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Analysis of HMGCS2 Expression and TG Lipidomics in the Perirenal Adipose Tissue of Obese Diabetic Nephropathy Mice 肥胖糖尿病肾病小鼠肾周脂肪组织HMGCS2表达及TG脂质组学分析
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-25 DOI: 10.1111/1753-0407.70125
Yuhong Huang, Miao Zeng, Mengxue Yang, Xiaodi Zheng, Lulu Jin, Rui Zhang, Yueyue Wu, Fei Li, Bo Yang, Jun Liu

Background and Aims

Renal HMGCS2 upregulation is associated with lipid deposition. However, the expression pattern and role of Hmgcs2 in the perirenal adipose tissue (PRAT) is not clear. This study was designed to elucidate the contribution of Hmgcs2 in the pathogenesis of obese diabetic kidney disease mice.

Methods

12-week-old db/db (diabetic) and db/m (control) mice were fed high-fat or normal diets, respectively. At 12, 16, and 20 weeks, mice (n = 4/group/timepoint) were euthanized for metabolic profiling (body weight, blood glucose, urinary ACR) and tissue collection (kidney, PRAT). Tissues were analyzed for TNF-α mRNA (qPCR), HMGCS2 expression (IHC/WB/IF), lipid deposition (Oil Red O), and histopathology (HE staining). PRAT triglycerides (colorimetric assay) and lipidomics (UPLC–MS/MS) were assessed. HMGCS2-knockout mice (CRISPR-generated) underwent metabolic tests (OGTT/ITT) before terminal tissue analysis.

Results

(1) Compared with db/mPRAT, db/db PRAT had significantly enlarged adipocytes and increased TG content. The expression of HMGCS2 in renal and PRAT was significantly greater in db/db mice. (2) Hmgcs2 was equally expressed in db/db renal and PRAT. PRAT expansion increases the inflammatory factor TNF-α, which occurs earlier in PRAT than in renal tissue.(3) Genetic ablation of HMGCS2 in mice significantly decreased renal and PRAT TG accumulation, concomitant with attenuated inflammation. (4) LC–MS/MS analysis revealed that TGs are the main PRAT lipid component. Db/db PRAT TG content was significantly greater than that in db/m. Db/db proximal PRAT TG content is greater than that of the distal region, with seven upregulated TG lipid molecules (TG (38:3)+NH4, TG (50:5)+NH4, TG (52:12e)+Na, TG (56:9e)+H, TG (57:6e)+H, FA (18:1)+H, and ST (m45:3)+NH4), among which TG (38:3) has the highest expression.

Conclusion

Our study strongly suggests that lipids, especially TGs, are deposited in the kidneys and PRAT of DKD mice, with proximal–distal PRAT differences. HMGCS2 may be involved in kidneys and PRAT TG deposition. PRAT-lipid-metabolism-induced inflammation may occur before blood-glucose-related kidney damage.

背景与目的肾HMGCS2上调与脂质沉积有关。然而,Hmgcs2在肾周脂肪组织(PRAT)中的表达模式和作用尚不清楚。本研究旨在阐明Hmgcs2在肥胖糖尿病肾病小鼠发病机制中的作用。方法12周龄db/db(糖尿病小鼠)和db/m(对照组小鼠)分别饲喂高脂饲料和正常饲料。在12、16和20周时,对小鼠(n = 4/组/时间点)实施安乐死,进行代谢分析(体重、血糖、尿ACR)和组织收集(肾脏、PRAT)。组织分析TNF-α mRNA (qPCR)、HMGCS2表达(IHC/WB/IF)、脂质沉积(Oil Red O)和组织病理学(HE染色)。评估PRAT甘油三酯(比色法)和脂质组学(UPLC-MS /MS)。hmgcs2敲除小鼠(crispr生成)在进行终末组织分析之前进行代谢测试(OGTT/ITT)。结果(1)与db/mPRAT相比,db/db PRAT显著增大脂肪细胞,增加TG含量。HMGCS2在肾和PRAT中的表达在db/db小鼠中显著增加。(2) Hmgcs2在db/db肾组织和PRAT组织中表达量相等。PRAT扩张增加炎症因子TNF-α,其在PRAT中比在肾组织中更早发生。(3)小鼠HMGCS2基因消融可显著降低肾脏和PRAT TG积累,并伴有炎症减轻。(4) LC-MS /MS分析显示tg是PRAT的主要脂质成分。Db/ Db PRAT TG含量显著高于Db/ m。近端PRAT区TG含量Db/ Db大于远端,7种TG脂质分子(TG (38:3)+NH4、TG (50:5)+NH4、TG (52:12e)+Na、TG (56:9e)+H、TG (57:6e)+H、FA (18:1)+H、ST (m45:3)+NH4)表达上调,其中TG(38:3)表达量最高。结论脂质,尤其是tg,在DKD小鼠的肾脏和PRAT中沉积,且PRAT近端和远端存在差异。HMGCS2可能参与肾脏和PRAT的TG沉积。prat -脂质代谢引起的炎症可能发生在血糖相关性肾损害之前。
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引用次数: 0
Comment on “Time Trends in Cardiovascular Event Incidence in New-Onset Type 2 Diabetes: A Population-Based Cohort Study From Germany” 《新发2型糖尿病心血管事件发生率的时间趋势:一项来自德国的基于人群的队列研究》
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-23 DOI: 10.1111/1753-0407.70130
Saraswati Sah, Rachana Mehta, Ranjana Sah
<p>We read with great interest the study by Sarabhai et al., which provides valuable insights into the temporal evolution of cardiovascular events in newly diagnosed type 2 diabetes (T2D) patients in Germany over a 17-year period [<span>1</span>]. Although the reduction in the 5-year incidence of coronary heart disease (CHD) and transient ischemic attack (TIA) is encouraging, we believe several methodological and conceptual limitations deserve further discussion to contextualize the findings.</p><p>First, the study's exclusion of laboratory parameters such as glycated hemoglobin (HbA1c), lipid panels, and renal function significantly constrains the capacity to adjust for the quality of glycemic and metabolic control—central determinants of cardiovascular outcomes in T2D [<span>2, 3</span>]. Reliance solely on ICD-10 codes, though validated for primary diagnoses, does not differentiate between stable and unstable angina, nor does it account for silent myocardial infarctions, which are prevalent in diabetic populations [<span>4</span>]. This coding limitation may partially explain the paradoxically unchanged incidence of myocardial infarction (MI) despite improvements in CHD.</p><p>Second, the use of chronic obstructive pulmonary disease (COPD) as a proxy for smoking status introduces exposure misclassification. Smoking is a potent modifiable risk factor for both MI and ischemic stroke (IS) [<span>5</span>], and its secular decline in Germany over this period likely contributed to cardiovascular risk reduction. Without direct smoking data, the differential attribution of risk to diabetes-specific interventions versus population-wide trends remains unresolved.</p><p>Third, the apparent stability in MI and IS incidence may also be an artifact of cohort composition rather than a true epidemiological plateau. Although the authors matched for age and sex, no stratification by socioeconomic status, regional healthcare access, or medication use—particularly statins and antihypertensives—was undertaken. These variables influence the uptake and effectiveness of cardioprotective interventions [<span>6</span>]. Furthermore, the analysis does not disaggregate event timing within the five-year follow-up, thereby overlooking early versus late event clustering, which may offer clues about legacy effects from undiagnosed prediabetes.</p><p>Fourth, the demographic distribution masks evolving baseline risk. Although mean age and sex proportions remained unchanged, the increased prevalence of hypertension and obesity in the later cohort signals rising baseline cardiovascular risk. Paradoxically, these upward shifts might dilute the observable impact of improved care. Consequently, the unchanged IS and MI rates may reflect counterbalancing effects between therapeutic progress and population-level risk escalation.</p><p>Finally, the study's conclusion that CHD and TIA reduction reflects successful diabetes management may overstate causality. CHD includes chronic, often
我们非常感兴趣地阅读了Sarabhai等人的研究,该研究为德国新诊断的2型糖尿病(T2D)患者心血管事件的时间演变提供了宝贵的见解,为期17年[10]。尽管5年冠心病(CHD)和短暂性脑缺血发作(TIA)发病率的降低令人鼓舞,但我们认为,一些方法学和概念上的局限性值得进一步讨论,以便将研究结果与背景联系起来。首先,该研究排除了实验室参数,如糖化血红蛋白(HbA1c)、脂质面板和肾功能,这明显限制了对血糖和代谢控制质量的调整能力,而血糖和代谢控制是糖尿病心血管结局的核心决定因素[2,3]。仅依赖ICD-10编码,虽然在初级诊断中得到了验证,但不能区分稳定型和不稳定型心绞痛,也不能解释在糖尿病人群中普遍存在的无症状心肌梗死[10]。这种编码限制可能部分解释了尽管冠心病有所改善,但心肌梗死(MI)发生率却矛盾地没有变化。其次,使用慢性阻塞性肺疾病(COPD)作为吸烟状况的代表会导致暴露错误分类。吸烟是心肌梗死和缺血性卒中(is)的一个有效的可改变的危险因素,在这一时期,吸烟在德国的长期下降可能有助于心血管风险的降低。在没有直接吸烟数据的情况下,糖尿病特定干预措施的风险归因与人群整体趋势的差异仍未得到解决。第三,心肌梗死和IS发病率的明显稳定性也可能是队列组成的人为因素,而不是真正的流行病学平台期。虽然作者的年龄和性别相匹配,但没有按社会经济地位、地区医疗保健获取或药物使用(特别是他汀类药物和抗高血压药物)进行分层。这些变量影响心脏保护干预措施的吸收和有效性。此外,该分析没有分解5年随访期间的事件时间,从而忽略了早期和晚期事件聚类,这可能为未确诊的前驱糖尿病的遗留影响提供线索。第四,人口分布掩盖了不断变化的基线风险。虽然平均年龄和性别比例保持不变,但后期队列中高血压和肥胖患病率的增加表明基线心血管风险上升。矛盾的是,这些向上的转变可能会淡化改善护理的可观察到的影响。因此,不变的IS和MI率可能反映了治疗进展和人群水平风险升级之间的平衡效应。最后,该研究的结论是冠心病和TIA的减少反映了成功的糖尿病管理,这可能夸大了因果关系。冠心病包括慢性的,通常是无症状的病理,需要长期的门诊治疗和诊断的进步。相比之下,心肌梗死和IS通常反映了急性的、不可逆的血管损伤终末累积,甚至可能在明显的T2D诊断之前。这提出了一种可能性,即本研究未解决的糖尿病前期血管损伤可能是结果停滞的主要驱动因素。总之,虽然该研究捕捉到了重要的时间变化,但对于从更广泛的流行病学转变中解开糖尿病特异性干预的贡献,更细粒度、生物标志物信息和纵向分层分析是必不可少的。Saraswati Sah:概念化,方法论,验证,写作-原稿,写作-审查和编辑。Rachana Mehta:写作-原稿,写作-审查和编辑。Ranjana Sah:监督,项目管理,写作-原稿,写作-审查和编辑。作者没有什么可报告的。作者没有什么可报告的。作者声明无利益冲突。
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引用次数: 0
Author Response to the Comment on “Time Trends in Cardiovascular Event Incidence in New-Onset Type 2 Diabetes: A Population-Based Cohort Study From Germany” 作者对“新发2型糖尿病心血管事件发生率的时间趋势:来自德国的一项基于人群的队列研究”评论的回应
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-23 DOI: 10.1111/1753-0407.70128
Theresia Sarabhai, Karel Kostev
<p>We sincerely thank the authors of the comment and appreciate the opportunity to respond to clarify specific aspects of our study.</p><p>First of all, we agree that laboratory parameters are key indicators of metabolic control and cardiovascular risk. Although the Disease Analyzer database includes laboratory data from a subset of practices, laboratory values were not consistently available over time and across patients in our cohort. Therefore, we opted not to include them in our analyses. To address this limitation, we adjusted for chronic comorbidities known to be associated with poor metabolic control, such as hypertension, dyslipidemia, and obesity (coded diagnoses). Previous studies demonstrated the validity of the Disease Analyzer database especially for case–control studies focusing on diabetes mellitus [<span>1</span>]. Furthermore, by focusing on first cardiovascular events in a well-defined incident T2D cohort without prior CVD, we aimed to reduce confounding and improve internal validity despite the absence of uniformly available laboratory markers.</p><p>We acknowledge the potential limitations of relying solely on ICD-10 codes, as we stated in the manuscript. However, the Disease Analyzer database has been extensively validated and has demonstrated a high positive predictive value for major cardiovascular diagnoses, including MI [<span>1-3</span>]. We appreciate the reference by Tsai et al. [<span>4</span>], which highlights the strong validity of ICD-10-CM codes for identifying AMI subtypes. Although their work confirms excellent performance metrics, our interest was not the subtype but rather the trend in overall MI incidence.</p><p>Indeed, smoking is a critical risk factor. As stated, individual smoking status is not recorded in the Disease Analyzer database. We therefore followed established practice in using COPD as a proxy, recognizing its limitations. As noted in the literature, around 90% of patients with COPD are current or former smokers [<span>5</span>]. However, not all smokers develop COPD, so COPD cannot fully replace smoking status, but provides an approximate indicator. We clearly acknowledged this limitation in the manuscript. Importantly, smoking prevalence in Germany has declined over the study period, which may have contributed to overall cardiovascular improvements. However, as these trends would influence both diabetic and nondiabetic populations alike, our interpretation focused on diabetes-specific outcomes in a matched T2D cohort.</p><p>We agree that socioeconomic status and medication use are important factors. Although these data were not available in sufficient detail in our database, our large, matched cohorts and adjustment for key comorbidities offer valuable insights into temporal patterns. The unchanged MI and IS incidence, despite improvements in CHD and TIA, likely reflects a balance between earlier vascular damage and therapeutic progress. Although we did not stratify events by time since diagno
我们真诚地感谢评论的作者,并感谢有机会回应澄清我们研究的具体方面。首先,我们同意实验室参数是代谢控制和心血管风险的关键指标。尽管疾病分析数据库包括来自实践子集的实验室数据,但实验室值在我们的队列中并不是始终如一地可用。因此,我们选择不将它们包括在我们的分析中。为了解决这一局限性,我们调整了已知与代谢控制不良相关的慢性合并症,如高血压、血脂异常和肥胖(编码诊断)。先前的研究证实了疾病分析数据库的有效性,特别是针对糖尿病的病例对照研究。此外,通过关注明确的T2D队列中没有CVD的首次心血管事件,我们旨在减少混淆并提高内部有效性,尽管缺乏统一可用的实验室标记。正如我们在手稿中所述,我们承认仅依赖ICD-10代码的潜在局限性。然而,Disease Analyzer数据库已被广泛验证,并显示出对主要心血管诊断的高阳性预测价值,包括心肌梗塞[1-3]。我们赞赏Tsai等人[4]的参考文献,该文献强调了ICD-10-CM代码在识别AMI亚型方面的强大有效性。虽然他们的工作证实了出色的表现指标,但我们的兴趣不是亚型,而是总体心肌梗死发病率的趋势。事实上,吸烟是一个关键的风险因素。如前所述,个人吸烟状况未记录在疾病分析数据库中。因此,在认识到COPD的局限性后,我们遵循了使用COPD作为替代指标的既定做法。如文献所述,约90%的COPD患者是当前或曾经的吸烟者。然而,并非所有吸烟者都会发展为慢性阻塞性肺病,因此慢性阻塞性肺病不能完全取代吸烟状态,但提供了一个近似的指标。我们在手稿中清楚地承认了这一局限性。重要的是,在研究期间,德国的吸烟率有所下降,这可能有助于整体心血管疾病的改善。然而,由于这些趋势会影响糖尿病和非糖尿病人群,我们的解释集中在匹配的T2D队列中糖尿病特异性结果。我们同意社会经济地位和药物使用是重要因素。虽然这些数据在我们的数据库中没有足够的细节,但我们的大型匹配队列和关键合并症的调整为时间模式提供了有价值的见解。尽管冠心病和TIA有所改善,但心肌梗死和心肌梗死发生率不变,可能反映了早期血管损伤和治疗进展之间的平衡。虽然我们没有根据诊断后的时间对事件进行分层,但我们的5年随访捕获了总体发病率模式。高血压和肥胖症的增加可能抵消了改善护理的一些好处。我们没有推断因果关系,而是将我们的发现解释为时间趋势,承认冠心病和TIA的下降可能是由临床改善和人口水平变化驱动的多因素。尽管存在局限性,但我们的研究为T2D事件的心血管趋势提供了新的见解。我们欢迎进一步的研究纳入生活方式、生物标志物和社会经济地位数据来扩展这些发现。向特蕾西娅·萨拉巴伊和卡雷尔·科斯特夫致以诚挚的问候。根据ICMJE指南,个人贡献如下:T.S.和K.K.手稿起草,以及响应协调。所有作者都已阅读并批准了回复的最终版本,并同意对工作的各个方面负责。作者没有什么可报告的。作者声明无利益冲突。
{"title":"Author Response to the Comment on “Time Trends in Cardiovascular Event Incidence in New-Onset Type 2 Diabetes: A Population-Based Cohort Study From Germany”","authors":"Theresia Sarabhai,&nbsp;Karel Kostev","doi":"10.1111/1753-0407.70128","DOIUrl":"https://doi.org/10.1111/1753-0407.70128","url":null,"abstract":"&lt;p&gt;We sincerely thank the authors of the comment and appreciate the opportunity to respond to clarify specific aspects of our study.&lt;/p&gt;&lt;p&gt;First of all, we agree that laboratory parameters are key indicators of metabolic control and cardiovascular risk. Although the Disease Analyzer database includes laboratory data from a subset of practices, laboratory values were not consistently available over time and across patients in our cohort. Therefore, we opted not to include them in our analyses. To address this limitation, we adjusted for chronic comorbidities known to be associated with poor metabolic control, such as hypertension, dyslipidemia, and obesity (coded diagnoses). Previous studies demonstrated the validity of the Disease Analyzer database especially for case–control studies focusing on diabetes mellitus [&lt;span&gt;1&lt;/span&gt;]. Furthermore, by focusing on first cardiovascular events in a well-defined incident T2D cohort without prior CVD, we aimed to reduce confounding and improve internal validity despite the absence of uniformly available laboratory markers.&lt;/p&gt;&lt;p&gt;We acknowledge the potential limitations of relying solely on ICD-10 codes, as we stated in the manuscript. However, the Disease Analyzer database has been extensively validated and has demonstrated a high positive predictive value for major cardiovascular diagnoses, including MI [&lt;span&gt;1-3&lt;/span&gt;]. We appreciate the reference by Tsai et al. [&lt;span&gt;4&lt;/span&gt;], which highlights the strong validity of ICD-10-CM codes for identifying AMI subtypes. Although their work confirms excellent performance metrics, our interest was not the subtype but rather the trend in overall MI incidence.&lt;/p&gt;&lt;p&gt;Indeed, smoking is a critical risk factor. As stated, individual smoking status is not recorded in the Disease Analyzer database. We therefore followed established practice in using COPD as a proxy, recognizing its limitations. As noted in the literature, around 90% of patients with COPD are current or former smokers [&lt;span&gt;5&lt;/span&gt;]. However, not all smokers develop COPD, so COPD cannot fully replace smoking status, but provides an approximate indicator. We clearly acknowledged this limitation in the manuscript. Importantly, smoking prevalence in Germany has declined over the study period, which may have contributed to overall cardiovascular improvements. However, as these trends would influence both diabetic and nondiabetic populations alike, our interpretation focused on diabetes-specific outcomes in a matched T2D cohort.&lt;/p&gt;&lt;p&gt;We agree that socioeconomic status and medication use are important factors. Although these data were not available in sufficient detail in our database, our large, matched cohorts and adjustment for key comorbidities offer valuable insights into temporal patterns. The unchanged MI and IS incidence, despite improvements in CHD and TIA, likely reflects a balance between earlier vascular damage and therapeutic progress. Although we did not stratify events by time since diagno","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144687907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prescription Medication Expenditures for Patients With Diabetes in the United States: 2012–2021 美国糖尿病患者的处方药支出:2012-2021
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-22 DOI: 10.1111/1753-0407.70106
Shanshan Li, Shaoxi Pan, Nan Xiao, Shaoxiang Jiang, Gorden G. Liu, Beini Lyu

Glucose-lowering medication expenditures per user by different payers among patients with diabetes.

糖尿病患者中不同支付者的人均降糖药物支出。
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引用次数: 0
The Role of Endothelin-1, Kidney Function and Diabetes in Patients With Coronary Artery Disease Underwent Percutaneous Coronary Intervention 内皮素-1、肾功能和糖尿病在冠心病患者经皮冠状动脉介入治疗中的作用
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-21 DOI: 10.1111/1753-0407.70127
Zixiang Ye, Enmin Xie, Yuan Du, Wenjia Zhang, Kefei Dou

Objective

This study aimed to explore the association between plasma big endothelin-1 (ET-1) and major adverse cardiovascular events (MACE) in CAD patients who underwent PCI with a focus on the influence of kidney function and diabetes status in secondary prevention.

Methods

A prospective cohort of CAD patients underwent PCI and patients with impaired kidney function and diabetes were initially screened and categorized separately, subdivided based on ET-1 levels. The primary outcome was MACE, including all-cause mortality, nonfatal myocardial infarction, unplanned revascularization, and stroke. Statistical analyses included Cox regression, competing risks analysis (competing for non-cardiovascular death), and restricted cubic spline to assess the relationships between ET-1 and MACE.

Results

This study included 1344 CAD patients with impaired kidney function and 10,577 CAD patients with DM. During a median follow-up of 3 years, 20% of renal dysfunction patients and 12.9% of DM patients experienced MACE. In CAD patients with renal dysfunction, elevated ET-1 levels were associated with increased MACE risk (adjusted HR 1.333, 95% CI 1.169–1.519, p < 0.001), with those in the highest group and DM showing a 2.134-fold (95% CI, 1.334–3.413, p < 0.001) increased MACE risk. In CAD patients with DM, patients with eGFR ≤ 60 mL/min/1.73 m2 and elevated ET-1 levels had a 2.297-fold (95% CI 1.822–2.895) increased risk of MACE.

Conclusion

ET-1 offered important prognostic value for CAD patients who underwent PCI, with especially bad prognoses observed in those with elevated ET-1 levels, renal dysfunction, and DM.

目的探讨冠心病患者行PCI后血浆大内皮素-1 (ET-1)与主要心血管不良事件(MACE)的关系,重点探讨二级预防中肾功能和糖尿病状况的影响。方法对行PCI的CAD患者和肾功能受损、糖尿病患者进行前瞻性队列筛选,分别进行分类,并根据ET-1水平进行细分。主要终点为MACE,包括全因死亡率、非致死性心肌梗死、计划外血运重建术和卒中。统计分析包括Cox回归、竞争风险分析(竞争非心血管死亡)和限制性三次样条来评估ET-1与MACE之间的关系。结果本研究纳入1344例冠心病合并肾功能受损患者和10577例冠心病合并糖尿病患者。在中位3年的随访期间,20%的肾功能不全患者和12.9%的糖尿病患者经历了MACE。在伴有肾功能不全的CAD患者中,ET-1水平升高与MACE风险增加相关(校正HR 1.333, 95% CI 1.169-1.519, p < 0.001),其中最高组和DM组的MACE风险增加2.134倍(95% CI, 1.334-3.413, p < 0.001)。在CAD合并DM患者中,eGFR≤60 mL/min/1.73 m2且ET-1水平升高的患者发生MACE的风险增加2.297倍(95% CI 1.822-2.895)。结论ET-1对行PCI的CAD患者有重要的预后价值,其中ET-1水平升高、肾功能不全、DM患者预后较差。
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引用次数: 0
Commentary on “Association of Serum Total Bilirubin to Cholesterol Ratio With Progression of Chronic Kidney Disease in Patients With Type 2 Diabetes: A Retrospective Cohort Study” 《2型糖尿病患者血清总胆红素/胆固醇比值与慢性肾病进展的相关性:一项回顾性队列研究》评论
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-21 DOI: 10.1111/1753-0407.70129
Tinghua Zhang

Several key factors influencing bilirubin levels and lipid metabolism were not measured or adjusted for in the study. Notably, hemoglobin, which affects bilirubin metabolism [5], was not included in the analysis. Furthermore, longitudinal changes in body mass index (BMI), blood pressure, or albuminuria during follow-up were also not accounted for. These unmeasured confounders may influence the observed association between the TBIL/TC ratio and CKD progression.

Chen et al. have highlighted the potential of the TBIL/TC ratio as a biomarker for CKD progression in type 2 diabetes. However, the issues of outcome misclassification, medication confounding, and oversimplified threshold analyses necessitate cautious interpretation of their findings. Future studies should aim to: (1) Validate these findings in ambulatory cohorts using KDIGO-endorsed sustained eGFR decline criteria; (2) Integrate time-varying adjustments for nephroprotective medications and account for genetic and environmental confounders; (3) Report absolute risks and conduct decision-curve analyses to better evaluate the clinical utility of the TBIL/TC ratio. Addressing these limitations will help clarify whether the TBIL/TC ratio offers incremental value beyond established renal risk markers.

Tinghua Zhang: wrote, reviewed, and edited the manuscript. Additionally, he conceptualized the study concept and design.

The author declares no conflicts of interest.

影响胆红素水平和脂质代谢的几个关键因素在研究中没有测量或调整。值得注意的是,影响胆红素代谢的血红蛋白没有包括在分析中。此外,随访期间体重指数(BMI)、血压或蛋白尿的纵向变化也未被考虑在内。这些未测量的混杂因素可能影响观察到的TBIL/TC比率与CKD进展之间的关联。Chen等人强调了TBIL/TC比值作为2型糖尿病CKD进展的生物标志物的潜力。然而,结果错误分类、药物混淆和过度简化的阈值分析等问题需要谨慎解释他们的发现。未来的研究应着眼于:(1)在使用kdigo认可的持续eGFR下降标准的流动队列中验证这些发现;(2)整合肾保护药物的时变调整,并考虑遗传和环境混杂因素;(3)报告绝对风险并进行决策曲线分析,更好地评价TBIL/TC比值的临床应用价值。解决这些限制将有助于澄清TBIL/TC比值是否提供超出既定肾脏风险标志物的增量价值。张廷华:撰写、审稿、编辑原稿。此外,他还对研究概念和设计进行了概念化。作者声明无利益冲突。
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引用次数: 0
Insulin Resistance in Type 1 Diabetes: Concepts and Implications for Therapy 1型糖尿病的胰岛素抵抗:概念和治疗意义
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-18 DOI: 10.1111/1753-0407.70126
Zachary Bloomgarden, Domenico Accili
<p>Many people with type 1 diabetes (T1D) appear to develop insulin resistance. In a 6-year post-Diabetes Control and Complications Trial (DCCT) follow-up of intensive treatment participants, comparison of the 61 having a family history of T2D with the 521 not reporting such a history showed BMI increasing by 3.8 versus 2.9 kg/m<sup>2</sup>, insulin requirement 0.73 versus 0.66 units/kg, and triglyceride 92 versus 76 [<span>1</span>].</p><p>Weight gain appears to be an important mediator of this insulin resistance. In the Pittsburgh Epidemiology of Diabetes Complications Study, adults with T1D had ~25% and 5% likelihood of having BMI 25–30 and ≥ 30, respectively, in 1986, with these figures increasing to ~35% and 25% by 2004 [<span>2</span>]; in the T1D Exchange Clinic Registry, by 2016–2018 more than two thirds of T1D adults age ≥ 26 were overweight or obese [<span>3</span>]. Comparing DCCT intensive treatment group participants in the top quartile of weight gain with those in the lower quartiles, insulin dose requirements, HbA1c, triglyceride, and BP were higher at DCCT close and 1- and 6-years post-trial, with those gaining the most weight being twice as likely to satisfy metabolic syndrome criteria at DCCT close, and 6 years later they were four times as likely to have metabolic syndrome [<span>4</span>]; in addition to the metabolic syndrome, metabolic-associated fatty liver disease affects approximately one in five people with T1D [<span>5</span>].</p><p>Another potential cause of insulin resistance in T1D may be hyperglucagonemia. Along with insulin deficiency, T1D is associated with hyperglucagonemia, with loss of insulin-induced glucagon suppression, and with increased α-cell mass [<span>6</span>]. Patients with T1D appear insensitive to the glucagon-suppressive effects of glucose and GLP-1, the latter potentially an indirect effect of decreased endogenous insulin secretion or, perhaps, a secondary state of insulin resistance. In addition to its action in increasing hepatic gluconeogenesis and glycogenolysis, glucagon accelerates hepatic amino acid metabolism and ureagenesis, with a potential physiologic feedback circuit in which amino acids such as alanine increase glucagon secretion, with glucagon then reducing amino acid levels; disruption of the liver–α-cell axis may cause hyperaminoacidemia and hyperglucagonemia, which may in turn contribute to hyperglycemia [<span>7</span>].</p><p>Insulin resistance becomes present early in the course of T1D [<span>8</span>]. The insulin resistance in T1D is not explained by body mass index, body fat percentage, visceral fat, plasma lipids, or physical activity, and is also not fully explained by the degree of hyperglycemia [<span>9</span>]. An additional cause of insulin resistance may be the hyperinsulinemia associated with peripheral insulin administration [<span>10</span>].</p><p>Insulin resistance in people with T1D appears, like that in type 2 diabetes, to be associated with the development o
许多1型糖尿病(T1D)患者似乎会产生胰岛素抵抗。在糖尿病控制和并发症试验(DCCT)后6年的强化治疗参与者随访中,61名有T2D家族史的患者与521名没有T2D家族史的患者进行比较,结果显示BMI增加3.8对2.9 kg/m2,胰岛素需求增加0.73对0.66单位/kg,甘油三酯增加92对76[1]。体重增加似乎是胰岛素抵抗的重要媒介。在匹兹堡糖尿病并发症流行病学研究中,1986年患有T1D的成年人BMI为25-30和≥30的可能性分别为~25%和5%,到2004年这一数字增加到~35%和25%;在T1D交换诊所登记处,到2016-2018年,超过三分之二的年龄≥26岁的T1D成年人超重或肥胖。比较体重增加前四分位数的DCCT强化治疗组参与者与体重增加后四分位数的参与者,胰岛素剂量要求、HbA1c、甘油三酯和血压在DCCT结束时和试验后1年和6年更高,体重增加最多的人在DCCT结束时满足代谢综合征标准的可能性是两倍,6年后他们患代谢综合征的可能性是四倍;除了代谢综合征外,大约五分之一的T1D[5]患者患有代谢相关的脂肪肝疾病。T1D患者胰岛素抵抗的另一个潜在原因可能是高血糖素血症。与胰岛素缺乏一起,T1D与高胰高血糖素血症、胰岛素诱导的胰高血糖素抑制丧失以及α-细胞质量[6]增加有关。T1D患者似乎对葡萄糖和GLP-1的胰高血糖素抑制作用不敏感,后者可能是内源性胰岛素分泌减少的间接影响,或者可能是胰岛素抵抗的继发性状态。胰高血糖素除了能促进肝脏糖异生和糖原分解外,还能加速肝脏氨基酸代谢和尿素生成,其潜在的生理反馈回路是氨基酸如丙氨酸增加胰高血糖素分泌,胰高血糖素随后降低氨基酸水平;肝- α-细胞轴的破坏可引起高氨基酸血症和高胰高血糖素血症,这反过来又可能导致高血糖。胰岛素抵抗在T1D[8]病程早期出现。T1D患者的胰岛素抵抗不能用体重指数、体脂率、内脏脂肪、血浆脂质或体力活动来解释,也不能完全用高血糖程度来解释。胰岛素抵抗的另一个原因可能是与外周胰岛素给药相关的高胰岛素血症。与2型糖尿病患者一样,T1D患者的胰岛素抵抗似乎与动脉粥样硬化并发症的发生有关。使用高胰岛素-正血糖钳来评估T1D患者和非糖尿病对照组的胰岛素敏感性,胰岛素抵抗与肥胖、高甘油三酯血症和冠状动脉钙评分升高有关。具有代谢综合征特征的DCCT患者的颈动脉内膜-中膜厚度高于没有这些特征的患者。在整个DCCT队列的1375名参与者中,49名在基线和18.5年随访时都有胰岛素抵抗的证据,与整个观察期间胰岛素敏感的人相比,患心血管疾病的可能性增加了四倍。在对儿童期发生T1D的成人进行的10年随访中,胰岛素抵抗也与冠状动脉疾病风险相关[13,14]。根据T1D患者的腰围估算,胰岛素抵抗与心血管疾病和全因死亡率相关[15,16]。T1D患者的胰岛素抵抗也可能与微血管并发症有关。在对764名最初没有糖尿病视网膜病变的T1D患者进行的7年随访中,根据空腹甘油三酯和腰臀比[17],有胰岛素抵抗证据的患者发生视网膜病变的可能性增加。基于这些考虑,针对2型糖尿病(T2D)开发的药物可能适用于特定的T1D患者。我们在近十年前讨论过这个话题,现在可以提一下一些更新。令人惊讶的是,很少有临床试验来确定体育活动是否对改善T1D患者的胰岛素敏感性有好处,尽管已发表的分析确实表明血糖和血脂异常可以改善bb0;这类办法应始终被认为是适当的。二甲双胍在改善青年T1D[21]患者的胰岛素敏感性方面具有潜在的益处,并可能与改善血糖[21]有关。 在美国,胰高血糖素样肽-1受体激动剂(GLP-1RA)和钠-葡萄糖共转运蛋白-2抑制剂(SGLT2i)越来越多地被用于T1D治疗b[22],人群研究显示,这些药物对血糖有一定的改善[23,24]。一项针对1965年接受GLP-1RA的11项T1D患者研究和844项对照研究的荟萃分析显示,GLP-1RA的效果一般,HbA1c降低0.21%,体重减轻4.04 kg,胰岛素剂量减少5.73单位/天,sglt1d患者试验的荟萃分析也显示了类似的效果,尽管存在糖尿病酮症酸中毒这一公认并发症的可能性增加[26,27]。因此,很大一部分T1D患者有胰岛素抵抗,通常在体重增加的情况下,我们注意到许多T2D治疗对T1D患者血糖有益的有趣证据。认识到T1D的并发症可能在一定程度上不同于T2D的发病机制,重要的悬而未决的问题是,是否像T2D一样,GLP-1RA和SGLT2i可能与T1D患者肾脏和心血管预后的改善有关。作者声明无利益冲突。
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引用次数: 0
The Effect of Liver Transplantation on Anti-Glycaemic Agents in Patients With Pre-Existing Diabetes Mellitus: A Population-Based Cohort Study 肝移植对既往糖尿病患者降糖药物的影响:一项基于人群的队列研究
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-15 DOI: 10.1111/1753-0407.70088
Amy Coulden, Christina Antza, Orighomisan Awala, Nihit Shah, Leelavathy Kandaswamy, Ananda Nahar, Angela Phillips, Sneha Upadhyaya, Ayesha Asif, Zara Khan, Feaz Babwah, Matthew Armstrong, Samiul Mostaf, Wasim Hanif

Background

Anecdotally, patients with diabetes mellitus after undertaking a liver transplant have reported improved glycaemic control and reduced insulin requirements, compared to other organ transplants where glycaemic control often worsens. This study aimed to evaluate possible changes in anti-glycaemic agent requirements pre- and post-liver transplantation and correlate them with the immunosuppression used and the reason for transplant.

Methods

In this observational, retrospective study, we investigated 258 adults with pre-existing diabetes mellitus who underwent liver transplant from October 2009 to January 2020 at a tertiary UK center. We compared pre- and post-transplant insulin treatment requirements.

Results

The mean age was 56 years, and the median duration of diabetes was 96 months. From a subgroup of 100 patients (38.8%) using insulin therapy, there was a reduction in insulin requirements from 60.5 ± 44.6 units/day before transplant to 51.1 ± 31.2 units/day at 1 month post-transplantation (15.5%, p = 0.02), 43.4 ± 29.5 units/day at 3 months post-transplantation (28.2%, p < 0.0001) and 33.6 ± 29.7 units/day at 6 months post-transplantation (44.4%, p < 0.0001). There was a significant correlation between the difference in insulin requirement before and 6 months post-transplant and the tacrolimus dose used as immunosuppressive therapy post-liver transplant. There was no correlation with the use of other immunosuppressive therapies and change in insulin requirement.

Conclusions

Insulin requirements significantly reduced post-liver transplant by almost 50%, despite initiation of immunosuppressive therapy. This is one of the first studies showing this effect, highlighting the role of the liver in regulating glucose metabolism, insulin utilization, and insulin resistance. Pooled data from other specialist centers need to be examined.

有趣的是,与其他器官移植后血糖控制往往恶化相比,接受肝移植后糖尿病患者的血糖控制得到改善,胰岛素需求降低。本研究旨在评估肝移植前后降糖药物需求的可能变化,并将其与所使用的免疫抑制和移植原因联系起来。方法:在这项观察性回顾性研究中,我们调查了2009年10月至2020年1月在英国一家三级中心接受肝移植的258名既往患有糖尿病的成年人。我们比较了移植前和移植后的胰岛素治疗需求。结果患者平均年龄56岁,糖尿病中位病程96个月。在使用胰岛素治疗的100例患者(38.8%)亚组中,胰岛素需求量从移植前的60.5±44.6个单位/天减少到移植后1个月的51.1±31.2个单位/天(15.5%,p = 0.02),移植后3个月的43.4±29.5个单位/天(28.2%,p < 0.0001),移植后6个月的33.6±29.7个单位/天(44.4%,p < 0.0001)。肝移植前和移植后6个月胰岛素需求量的差异与肝移植后他克莫司用作免疫抑制治疗的剂量有显著相关性。与使用其他免疫抑制疗法和胰岛素需要量的变化没有相关性。结论:尽管开始免疫抑制治疗,肝移植后胰岛素需求显著降低近50%。这是最早显示这种作用的研究之一,强调了肝脏在调节葡萄糖代谢、胰岛素利用和胰岛素抵抗中的作用。需要对其他专业中心的汇总数据进行检查。
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引用次数: 0
Association of Different Types of Diabetic Autonomic Neuropathy With Left Ventricular Diastolic Dysfunction in Patients With Type 2 Diabetes: A Cross-Sectional Study 2型糖尿病患者不同类型的糖尿病自主神经病变与左室舒张功能障碍的关联:一项横断面研究
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-14 DOI: 10.1111/1753-0407.70124
Ruixue Feng, Donge Yan, Mingxin Bai, Xingwu Ran, Dawei Chen, Chun Wang, Lihong Chen, Shuang Lin, Sen He, Yan Liu, Murong Wu, Zhiyi Lei, Yun Gao

Background

To investigate the association between different categories of diabetic autonomic neuropathy (DAN) and left ventricular diastolic dysfunction (LVDD) in patients with type 2 diabetes mellitus (T2DM).

Methods

We conducted a cross-sectional study of 3440 participants with T2DM recruited in Diabetic Foot Care Center of West China Hospital, Sichuan University from January 2016 to February 2024. LVDD was assessed via echocardiography, defined as an average E/e′ ratio > 14. Twenty-four hour Holter ECG, postvoid residual volume (PVR) examinations, and gastric emptying scintigraphy were employed to evaluate cardiac autonomic dysfunction, diabetic neurogenic bladder (DNB), and diabetic gastrointestinal autonomic neuropathy (DGAN), respectively. Logistic regression and propensity score matching (PSM) analyses were employed to examine the associations.

Results

Severe cardiac autonomic dysfunction (SDNN < 50 ms) was independently associated with LVDD, with odds ratios (OR) 1.731 (95% CI: 1.103–2.719, p = 0,018) after adjustment for potential confounding factors. LVDD tended to be independently associated with DNB (OR 1.356; 95% CI [0.992, 1.856]; p = 0.056). PSM analysis further validated the independent associations of SDNN < 50 ms (OR 1.587, 95% CI 1.028, 2.450, p = 0.037) and DNB (OR 1.454, 95% CI 1.011, 2.090, p = 0.043). However, DGAN was not independently associated with LVDD. Additionally, women had a higher risk of LVDD compared to men (OR 1.995, 95% CI 1.379, 2.885, p < 0.001).

Conclusions

Severe (SDNN < 50 ms), rather than mild–moderate, cardiac autonomic dysfunction, and DNB are independently associated with LVDD in individuals with T2DM. Additionally, women have a higher risk of LVDD than men.

研究2型糖尿病(T2DM)患者不同类型的糖尿病自主神经病变(DAN)与左室舒张功能障碍(LVDD)的关系。方法对2016年1月至2024年2月在四川大学华西医院糖尿病足护理中心招募的3440名T2DM患者进行横断面研究。通过超声心动图评估LVDD,定义为平均E/ E比值>; 14。采用24小时动态心电图(Holter ECG)、空后残余容量(PVR)检查和胃排空显像分别评估心脏自主神经功能障碍、糖尿病神经源性膀胱(DNB)和糖尿病胃肠道自主神经病变(DGAN)。采用Logistic回归和倾向评分匹配(PSM)分析来检验相关性。结果校正潜在混杂因素后,严重心脏自主神经功能障碍(SDNN < 50 ms)与LVDD独立相关,优势比(OR)为1.731 (95% CI: 1.103-2.719, p = 0.018)。LVDD倾向于与DNB独立相关(OR 1.356;95% ci [0.992, 1.856];p = 0.056)。PSM分析进一步验证了SDNN <; 50 ms (OR 1.587, 95% CI 1.028, 2.450, p = 0.037)和DNB (OR 1.454, 95% CI 1.011, 2.090, p = 0.043)的独立相关性。然而,DGAN与LVDD并不独立相关。此外,与男性相比,女性LVDD的风险更高(OR 1.995, 95% CI 1.379, 2.885, p < 0.001)。结论重度(SDNN < 50 ms)心脏自主神经功能障碍和DNB与T2DM患者LVDD独立相关,而非轻度-中度。此外,女性比男性有更高的LVDD风险。
{"title":"Association of Different Types of Diabetic Autonomic Neuropathy With Left Ventricular Diastolic Dysfunction in Patients With Type 2 Diabetes: A Cross-Sectional Study","authors":"Ruixue Feng,&nbsp;Donge Yan,&nbsp;Mingxin Bai,&nbsp;Xingwu Ran,&nbsp;Dawei Chen,&nbsp;Chun Wang,&nbsp;Lihong Chen,&nbsp;Shuang Lin,&nbsp;Sen He,&nbsp;Yan Liu,&nbsp;Murong Wu,&nbsp;Zhiyi Lei,&nbsp;Yun Gao","doi":"10.1111/1753-0407.70124","DOIUrl":"https://doi.org/10.1111/1753-0407.70124","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>To investigate the association between different categories of diabetic autonomic neuropathy (DAN) and left ventricular diastolic dysfunction (LVDD) in patients with type 2 diabetes mellitus (T2DM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a cross-sectional study of 3440 participants with T2DM recruited in Diabetic Foot Care Center of West China Hospital, Sichuan University from January 2016 to February 2024. LVDD was assessed via echocardiography, defined as an average E/e′ ratio &gt; 14. Twenty-four hour Holter ECG, postvoid residual volume (PVR) examinations, and gastric emptying scintigraphy were employed to evaluate cardiac autonomic dysfunction, diabetic neurogenic bladder (DNB), and diabetic gastrointestinal autonomic neuropathy (DGAN), respectively. Logistic regression and propensity score matching (PSM) analyses were employed to examine the associations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Severe cardiac autonomic dysfunction (SDNN &lt; 50 ms) was independently associated with LVDD, with odds ratios (OR) 1.731 (95% CI: 1.103–2.719, <i>p</i> = 0,018) after adjustment for potential confounding factors. LVDD tended to be independently associated with DNB (OR 1.356; 95% CI [0.992, 1.856]; <i>p</i> = 0.056). PSM analysis further validated the independent associations of SDNN &lt; 50 ms (OR 1.587, 95% CI 1.028, 2.450, <i>p</i> = 0.037) and DNB (OR 1.454, 95% CI 1.011, 2.090, <i>p</i> = 0.043). However, DGAN was not independently associated with LVDD. Additionally, women had a higher risk of LVDD compared to men (OR 1.995, 95% CI 1.379, 2.885, <i>p</i> &lt; 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Severe (SDNN &lt; 50 ms), rather than mild–moderate, cardiac autonomic dysfunction, and DNB are independently associated with LVDD in individuals with T2DM. Additionally, women have a higher risk of LVDD than men.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Global, Regional, and National Epidemiology of Vision Impairment due to Diabetic Retinopathy Among Working-Age Population, 1990–2021 1990-2021年全球、地区和国家工作年龄人口糖尿病视网膜病变视力损害流行病学研究
IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Pub Date : 2025-07-14 DOI: 10.1111/1753-0407.70121
Yang Meng, Yuan Liu, Runping Duan, Baoyi Liu, Zhuangling Lin, Yuan Ma, Lan Jiang, Zijian Qin, Tao Li

Background

To evaluate the global, regional, and national trends of vision impairment associated with diabetic retinopathy (DR) in the working-age population (20–65 years) from 1990 to 2021.

Methods

This was a population-based analysis using data from the Global Burden of Disease Study 2021. Vision impairment was defined as low vision (Snellen visual acuity of < 6/18 to ≥ 3/60) and blindness (Snellen visual acuity of < 3/60 or central visual field < 10°). The burden of DR-related vision impairment, that is, prevalence and years lived with disability (YLD), was analyzed by sex, age, location, and sociodemographic index (SDI). A Bayesian age-period-cohort analysis was employed to forecast the future burden up to 2035.

Results

From 1990 to 2021, the global prevalence rate and YLD rate of DR-related vision impairment increased significantly. In 2021, 2.85 million prevalent cases and 250 117 YLDs were reported, representing 2.8-fold and 3.0-fold increases compared to 1990, respectively. South Asia and China were identified as the most severely burdened region and country in 2021, respectively. Throughout 1990–2021, females consistently bore a greater burden than males. In terms of SDI, the burden was predominantly concentrated in middle-SDI countries. Predictive analysis suggests a continued increase in the number of patients and YLDs by 2035.

Conclusions

Globally, there has been a substantial increase in the burden of DR-related vision impairment among working-age individuals, with disparities observed in terms of sex, location, and SDI. Given the projected worsening of this burden, targeted interventions are needed to address this global health challenge.

研究背景:评估1990年至2021年工作年龄人群(20-65岁)中与糖尿病视网膜病变(DR)相关的视力损害的全球、地区和国家趋势。方法:这是一项基于人群的分析,使用2021年全球疾病负担研究的数据。视力障碍定义为低视力(Snellen视力为6/18 ~≥3/60)和失明(Snellen视力为3/60或中心视野为10°)。根据性别、年龄、地区和社会人口指数(SDI)分析dr相关视力损害的负担,即患病率和残疾生活年数(YLD)。采用贝叶斯年龄-时期-队列分析预测到2035年的未来负担。结果从1990年到2021年,dr相关性视力损害的全球患病率和YLD率显著上升。2021年,报告了285万例流行病例和250 117例yld,分别比1990年增加2.8倍和3.0倍。2021年,南亚和中国分别被确定为负担最严重的地区和国家。在1990年至2021年期间,女性的负担一直高于男性。就SDI而言,负担主要集中在中等SDI国家。预测分析表明,到2035年,患者和死亡人数将继续增加。在全球范围内,工作年龄人群中dr相关视力损害的负担大幅增加,性别、地点和SDI方面存在差异。鉴于这一负担预计会恶化,需要采取有针对性的干预措施来应对这一全球卫生挑战。
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引用次数: 0
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Journal of Diabetes
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