD in male type 2 diabetes mellitus patients, which may be attributed to the close association between the E2/T ratio and inflammation. The E2/T ratio may serve as a simple and practical indicator to assess the risk of MASLD in male type 2 diabetes mellitus patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 1","pages":"129-141"},"PeriodicalIF":3.0,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70202","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627217","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}
Leukocytes are implicated in the inflammatory cascades of diabetic retinopathy (DR), but their causal roles remain ambiguous. This study employed a two-sample Mendelian randomization (MR) analysis to dissect the causal effects of circulating leukocyte counts on DR risk.
Materials and Methods
We utilized summary statistics from large-scale genome-wide association studies (GWAS) for five leukocyte subtypes and DR in European-ancestry populations. The inverse-variance weighted (IVW) method was primary, supported by comprehensive sensitivity analyses including MR-Egger, weighted median, and the MR-Pleiotropy Residual Sum and Outlier (MR-PRESSO) test to ensure result robustness.
Results
A total of 2,136 leukocyte-related SNPs were extracted as instrumental variables for causal inference. MR analysis revealed that increased lymphocyte counts are associated with reduced DR risk (IVW OR = 0.93, 95% CI = 0.86–0.99, P = 0.03), while the initial association between higher eosinophil counts and DR risk (IVW OR = 1.11, 95% CI = 1.03–1.19, P < 0.01) was attenuated following correction for outliers. No significant associations were observed for basophil, monocyte, or neutrophil counts. Sensitivity analyses found no evidence of pleiotropy or substantial influence from single SNPs.
Conclusions
Our findings provide genetic evidence supporting a potential causal association between lymphocyte counts and diabetic retinopathy risk, while the association for eosinophil counts was attenuated after correction for outliers. These results highlight the importance of further investigating the physiological role of lymphocytes in diabetic retinopathy to inform effective prevention and treatment strategies.
目的/简介：白细胞与糖尿病视网膜病变（DR）的炎症级联反应有关，但其因果关系尚不明确。本研究采用双样本孟德尔随机化（MR）分析来剖析循环白细胞计数对DR风险的因果影响。材料和方法：我们利用了欧洲血统人群中5种白细胞亚型和DR的大规模全基因组关联研究（GWAS）的汇总统计数据。主要采用反方差加权（IVW）方法，并辅以综合敏感性分析，包括MR-Egger、加权中位数和mr -多效性残差和异常值（MR-PRESSO）检验，以确保结果的稳健性。结果：共提取了2136个与白细胞相关的snp作为因果推理的工具变量。MR分析显示，淋巴细胞计数增加与DR风险降低相关（IVW OR = 0.93, 95% CI = 0.86-0.99, P = 0.03），而嗜酸性粒细胞计数较高与DR风险之间的初始关联（IVW OR = 1.11, 95% CI = 1.03-1.19， P）。结论：我们的研究结果提供了遗传学证据，支持淋巴细胞计数与糖尿病视网膜病变风险之间的潜在因果关系，而嗜酸性粒细胞计数的关联在校正异常值后减弱。这些结果强调了进一步研究淋巴细胞在糖尿病视网膜病变中的生理作用，为有效的预防和治疗策略提供信息的重要性。
{"title":"Causal association between circulating leukocyte characteristics and diabetic retinopathy based on two-sample Mendelian randomization","authors":"Yan Wang, Yunxian Gao, Zhiqiang Wang, Luhua Wu, Lixia Guo, Xiaoqiang Zhang, Jiaxin Wu, Shanshan Shang","doi":"10.1111/jdi.70196","DOIUrl":"10.1111/jdi.70196","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>Leukocytes are implicated in the inflammatory cascades of diabetic retinopathy (DR), but their causal roles remain ambiguous. This study employed a two-sample Mendelian randomization (MR) analysis to dissect the causal effects of circulating leukocyte counts on DR risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We utilized summary statistics from large-scale genome-wide association studies (GWAS) for five leukocyte subtypes and DR in European-ancestry populations. The inverse-variance weighted (IVW) method was primary, supported by comprehensive sensitivity analyses including MR-Egger, weighted median, and the MR-Pleiotropy Residual Sum and Outlier (MR-PRESSO) test to ensure result robustness.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 2,136 leukocyte-related SNPs were extracted as instrumental variables for causal inference. MR analysis revealed that increased lymphocyte counts are associated with reduced DR risk (IVW OR = 0.93, 95% CI = 0.86–0.99, <i>P</i> = 0.03), while the initial association between higher eosinophil counts and DR risk (IVW OR = 1.11, 95% CI = 1.03–1.19, <i>P</i> < 0.01) was attenuated following correction for outliers. No significant associations were observed for basophil, monocyte, or neutrophil counts. Sensitivity analyses found no evidence of pleiotropy or substantial influence from single SNPs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings provide genetic evidence supporting a potential causal association between lymphocyte counts and diabetic retinopathy risk, while the association for eosinophil counts was attenuated after correction for outliers. These results highlight the importance of further investigating the physiological role of lymphocytes in diabetic retinopathy to inform effective prevention and treatment strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 2","pages":"267-279"},"PeriodicalIF":3.0,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12863003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627055","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}
<p>To the Editor,</p><p>We read with great interest the article by Saremi <i>et al</i>.<span><sup>1</sup></span>, which investigated the association of the leptin promoter G2548A variant and plasma leptin levels with the risk of Type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD) in an Iranian population. The study provides valuable preliminary insights into this genetic association in a previously understudied population. However, we wish to raise two methodological concerns that merit clarification to strengthen the interpretation of the findings.</p><p>First, the central biological premise of the study—that the polymorphism influences disease risk via elevated plasma leptin levels—appears inconsistent with the core comparative data. The authors conclude that the GG genotype and higher plasma leptin levels contribute to T2DM with CAD. However, table 2 demonstrates that the mean plasma leptin level was not significantly different between the case (T2DM + CAD) and control groups (14 ± 17.2 μg/mL vs. 15.9 ± 8.3 μg/mL, <i>P</i> = 0.224). This lack of a significant association in the primary group comparison challenges the proposed mechanistic pathway. The relationship between leptin and cardiometabolic diseases is complex and often non-linear, and a null finding in this fundamental analysis warrants careful discussion<span><sup>2</sup></span>. To substantiate the proposed mechanism, an analysis testing for an interaction effect between the genotype and leptin level on the disease outcome would be highly informative.</p><p>Second, the generalizability of the findings may be limited by the marked gender imbalance in the study cohort, which comprised 68% females and only 32% males. While the groups were matched, the overwhelming female predominance raises the possibility that the overall reported genetic associations are heavily influenced by the female subgroup. This concern is supported by the authors' own finding of a strong association between obesity and T2DM risk exclusively in females (OR = 2.89, <i>P</i> < 0.001). It is well established that genetic effects on complex traits like obesity and T2DM can exhibit significant sexual dimorphism<span><sup>3</sup></span>. Therefore, the conclusion that the LEP variant is a risk factor for the general “Iranian population” may be premature without demonstrating that the effect is consistent across genders. Presenting sex-stratified analyses for the primary genetic associations would greatly enhance the translational impact and validity of the conclusions.</p><p>In summary, we believe that addressing the apparent discrepancy between the proposed mechanism and the group comparison for leptin levels, and considering the influence of gender imbalance on the generalizability of the findings, is crucial for a robust interpretation of the evidence. Clarifying these points would significantly strengthen the contribution of this interesting study to the field.</p><p>The authors declare no conflic
致编辑：我们怀着极大的兴趣阅读了Saremi等人的文章1，该文章调查了伊朗人群中瘦素启动子G2548A变异和血浆瘦素水平与2型糖尿病（T2DM）和冠状动脉疾病（CAD）风险的关系。这项研究为之前未被充分研究的人群提供了有价值的初步见解。然而，我们希望提出两个值得澄清的方法问题，以加强对调查结果的解释。首先，该研究的核心生物学前提——多态性通过升高的血浆瘦素水平影响疾病风险——似乎与核心比较数据不一致。作者得出结论，GG基因型和较高的血浆瘦素水平有助于T2DM合并CAD。然而，表2显示，T2DM + CAD组与对照组的平均血浆瘦素水平差异无统计学意义（14±17.2 μg/mL vs. 15.9±8.3 μg/mL, P = 0.224）。在初级组比较中缺乏重要的关联，这对提出的机制途径提出了挑战。瘦素与心脏代谢疾病之间的关系是复杂的，往往是非线性的，在这一基础分析中的零发现值得仔细讨论。为了证实所提出的机制，对基因型和瘦素水平对疾病结果的相互作用的分析测试将是非常有用的。其次，研究结果的普遍性可能受到研究队列中明显的性别失衡的限制，该队列中68%的女性和32%的男性。虽然这些群体是匹配的，但压倒性的女性优势提高了总体报告的遗传关联受到女性亚群体严重影响的可能性。这一担忧得到了作者自己的研究结果的支持，即肥胖和2型糖尿病风险之间存在强烈关联，仅在女性中存在（OR = 2.89, P < 0.001）。众所周知，遗传对肥胖和2型糖尿病等复杂性状的影响可以表现出显著的性别二态性。因此，LEP变异是一般“伊朗人口”的危险因素的结论可能为时过早，因为没有证明这种影响在性别之间是一致的。对主要遗传关联进行性别分层分析将大大提高结论的翻译影响和有效性。总之，我们认为，解决所提出的机制与瘦素水平的组比较之间的明显差异，并考虑性别失衡对研究结果的普遍性的影响，对于证据的有力解释至关重要。澄清这些要点将大大加强这项有趣的研究对该领域的贡献。作者声明无利益冲突。研究方案的批准：无。知情同意：无。注册批准日期及注册编号。研究/试验：无。动物研究：无。数据共享不适用于本文，因为本研究没有创建或分析新的数据。
{"title":"Considerations on mechanistic coherence and generalizability in the study of leptin G2548A variant and T2DM with CAD","authors":"Yingxia Jiang, Yangying Chu","doi":"10.1111/jdi.70192","DOIUrl":"10.1111/jdi.70192","url":null,"abstract":"<p>To the Editor,</p><p>We read with great interest the article by Saremi <i>et al</i>.<span><sup>1</sup></span>, which investigated the association of the leptin promoter G2548A variant and plasma leptin levels with the risk of Type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD) in an Iranian population. The study provides valuable preliminary insights into this genetic association in a previously understudied population. However, we wish to raise two methodological concerns that merit clarification to strengthen the interpretation of the findings.</p><p>First, the central biological premise of the study—that the polymorphism influences disease risk via elevated plasma leptin levels—appears inconsistent with the core comparative data. The authors conclude that the GG genotype and higher plasma leptin levels contribute to T2DM with CAD. However, table 2 demonstrates that the mean plasma leptin level was not significantly different between the case (T2DM + CAD) and control groups (14 ± 17.2 μg/mL vs. 15.9 ± 8.3 μg/mL, <i>P</i> = 0.224). This lack of a significant association in the primary group comparison challenges the proposed mechanistic pathway. The relationship between leptin and cardiometabolic diseases is complex and often non-linear, and a null finding in this fundamental analysis warrants careful discussion<span><sup>2</sup></span>. To substantiate the proposed mechanism, an analysis testing for an interaction effect between the genotype and leptin level on the disease outcome would be highly informative.</p><p>Second, the generalizability of the findings may be limited by the marked gender imbalance in the study cohort, which comprised 68% females and only 32% males. While the groups were matched, the overwhelming female predominance raises the possibility that the overall reported genetic associations are heavily influenced by the female subgroup. This concern is supported by the authors' own finding of a strong association between obesity and T2DM risk exclusively in females (OR = 2.89, <i>P</i> < 0.001). It is well established that genetic effects on complex traits like obesity and T2DM can exhibit significant sexual dimorphism<span><sup>3</sup></span>. Therefore, the conclusion that the LEP variant is a risk factor for the general “Iranian population” may be premature without demonstrating that the effect is consistent across genders. Presenting sex-stratified analyses for the primary genetic associations would greatly enhance the translational impact and validity of the conclusions.</p><p>In summary, we believe that addressing the apparent discrepancy between the proposed mechanism and the group comparison for leptin levels, and considering the influence of gender imbalance on the generalizability of the findings, is crucial for a robust interpretation of the evidence. Clarifying these points would significantly strengthen the contribution of this interesting study to the field.</p><p>The authors declare no conflic","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 2","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12862993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627132","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}
To assess racial and ethnic differences in gestational diabetes mellitus (GDM) prevalence and perinatal outcomes among U.S. women with normal prepregnancy body mass index (BMI).
Design, Setting, and Participants
Retrospective, population-based cohort study using 2021–2023 US National Vital Statistics System data. Included singleton live births to women aged 18–44 years with BMI 18.5–24.9 kg/m2. Exclusions were preexisting hypertension or diabetes, multiple gestations, missing covariates, or implausible data.
Exposures
Race/ethnicity: White, Black, Asian, and Other (Native American/Alaska Native, Native Hawaiian/Pacific Islander, and multiracial).
Main Outcomes and Measures
Primary outcome: GDM prevalence by race. Logistic regression estimated adjusted odds ratios (aORs) with White women as the reference. Secondary outcomes: preterm delivery macrosomia, NICU admission, and neonatal respiratory failure.
Results
A total of 3,754,684 women, GDM prevalence was highest in Asians (12.5%). Compared with White women, Asians had nearly threefold higher odds of GDM (aOR, 2.95; 95% CI, 2.91–3.00). GDM was associated with preterm delivery (aOR, 1.23; 95% CI, 1.22–1.25), NICU admission (aOR, 1.26; 95% CI, 1.24–1.28), and neonatal respiratory failure (aOR, 1.27; 95% CI, 1.22–1.32), in all racial groups. Macrosomia was increased only in Black (aOR, 1.55; 95% CI, 1.43–1.68) and Other (aOR, 1.21; 95% CI, 1.08–1.34).
Conclusions
Among women with normal BMI, substantial racial disparities in GDM prevalence and outcomes exist, with Asian women at the highest risk. Our results support earlier and ethnicity-tailored GDM screening among women with normal BMI—particularly Asian women—plus proactive counseling on glucose monitoring and culturally adapted lifestyle interventions during pregnancy.
{"title":"Racial disparities in the prevalence and perinatal outcomes of gestational diabetes among women with normal body mass index","authors":"Hongdan Zhu, Jing Pan, Haitao Pan","doi":"10.1111/jdi.70195","DOIUrl":"10.1111/jdi.70195","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To assess racial and ethnic differences in gestational diabetes mellitus (GDM) prevalence and perinatal outcomes among U.S. women with normal prepregnancy body mass index (BMI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design, Setting, and Participants</h3>\u0000 \u0000 <p>Retrospective, population-based cohort study using 2021–2023 US National Vital Statistics System data. Included singleton live births to women aged 18–44 years with BMI 18.5–24.9 kg/m<sup>2</sup>. Exclusions were preexisting hypertension or diabetes, multiple gestations, missing covariates, or implausible data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Exposures</h3>\u0000 \u0000 <p>Race/ethnicity: White, Black, Asian, and Other (Native American/Alaska Native, Native Hawaiian/Pacific Islander, and multiracial).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main Outcomes and Measures</h3>\u0000 \u0000 <p>Primary outcome: GDM prevalence by race. Logistic regression estimated adjusted odds ratios (aORs) with White women as the reference. Secondary outcomes: preterm delivery macrosomia, NICU admission, and neonatal respiratory failure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 3,754,684 women, GDM prevalence was highest in Asians (12.5%). Compared with White women, Asians had nearly threefold higher odds of GDM (aOR, 2.95; 95% CI, 2.91–3.00). GDM was associated with preterm delivery (aOR, 1.23; 95% CI, 1.22–1.25), NICU admission (aOR, 1.26; 95% CI, 1.24–1.28), and neonatal respiratory failure (aOR, 1.27; 95% CI, 1.22–1.32), in all racial groups. Macrosomia was increased only in Black (aOR, 1.55; 95% CI, 1.43–1.68) and Other (aOR, 1.21; 95% CI, 1.08–1.34).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Among women with normal BMI, substantial racial disparities in GDM prevalence and outcomes exist, with Asian women at the highest risk. Our results support earlier and ethnicity-tailored GDM screening among women with normal BMI—particularly Asian women—plus proactive counseling on glucose monitoring and culturally adapted lifestyle interventions during pregnancy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 1","pages":"142-149"},"PeriodicalIF":3.0,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70195","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145601364","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}
Cheng Li, Lingyan Qiao, Juan Ge, Sicui Hu, Hongxiu Yang, Conghui Hu, Tang Li
Background
Type 1 diabetes mellitus (T1DM) arises from autoimmune destruction of pancreatic β-cells. Pleomorphic adenoma gene-like 1 (PLAGL1) overexpression has been linked to β-cell apoptosis, but molecular mechanisms remain incompletely understood. This study explored whether PLAGL1 exacerbates T1DM by promoting oxidative stress-induced DNA damage and activating the cGAS/STING inflammatory pathway.
Methods
The mouse β-cell line NIT-1 was transfected with PLAGL1 overexpression plasmids or specific siRNA. Mitochondrial and nuclear DNA damage was assessed through comet assays, 8-OHdG ELISA, and Western blot analysis of key DNA repair proteins, including XRCC1, OGG1, and PARP1. Oxidative stress was evaluated by measuring superoxide dismutase (SOD) activity and the glutathione redox state (GSH/GSSG ratio), while apoptosis was examined via expression levels of BCL2, BAX, and cleaved Caspase-3. To investigate pathway involvement, pharmacological inhibitors—RU.521 (targeting cGAS) and H-151 (targeting STING)—were applied. In NOD mice, PLAGL1 overexpression was combined with cGAS/STING inhibition; glucose tolerance was subsequently evaluated, and pancreatic tissue was subjected to histopathological examination.
Results
Overexpression of PLAGL1 triggered substantial mitochondrial and nuclear DNA damage, which was accompanied by elevated oxidative stress and compromised DNA repair. Consequently, cytoplasmic DNA accumulated, leading to activation of the cGAS/STING pathway and subsequent β-cell apoptosis and functional decline. Treatment with the cGAS inhibitor RU-521 or the STING inhibitor H-151 markedly attenuated apoptosis and restored insulin secretion in PLAGL1-overexpressing NIT-1 cells. In NOD mice, PLAGL1 overexpression accelerated diabetes progression, whereas inhibition of the cGAS/STING axis preserved β-cell mass, improved glucose homeostasis, and sustained insulin output. Histological evaluation further confirmed that inhibition of this signaling pathway helped maintain normal islet architecture.
Conclusion
Our findings demonstrated that PLAGL1 exacerbates β-cell loss in type 1 diabetes by driving oxidative DNA damage and activating the cGAS/STING signaling cascade. Therapeutic intervention targeting this axis may therefore represent a promising strategy to protect β-cells and attenuate disease progression.
{"title":"PLAGL1 overexpression exacerbates type 1 diabetes by inducing β-cell apoptosis via oxidative stress-dependent dual DNA damage and cGAS/STING pathway activation","authors":"Cheng Li, Lingyan Qiao, Juan Ge, Sicui Hu, Hongxiu Yang, Conghui Hu, Tang Li","doi":"10.1111/jdi.70204","DOIUrl":"10.1111/jdi.70204","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Type 1 diabetes mellitus (T1DM) arises from autoimmune destruction of pancreatic β-cells. Pleomorphic adenoma gene-like 1 (PLAGL1) overexpression has been linked to β-cell apoptosis, but molecular mechanisms remain incompletely understood. This study explored whether PLAGL1 exacerbates T1DM by promoting oxidative stress-induced DNA damage and activating the cGAS/STING inflammatory pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The mouse β-cell line NIT-1 was transfected with PLAGL1 overexpression plasmids or specific siRNA. Mitochondrial and nuclear DNA damage was assessed through comet assays, 8-OHdG ELISA, and Western blot analysis of key DNA repair proteins, including XRCC1, OGG1, and PARP1. Oxidative stress was evaluated by measuring superoxide dismutase (SOD) activity and the glutathione redox state (GSH/GSSG ratio), while apoptosis was examined via expression levels of BCL2, BAX, and cleaved Caspase-3. To investigate pathway involvement, pharmacological inhibitors—RU.521 (targeting cGAS) and H-151 (targeting STING)—were applied. In NOD mice, PLAGL1 overexpression was combined with cGAS/STING inhibition; glucose tolerance was subsequently evaluated, and pancreatic tissue was subjected to histopathological examination.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Overexpression of PLAGL1 triggered substantial mitochondrial and nuclear DNA damage, which was accompanied by elevated oxidative stress and compromised DNA repair. Consequently, cytoplasmic DNA accumulated, leading to activation of the cGAS/STING pathway and subsequent β-cell apoptosis and functional decline. Treatment with the cGAS inhibitor RU-521 or the STING inhibitor H-151 markedly attenuated apoptosis and restored insulin secretion in PLAGL1-overexpressing NIT-1 cells. In NOD mice, PLAGL1 overexpression accelerated diabetes progression, whereas inhibition of the cGAS/STING axis preserved β-cell mass, improved glucose homeostasis, and sustained insulin output. Histological evaluation further confirmed that inhibition of this signaling pathway helped maintain normal islet architecture.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings demonstrated that PLAGL1 exacerbates β-cell loss in type 1 diabetes by driving oxidative DNA damage and activating the cGAS/STING signaling cascade. Therapeutic intervention targeting this axis may therefore represent a promising strategy to protect β-cells and attenuate disease progression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 1","pages":"12-24"},"PeriodicalIF":3.0,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70204","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145601386","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}
The MiniMed™ 780G® is effective for improving glycemic control; however, few studies have specifically examined the impact of upgrading from MiniMed™ 770G® to MiniMed™ 780G® in adults. We determined the effects of upgrading from MiniMed™ 770G® to MiniMed™ 780G® (780G) on glucose management, psychological distress, daily life quality, and sleep in type 1 diabetes mellitus (T1DM).
Materials and Methods
In this single-center prospective study, we observed 21 adults who transitioned from the MiniMed™ 770G® to the 780G for 3 months. Glycemic outcomes, insulin delivery parameters, frequency of alarms, and sensor calibrations were assessed. Patient-reported outcomes were evaluated using the Problem Areas in Diabetes (PAID), the Diabetes Treatment Satisfaction Questionnaire status version, the Diabetes Therapy-Related Quality of Life, and the Pittsburgh Sleep Quality Index.
Results
Glycated hemoglobin (HbA1c) decreased (7.5 ± 1.3%–7.0 ± 0.8%, mean difference: −0.5%, 95% Confidence Interval (CI): −0.9 to −0.1; P = 0.018). Time in tight range (TITR) showed trends toward improvement (44.9 ± 15.5%–48.9 ± 15.5%, mean difference: 4.0%, 95% CI: −0.7 to 8.6; P = 0.090). Alarm frequency declined (11.9 ± 8.7–7.1 ± 5.5 times/day, mean difference: −4.8, 95% CI: −7.0 to −2.6; P = 0.0002), and calibration frequency decreased (3.6 ± 2.2–0.8 ± 0.6 times/day, mean difference: −2.8, 95% CI: −3.7 to −1.9; P < 0.0001). The PAID score improved, decreasing from 38.7 ± 19.9 to 31.7 ± 19.3 (mean difference: −7.0, 95% CI: −14.7 to 0.7; P = 0.074).
Conclusions
Favorable changes in HbA1c, TITR, and PAID scores suggest potential glycemic and psychological benefits.
{"title":"Efficacy of MiniMed™ 780G® on glucose management, sleep quality, and psychological aspects in persons with type 1 diabetes treated with MiniMed™ 770G®: A 3-month prospective single-center observational study","authors":"Tomoaki Akiyama, Kazuki Orime, Ryoichi Akamatsu, Taichi Suezono, Mako Akiyama, Arisa Matsuura, Ayano Kaneko, Tadashi Yamakawa, Satoru Shinoda, Yasuo Terauchi","doi":"10.1111/jdi.70198","DOIUrl":"10.1111/jdi.70198","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims/Introduction</h3>\u0000 \u0000 <p>The MiniMed™ 780G® is effective for improving glycemic control; however, few studies have specifically examined the impact of upgrading from MiniMed™ 770G® to MiniMed™ 780G® in adults. We determined the effects of upgrading from MiniMed™ 770G® to MiniMed™ 780G® (780G) on glucose management, psychological distress, daily life quality, and sleep in type 1 diabetes mellitus (T1DM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>In this single-center prospective study, we observed 21 adults who transitioned from the MiniMed™ 770G® to the 780G for 3 months. Glycemic outcomes, insulin delivery parameters, frequency of alarms, and sensor calibrations were assessed. Patient-reported outcomes were evaluated using the Problem Areas in Diabetes (PAID), the Diabetes Treatment Satisfaction Questionnaire status version, the Diabetes Therapy-Related Quality of Life, and the Pittsburgh Sleep Quality Index.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Glycated hemoglobin (HbA1c) decreased (7.5 ± 1.3%–7.0 ± 0.8%, mean difference: −0.5%, 95% Confidence Interval (CI): −0.9 to −0.1; <i>P</i> = 0.018). Time in tight range (TITR) showed trends toward improvement (44.9 ± 15.5%–48.9 ± 15.5%, mean difference: 4.0%, 95% CI: −0.7 to 8.6; <i>P</i> = 0.090). Alarm frequency declined (11.9 ± 8.7–7.1 ± 5.5 times/day, mean difference: −4.8, 95% CI: −7.0 to −2.6; <i>P</i> = 0.0002), and calibration frequency decreased (3.6 ± 2.2–0.8 ± 0.6 times/day, mean difference: −2.8, 95% CI: −3.7 to −1.9; <i>P</i> < 0.0001). The PAID score improved, decreasing from 38.7 ± 19.9 to 31.7 ± 19.3 (mean difference: −7.0, 95% CI: −14.7 to 0.7; <i>P</i> = 0.074).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Favorable changes in HbA1c, TITR, and PAID scores suggest potential glycemic and psychological benefits.</p>\u0000 </section>\u0000 </div>","PeriodicalId":51250,"journal":{"name":"Journal of Diabetes Investigation","volume":"17 1","pages":"165-173"},"PeriodicalIF":3.0,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdi.70198","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145601419","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}
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