Dysregulation of microRNAs (miRNAs) has been associated with podocyte injury in diabetic nephropathy (DN). This study aimed to investigate the role and underlying mechanism of miR-208a-3p in the development of DN. An in vitro DN model was established by treating podocytes with high glucose (HG). Gene expression was analyzed using reverse transcription quantitative polymerase chain reaction, and protein levels were determined by Western blotting. Immunofluorescence staining was performed to assess microtubule-associated protein 1A/1B-light chain 3 (LC3) intensity as an autophagy marker. Podocyte viability and apoptosis were evaluated via Cell Counting Kit-8 assay and flow cytometry, respectively. Intracellular reactive oxygen species (ROS) levels were measured using 2',7'-dichlorofluorescin diacetate staining. miR-208a-3p was significantly upregulated in HG-stimulated podocytes. HG exposure promoted apoptosis and oxidative stress, while suppressing autophagy and cell viability, effects that were reversed by miR-208a-3p inhibition. Mechanistically, miR-208a-3p directly targeted vav guanine nucleotide exchange factor 3 (VAV3). HG suppressed AKT/mTOR signaling, whereas miR-208a-3p silencing activated it. Conversely, VAV3 knockdown inactivated AKT/mTOR signaling. VAV3 downregulation or treatment with LY294002, an AKT/mTOR inhibitor, abolished the protective effects of miR-208a-3p silencing against HG-induced podocyte injury. These findings indicate that miR-208a-3p silencing attenuates HG-induced podocyte injury by promoting autophagy via targeting the VAV3/AKT/mTOR pathway.

Objective:To investigate the serum levels of Chemokine CCL26 (CCL26) and Receptors, CCR3 (CCR3) in patients with Diabetes Mellitus, Type 2 (T2DM) complicated by lower extremity artery disease (LEAD), and to evaluate their potential as diagnostic biomarkers for T2DM with LEAD. Methods:A retrospective study was conducted involving 197 patients with T2DM between June 2022 and February 2025. Patients were divided into T2DM group (n=157) and LEAD group (n=40). Clinical data and fasting venous blood were collected to measure serum CCL26 and CCR3 levels. Pearson correlation analysis was used to assess the correlation between CCL26 and CCR3. Lasso regression and logistic regression models were employed to identify risk factors for LEAD. The receiver operating characteristic (ROC) curve was constructed to evaluate the predictive efficacy of CCL26 and CCR3 for LEAD. Results:The LEAD group had significantly higher BMI, disease duration, HbA1C, FINS, and HOMA-IR compared to the T2DM group (P<0.05). Serum levels of CCL26 and CCR3 were elevated in the LEAD group (P<0.05). A positive correlation was found between CCL26 and CCR3 (r=0.337, P=0.034). Lasso regression identified 12 indicators, including CCL26 and CCR3, as predictors of LEAD. Logistic regression revealed that BMI, disease duration, HbA1C, CCL26, and CCR3 were independent risk factors for LEAD (P<0.05). The combined detection of serum CCL26 and CCR3 had an AUC of 0.812, indicating high predictive value for LEAD in T2DM patients. Conclusion:Serum CCL26 and CCR3 levels are elevated in T2DM patients with LEAD and are closely associated with its occurrence. Combined detection of these biomarkers shows good predictive value for LEAD in T2DM patients.

ObjectiveThis study explored the utility of NLR (neutrophil-to-lymphocyte ratio) as a marker to predict Lower Extremity Peripheral Artery Disease (PAD) in the Chinese population, as well as to assess its consistency and diagnostic value with digital subtraction angiography.MethodsPatients were distributed into three groups according to the angiography in lower limb arterial: group L1, plaque with no stenosis; group L2, plaque with luminal stenosis and group L3, total vascular occlusion. Changes in the neutrophil-to-lymphocyte ratio were documented and compared among groups.ResultsCompared to group L1, NLR was significantly increased in L2 (1.76 vs 2.35, p=0.037) and L3 (1.76 vs 3.60, p<0.001), with a gradual decrease in ABI (Ankle-Brachial Index, 1.11 vs 1.02 vs 0.94, p<0.001). Those older patients with higher prevalence of hypertension (p=0.002), obesity (p=0.032), or reduced high-density lipoprotein cholesterol (p=0.020) were more likely to develop PAD; higher glycosylated hemoglobin (p=0.045), low-density lipoprotein cholesterol (p=0.006), and systolic blood pressure (p<0.001) levels led to a greater tendency to suffer stenosis or even occlusion; the probability of severe stenosis (>70%) increased to 2.075 times for every 1 increase in NLR, while it was 46.8% for every 0.1 increase in ABI. The optimal NLR cut-off value to predict severe stenosis in PAD was 2.73. Receiver operating characteristic curve analysis of the inflammatory biomarkers and severe stenosis prediction displayed an area under the curve of 0.81.ConclusionNLR could serve as a new noninvasive and accurate marker in predicting PAD.

目的 研究去整合素-金属蛋白酶(deintegrin metalloproteinase,ADAM)17、Notch1及α-平滑肌动蛋白(alpha-smooth muscle actin,α-SMA)在子宫内膜异位症(EMs)组织中的表达,及其与子宫内膜异位症的临床病理特征之间的相关性.方法 选取2019年10月至2020年10月潍坊医学院附属医院收治的EMs病人异位内膜40例(异位内膜组)、在位内膜25例(在位内膜组),正常内膜25例作为对照组.采用免疫组化法及半定量分析法分别检测ADAM17、Notch1、α-SMA在三组中的表达.分析异位内膜组织中ADAM17、Notch1、α-SMA的表达与病理特征的关系.采用Pearson相关分析分析ADAM17、Notch1、α-SMA在三组中的表达的相关性.结果 ADAM17、Notch1、α-SMA在异位内膜组中的表达高于在位内膜组(4.77±1.35比3.24±1.09,4.40±1.24比3.44±0.96,4.42±1.30比3.36±0.95),差异有统计学意义(P<0.05),在位内膜组的表达高于正常内膜组(2.36±1.22、2.24±1.01、2.16±1.028),差异有统计学意义(P<0.05).异位内膜组中ADAM17、Notch1、α-SMA在Ⅲ～Ⅳ期中的表达高于Ⅰ～Ⅱ期,差异有统计学意义(P<0.05).EMs病人异位内膜组中ADAM17、Notch1、α-SMA的表达与年龄及囊肿大小差异无统计学意义(P>0.05).ADAM17、Notch1、α-SMA在异位内膜中的表达两两之间具有正相关性(P<0.05).结论 ADAM17、Notch1、α-SMA在EMs发生及发展中起重要作用,ADAM17可能通过Notch通路参与EMs的纤维化发生并调控EMs的纤维化严重程度.

Iron is one of the most important trace elements in life activities. It participates in a variety of important physiological processes in the body through oxidation-reduction reaction. A large number of studies show that iron overload (IO) is closely related to the progression of diabetes and its various chronic complications. However, the mechanism of iron overload in the pathogenesis of diabetes and the mechanism of iron overload in atherosclerosis (AS) are still controversial, and the relationship between iron overload and diabetic lower extremity arterial disease (LEAD) remains still unclear. Some recent reviews and original research articles suggest further studies to explain the complex relationship between iron metabolism and atherosclerosis. This article reviews the relationship between iron overload and diabetes and its relationship with LEAD, and discusses its mechanisms from various aspects, such as lipid peroxidation induced by iron overload, so as to provide clinical diagnosis and treatment ideas for diabetic lower extremity arterial disease. It is hoped that early evaluation, diagnosis and treatment of LEAD will be inspired.

*These authors contributed equally to this work Background: Type 2 diabetes (T2D) is characterized by progressive β-cell dysfunction. Regulatory microRNAs (miRNAs) may be associated with this. Methods: Serum miR-26a-5p and RNF6 levels were detected in T2D patients and healthy volunteers via qRT-PCR. Subsequently, the role of specific dysregulated miR-26a-5p or RNF6 in regulating insulin content, cell proliferation, and apoptosis was studied in INS-1 cells. The targeting correlation between miR-26a-5p and RNF6 was detected using a luciferase assay. Results: RNF6 expression was significantly decreased in T2D individuals and INS-1 cells treated with high glucose, while miR-26a-5p expression was increased. In INS-1 cells, RNF6 overexpression or miR-26a-5p downregulation significantly increased insulin content and secretion, induced proliferation, and inhibited apoptosis. RNF6 has been identified as an miR-26a-5p target, which negatively regulates RNF6 to worsen INS-1 cell function. Conclusion: RNF6 promoted insulin secretion and induced cell proliferation in INS-1 cells. This may be related to miR-26a-5p targeting and negatively regulating T2D pathogenesis.

Background Type 2 diabetes (T2D) is characterized by progressive β-cell dysfunction. Regulatory microRNAs (miRNAs) may be associated with this. Methods Serum miR-26a-5p and RNF6 levels were detected in T2D patients and healthy volunteers via qRT-PCR. Subsequently, the role of specific dysregulated miR-26a-5p or RNF6 in regulating insulin content, cell proliferation, and apoptosis was studied in INS-1 cells. The targeting correlation between miR-26a-5p and RNF6 was detected using a luciferase assay. Results RNF6 expression was significantly decreased in T2D individuals and INS-1 cells treated with high glucose, while miR-26a-5p expression was increased. In INS-1 cells, RNF6 overexpression or miR-26a-5p downregulation significantly increased insulin content and secretion, induced proliferation, and inhibited apoptosis. RNF6 has been identified as an miR-26a-5p target, which negatively regulates RNF6 to worsen INS-1 cell function. Conclusion RNF6 promoted insulin secretion and induced cell proliferation in INS-1 cells. This may be related to miR-26a-5p targeting and negatively regulating T2D pathogenesis.

目的 探讨中性粒细胞与淋巴细胞比值(NLR)、糖类抗原125(CA125)在子宫内膜异位症(EMT)中的表达及临床意义.方法 选取50例行腹腔镜手术且术后病理确诊为EMT的患者为研究组,其中Ⅰ～Ⅱ期为轻度组(20例),Ⅲ～Ⅳ期为重度组(30例),选取同期因卵巢良性肿瘤行腹腔镜手术的30例作为对照组,通过ROC曲线分析,评价NLR、CA125及联合检测NLR+CA125在诊断EMT中的敏感性及特异性.结果 ①研究组中血清NLR、CA125及联合标记物水平明显高于对照组(P＜0.001),且CA125、联合标记物在轻重度组中差异亦有统计学意义(P＜0.05),而NLR在轻重度组中差异无统计学意义(P＞0.05);②通过ROC曲线对NLR、CA125及联合标记物进行分析时发现,联合标记物预测子宫内膜异位症的AUC高于CA125与NLR;③CA125、联合标记物与病情的严重程度呈正相关(P＜0.05),而NLR与病情严重程度无明显相关性(P＞0.05).结论 NLR参与内异症的发生,但与病情严重程度无关,联合检测NLR、CA125可明显提高内异症的诊断率,对分期有较高的临床意义.

新型冠状病毒肺炎(COVID-19)患者的预后与其潜在的基础疾病相关,糖尿病患者易合并心、脑、肾等慢性并发症,往往预后不良.糖尿病及治疗中可能出现的血糖波动在COVID-19病程的发展中起着不可忽视的作用.本文根据疫情暴发以来我院诊治COVID-19合并糖尿病患者的临床经验及实际操作,对于这类特殊人群的诊治提出相关建议.

目的 探讨T2DM患者外周血游离mtDNA(线粒体DNA)和外周血白细胞线粒体功能对脂肪组织IR的影响.方法 选取2017年1月至2019年3月于武汉大学中南医院内分泌科住院的新诊断未用药的T2DM患者80例(T2DM组),另选取同期健康人群64名为正常对照(NC)组.Seahorse XFe96检测仪检测两组白细胞线粒体功能.提取外周血mtDNA,RT-PCR检测mtDNA拷贝数,脂肪组织IR指数(Adipo-IR)评价脂肪组织IR水平,并检测血脂、BG和Ins、hsC-RP、TNF-α及活性氧簇(ROS).结果 与NC组比较,T2DM组外周血游离mtDNA、Adipo-IR升高(P<0.01).随着Adipo-IR升高,外周血游离mtDNA水平逐渐升高,白细胞线粒体剩余呼吸功能和最大呼吸功能逐渐降低.外周血游离mtDNA与ROS、TNF-α、hsC-RP及Adipo-IR呈正相关(P<0.05或P<0.01).外周血白细胞线粒体剩余呼吸功能和最大呼吸功能与ROS、TNF-α、hsC-RP呈负相关(P<0.05).Logistic回归分析显示,外周血游离mtDNA,外周血白细胞线粒体剩余呼吸功能、白细胞线粒体最大呼吸功能均为脂肪组织IR的影响因素.结论 外周血白细胞线粒体功能和游离mtDNA水平可能影响脂肪组织IR.

目的 检测PI3K和MMP-9在子宫内膜异位症(EMs)组织中的表达及意义.方法 选取2017年9月～2019年6月在潍坊医学院附属医院住院治疗的EMs患者异位内膜45例(异位内膜组)、在位内膜36例(在位内膜组).正常内膜43例作为正常子宫内膜组.采用免疫组化法及半定量分析法分别检测PI3K,MMP-9在3组中的表达,采用Pearson相关分析分析PI3K和MMP-9在3组中表达的相关性.结果 PI3K,MMP-9在异位内膜组中的表达高于在位内膜组,在位内膜组的表达高于正常子宫内膜组,差异均有显著性(P＜0.05).异位内膜组和在位内膜组中PI3K和MMP-9在分泌期的表达高于增生期,差异有显著性(P＜0.05),正常子宫内膜组中MMP-9和PI3K在分泌期和增生期的表达无明显差异(P＞0.05).异位内膜组和在位内膜组中PI3K与MMP-9呈正相关(P＜0.05),正常子宫内膜组中MMP-9和PI3K之间无明显相关性.结论 PI3K和MMP-9在EMs异位内膜和在位内膜组中高表达,且呈正相关,提示二者在EMs的发生发展中起重要作用.

目的 研究骨桥蛋白(OPN)、磷脂酰肌醇3-激酶(PI3K)及基质金属蛋白酶-9(MMP-9)在子宫内膜异位症组织中的表达,及其与子宫内膜异位症临床病理特征之间的相关性.方法 前瞻性选取潍坊医学院附属医院收治的子宫内膜异位症患者异位内膜35例(异位内膜组)、在位内膜26例(在位内膜组),正常内膜27例作为对照组.采用免疫组化法及半定量分析法分别检测OPN、PI3K、MMP-9在三组中的表达.分析异位内膜组织中OPN、PI3K与MMP-9的表达与病理特征的关系.采用Pearson相关分析分析OPN、PI3K和MMP-9在三组中的表达的相关性.结果 OPN、PI3K、MMP-9在异位内膜组中的表达高于在位内膜组,在位内膜组的表达高于正常内膜组,差异均有统计学意义(P<0.05).异位内膜组中OPN和MMP-9在Ⅲ ～ Ⅳ期中的表达高于Ⅰ ～ Ⅱ期,差异有统计学意义(P<0.05).PI3K在Ⅲ ～ Ⅳ期与Ⅰ ～ Ⅱ期的表达中差异无统计学意义(P>0.05).EMs患者异位内膜组中OPN、PI3K和MMP-9的表达与年龄和囊肿直径大小差异无统计学意义(P>0.05).OPN、PI3K与MMP-9在异位内膜中的表达两两之间具有正相关性(P<0.05).结论 OPN、PI3K和MMP-9在EMs异位内膜和在位内膜中高表达,且两两呈正相关性,三者在EMs发病中起重要作用.

目的 探讨糖尿病足患者感染程度与身体状况、生存状况、溃疡程度及感染类型的相关性.方法 选取2016年7月-2018年7月华中科技大学同济医学院附属武汉中心医院内分泌科收治的发生感染的糖尿病足患者131例作为研究对象,收集患者的一般资料[包括体质量指数(BMI)、糖尿病血管并发症、糖尿病神经并发症]和实验室检查指标[包括空腹血糖、糖化血红蛋白(HbAlc)、白蛋白、血红蛋白、总蛋白、中性粒细胞、C-反应蛋白、尿素氮、24 h尿蛋白],根据患者糖尿病足感染程度分为轻度感染组(n=42)、中度感染组(n=51)和重度感染组(n=38),比较各组患者的身体状况、生存状况、溃疡程度以及感染类型.结果 随着感染程度加重,患者BMI、蛋白水平下降,心血管并发症增多,血糖控制变差,炎性反应增强,尿蛋白排出增加;截肢/趾率、愈合时间、治疗费用不断升高;华格纳(Wanger)分级达到4级以上的比例明显升高;混合感染率升高且感染菌由革兰阳性球菌为主转变为肠杆菌科中的革兰阴性杆菌为主.结论 糖尿病足患者随着感染程度加重,身体状况和生存状况变差,溃疡程度加重,以革兰阴性杆菌为主的混合感染比例逐渐增高.

目的 探讨骨桥蛋白(OPN)及整合素β3(CD61)在子宫内膜异位症患者的在位子宫内膜及异位子宫内膜中的表达及意义.方法 选择201 8年1月～2018年7月因子宫内膜异位症行腹腔镜手术治疗的患者30例,收集其异位子宫内膜及在位子宫内膜组织,其中Ⅰ～Ⅱ期1 5例,Ⅲ～Ⅳ期15例.选择因子宫肌瘤行全子宫切除术的患者15例,收集其在位子宫内膜组织作为对照组.采用免疫组化及半定量分析法分别检测OPN,CD61在子宫内膜组织中的表达.结果 ①OPN及CD61在Ⅲ～Ⅳ期异位内膜组织中的表达高于Ⅰ～Ⅱ期异位内膜组织、Ⅲ～Ⅳ期在位内膜组织、Ⅰ～Ⅱ期在位内膜组织及对照组,差异均有显著性(P＜0.01).②OPN,CD61在异位及在位子宫内膜组织中的表达显著相关,在正常子宫内膜组织中的表达无相关性.结论 ①OPN,CD61在异位子宫内膜组织中的表达高于在位子宫内膜组织,在位子宫内膜组织高于对照组,推测两者在子宫内膜异位症的发生发展中起重要作用.②OPN,CD61在Ⅲ～Ⅳ期患者的在位子宫内膜组织中的表达高于Ⅰ～Ⅱ期在位子宫内膜组织,在Ⅰ～Ⅱ期在位子宫内膜组织中的表达高于对照组,推测子宫内膜异位症的致病关键系子宫在位内膜本身.③OPN,CD61在异位及在位子宫内膜组织中的表达显著相关,推测其在子宫内膜异位症的发生发展中具有协同作用.

目的 比较绝经后骨质疏松症女性和健康对照人群的血清锌(Zn)、铜(Cu)和血脂水平,并确定上述参数与骨密度(bone mineral density,BMD)之间是否存在关联.方法 研究对象为116名绝经后妇女,包括58例骨质疏松症患者[骨质疏松组,年龄(58.9±3.7)岁]和58名对照者[健康对照组,年龄(55.1±1.9)岁].使用原子吸收分光光度法测定血清锌和铜含量,通过双能X线骨密度仪检测所有女性腰椎(L1～4)和左侧股骨颈的骨密度.结果 两组患者血清锌和铜含量相近(P>0.05);骨质疏松组血清低密度脂蛋白(LDL)和总胆固醇(TC)水平与对照组相比差异有统计学意义(P<0.05);相关分析显示体质量指数(bone mass index,BMI)与BMD值之间存在显著相关性(P<0.05);血清Zn、Cu水平与血脂无显著相关性(P>0.05);BMD与LDL(r=-0.302,P=0.002)和总胆固醇水平(r=-0.252,P=0.007)之间呈负相关.结论 本研究表明血脂异常可能是绝经后妇女骨质疏松症的独立危险因素.此外,微量元素对BMD没有直接和相关的影响.

目的:探讨利拉鲁肽联合利格列汀治疗2型糖尿病肥胖患者的临床疗效.方法:选取2016年1月至2018年1月本院收治的104例2型糖尿病肥胖患者,按照随机数字表法将患者分为对照组(n=52)和治疗组(n=52).对照组给予利格列汀治疗,治疗组给予利拉鲁肽联合利格列汀治疗,两组疗程均为3个月.比较两组治疗前后体质量指数(BMI)、血糖指标[糖化血红蛋白(HbAlc)、空腹血糖(FPG)、餐后2小时血糖(2hPG)]、血压指标[收缩压(SBP)、舒张压(DBP)]、胰岛功能指标[胰岛素抵抗指数(HOMA-IR)、胰岛β细胞功能(HOMA-β)]、骨代谢指标[N端中段骨钙素(N-MID-OT)、β胶联降解产物(β-CTX)]、氧化应激指标[丙二醛(MDA)、脂质过氧化氢(LHP)、谷胱甘肽过氧化物酶(GSH-Px)]和炎症指标[肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、C反应蛋白(CRP)]水平,记录两组治疗过程中不良反应的发生情况.结果:治疗后,两组的BMI、血糖指标、血压指标、HOMA-IR、-CTX、MDA、LHP、炎症指标水平均低于治疗前,HOMA-β、N-MID-OT、GSH-Px水平均高于治疗前(P＜0.05),且治疗组以上指标的改善程度明显优于对照组.治疗组不良反应发生率为15.38％(8/52),与对照组的11.54％(6/52)比较差异无统计学意义(P＞0.05).结论:利拉鲁肽联合利格列汀治疗2型糖尿病肥胖患者安全有效,能够明显降低患者体重、血糖、血压水平,改善胰岛功能和骨代谢,减轻氧化应激和炎症反应.

In recent years,cytokine-based therapy for diabetic foot has attracted much attention,and the dynamic balance between angiogenesis-promoting factors and inhibitors was the key to maintain the normal occurrence of wound healing.Mechanism of cytokines of angiogenesis-promoting (vascular endothelial growth factor,hypoxia-inducible factor-1,fibroblast growth factor,platelet-derived growth factor,et al.)and inhibitors (pigment epithelium derived factor and kallikrein binding protein) were expounded.The aim was to provide a new protocol for the treatment of diabetic foot with cytokines.

目的 探讨桂皮醛(CA)在棕榈酸(PA)诱导的巨噬细胞(RAW264.7)炎症反应中的分子机制.方法 将RAW264.7随机分为空白对照组(NC)、PA处理组(PA组)和不同浓度CA处理组(10μmol/L CA组、20μmol/L CA组、40μmol/L CA组).MTT法检测不同浓度CA对RAW264.7的影响,确定CA作用时间和浓度.PCR检测各组脂多糖诱导的肿瘤坏死因子(LITAF),肿瘤坏死因子α(TNF-α)、白介素6(IL-6)mRNA表达,ELISA检测各组TNF-α和IL-6的蛋白水平,Western blot检测各组LITAF蛋白水平.结果 与PA组相比,10μmol/L CA组、20μmol/L CA组和40μmol/L CA组均能显著抑制细胞内TNF-α、IL-6的mRNA和蛋白水平(P<0.05或P<0.01),且随着CA浓度增加,抑制炎症作用越强.与PA组相比,10μmol/L CA组、20μmol/L CA组和40μmol/L CA组LITAF mRNA和蛋白表达降低(P<0.05).结论 CA具有抗炎活性,其机制可能通过抑制LITAF信号通路,降低脂肪酸诱导TNF-α、IL-6表达,调控慢性低度炎症反应,为糖尿病及并发症提供可能的治疗选择.

目的 探讨血清P选择素(sP-selectin)、胰高血糖素样肽-1(GLP-1)的变化与新诊断2型糖尿病(T2DM)患者胰岛素抵抗的关系.方法 选取华中科技大学同济医学院附属武汉中心医院2018年6月 ～2018年12月初诊断的T2DM患者60例(A组)、具有5年以上糖尿病病程的T2DM患者60例(B组)和健康体检人员60例(C组);检测各组血清sP-selectin、GLP-1、空腹胰岛素(FINS)、空腹血糖(FPG)、胰岛素抵抗指数(HOMA-IR)、糖化血红蛋白(HbA1c)及胰岛素敏感指数(ISI),分析血清sP-selectin、GLP-1与HOMA-IR、ISI的相关性.结果 B组的血清sP-selectin显著高于A组和C组(P<0.05),血清GLP-1显著低于A组和C组(P<0.05);A组的血清sP-selectin显著高于C组(P<0.05),血清GLP-1显著低于C组(P<0.05);A组的HOMA-IR、HbA1c、FINS、FPG均显著高于C组(P<0.05),ISI低于C组(P<0.05);初诊断T2DM患者的血清sP-selectin与HOMA-IR呈正相关(P<0.05)、与ISI呈负相关(P<0.05);血清GLP-1与HOMA-IR呈负相关(P<0.05)、与ISI呈正相关(P<0.05).初诊断T2DM患者的血清sP-selectin、腰围(WC)、病程、BMI升高及GLP-1降低将会增大患者HOMA-IR升高的风险(P<0.05);血清sP-selectin、WC、病程升高及GLP-1降低会增大患者ISI降低的风险.结论 血清sP-selectin、GLP-1水平变化参与了初诊断T2DM患者发生胰岛素抵抗的病理过程.

目的 探讨2型糖尿病(T2DM)患者血清P选择素(sP-selectin)、E选择素(sE-selectin)、脂肪细胞型脂肪酸结合蛋白(A-FABP)、游离脂肪酸(FFA)的表达与患者胰岛素抵抗(IR)的关系.方法 选取我院新诊断T2DM患者90例(2016年1月-2018年7月)作为T2DM组、健康体检对象90例作为对照组,检测两组的血清sP-selectin、sE-selectin、A-FABP、FFA水平,并分析上述指标与T2DM患者胰岛素抵抗指数(HOMA-IR)的相关性.结果 T2DM组患者的sP-selec-tin、sE-selectin、A-FABP、FFA水平显著高于对照组,差异具有统计学意义(P﹤0.05).结论 T2DM患者血清sP-selectin、sE-selectin、A-FABP、FFA水平升高比较显著,并且可能与患者胰岛素抵抗程度有一定的相关性.