Introduction: Cognitive dysfunction is a common complication of the central nervous system in diabetic patients. To explore the molecularmechanism of diabetic cognitive dysfunction (DCD). Material and methods: The db/db mice and high-glucose (HG)-treated human brain astrocytes (SVG p12) and mouse hippocampalneuron cells (mHNCs) were used for mechanistic exploration. Learning and memory abilities in mice were tested using the Morris watermaze assay. The expression of lncRNA NEAT1 and miR-30e-5p and the mRNA levels of FLT1, NGF, and GPX4 were detected by RT-qPCR.Western blotting was used to analyze FLT1 and p-tau protein levels. Cell viability and apoptosis were evaluated using the CCK-8 methodand flow cytometry. Ferroptosis was assessed by measuring Fe2+ and 4-HNE levels and GPX4 expression. Target sites among NEAT1,miR-30e-5p, and FLT1 were detected using a dual-luciferase reporter assay, and their predictive value for DCD was assessed using ROCcurves and binary logistic regression analysis. Results: The db/db mice showed significant cognitive deficits. NEAT1 and FLT1 were highly expressed in the hippocampus of db/db mice and HG-treated nerve cells, whereas miR-30e-5p was expressed at low levels. Silencing NEAT1 rescued HG-induced nerve cell viabilityimpairment and ferroptosis. NEAT1 directly targeted miR-30e-5p and negatively regulated it, and miR-30e-5p directly targeted FLT1.The miR-30e-5p inhibitor partially reversed the effects of NEAT1 silencing, whereas silencing FLT1 rescued the effects of the miR-30e-5pinhibitor. NEAT1, miR-30e-5p, and FLT1 were classifiers for differentiating patients with diabetes mellitus from those with DCD, withareas under the curves (AUCs) of 0.718, 0.816, and 0.716, respectively. Their combination showed more reliable diagnostic performance(AUC = 0.896). Conclusions: The NEAT1/miR-30e-5p/FLT1 axis may mediate DCD pathogenesis by regulating ferroptosis in brain nerve cells under HG conditions. These molecules may serve as new biomarkers of DCD occurrence.

GZR18 is a long-acting glucagon-like peptide-1 receptor agonist that is under development for the treatment of type 2 diabetes mellitus (T2DM). In this randomized, double-blind, placebo-controlled phase 1b/2a trial in Chinese adults with T2DM, the safety and efficacy of once-weekly GZR18 are evaluated using different dose-titration regimens in two separate parts: Part A (0.5-4 mg over 26 weeks) and Part B (1.5-13 mg over 23 weeks). Overall, 72 participants are enrolled, of whom 62 complete the trial. GZR18 significantly reduces glycated hemoglobin (HbA1c) in both parts (Part A: -1.32% for GZR18 versus 0.86% for placebo; Part B: -1.81% for GZR18 versus 0.12% for placebo). Improvements in body weight and other metabolic parameters are also observed. GZR18 is safe and well tolerated, with mostly mild-to-moderate gastrointestinal adverse events; no severe hypoglycemia or treatment-related serious adverse events occurred. These findings support further development of GZR18 in larger, longer-term trials. The trial is registered at ClinicalTrials.gov (NCT06256523).

Background: Chronic periodontitis is a common inflammatory condition that may contribute to systemic inflammation and microvascular complications in type 2 diabetes mellitus (T2DM). However, longitudinal evidence linking periodontitis to diabetic peripheral neuropathy (DPN) remains scarce. Objective: To investigate whether chronic periodontitis is associated with an increased risk of incident DPN in patients with T2DM. Methods: We conducted a single-center retrospective cohort study using electronic medical records from 2017 to 2022. A total of 3,996 T2DM patients without baseline DPN were included, of whom 318 had incident chronic periodontitis. Propensity score matching (1:1) was applied to balance baseline characteristics, resulting in 604 patients (302 with periodontitis, 302 without). The primary outcome was incident DPN, identified using ICD-10 codes and confirmed by neurologist/endocrinologist diagnosis or abnormal nerve conduction studies. Cox proportional hazards models were used to estimate hazard ratios (HRs) adjusted for age, sex, diabetes duration, HbA1c, health insurance type, and metformin use. Results: Over a median follow-up of 3.8 years, the incidence of DPN was significantly higher in the periodontitis group (42.7% vs. 27.5%, P < 0.001). The adjusted HR for DPN associated with chronic periodontitis was 1.63 (95% CI: 1.22-2.18, P < 0.001). Subgroup analyses confirmed consistent associations across age, sex, and glycemic control strata. Sensitivity analyses, including alternative matching, lag-time analysis, and exclusion of metformin users, supported the robustness of the findings. Conclusion: Chronic periodontitis is an independent risk factor for the development of DPN in patients with T2DM. These findings highlight the importance of integrated oral health management in diabetes care to potentially mitigate neuropathic complications.

Objectives:Diabetic lower extremity arterial disease (LEAD) is a manifestation of diabetic lower extremity vascular complications. This study aimed to screen the key single nucleotide polymorphism (SNP) gene signature in patients with type 2 diabetes mellitus (T2DM) and LEAD.Methods:A total of 147 patients with T2DM complicated by LEAD and 144 patients with T2DM without LEAD were enrolled for transcriptome sequencing. The Plink software was used to preprocess the data. Five machine learning methods were adopted to build the SNP diagnosis models. The receiver operating characteristic (ROC) curve was used to quantify the predicted probabilities of the model. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the cluster Profiler package. Finally, regression statistical analysis was used to correlate the key SNPs with clinical information and biochemical indicators.Results:A total of 24 SNPs were retained and 10 SNPs were risk allele genes. Nine SNPs (rs7412, rs1800629, rs699947, rs3918242, rs668, rs1800470, rs1800449, rs1800469, and rs1024611) were identified as the key SNPs sites. GO and KEGG pathway analyses revealed that these genes are mainly enriched in fluid shear stress and atherosclerosis. Finally, rs1800449 was associated with low-density lipoprotein cholesterol (LDL-C). With high density lipoprotein cholesterol (HDL-C), related site was rs1024611. The sites associated with total cholesterol (CHOL) were rs1800449 and rs7412.The site associated with apolipoprotein B (APOB) and apolipoprotein A1 (APOA1) were rs1800470 and rs1800469.Conclusion:This study authenticated nine SNPs for the diagnosis of T2DM patients with LEAD, which will be of great significance in the development of diagnostic molecular biomarkers for T2DM patients.

ObjectiveTo evaluate the effects of non-surgical periodontal therapy on systemic and local levels of tumor necrosis factor-alpha (TNF-α) and their relationship with glycolipid metabolism in patients with type 2 diabetes mellitus (T2DM) and periodontitis.MethodsIn this prospective cohort study, 234 patients with T2DM and periodontitis underwent standardized non-surgical periodontal therapy, including scaling and root planing, supplemented with systemic antibiotics. Clinical parameters (gingival bleeding index, periodontitis staging and grading), serum levels of TNF-α, HbA1c, leptin, adiponectin, resistin, free fatty acids (FFA), and levels of TNF-α, leptin, adiponectin, and resistin in gingival crevicular fluid (GCF) were assessed at baseline, 4 weeks, and 8 weeks post-treatment. Correlations were analyzed using Spearman’s rank correlation with false discovery rate correction.ResultsPeriodontal therapy resulted in significant improvements in all clinical periodontal parameters (P<0.01). Systemic and local GCF levels of TNF-α, leptin, resistin, and FFA demonstrated significant and progressive reductions, while adiponectin levels increased significantly at 4 and 8 weeks (P<0.01). HbA1c and FBG levels were also significantly improved by week 8 (P<0.01). TNF-α dynamics were strongly correlated with adipokine levels and clinical indices, with the most robust correlations observed within the GCF microenvironment.ConclusionSystematic periodontal therapy effectively reduces local and systemic inflammation, improves glycemic control, and ameliorates glycolipid metabolic disorders in patients with T2DM and periodontitis. The strong interrelationships observed, particularly within the GCF, underscore the potential role of TNF-α as a key mediator in the mouth-systemic metabolic interplay.

Phase I study showed comparable pharmacodynamic, safety and pharmacokinetic profiles of denosumab biosimilar CMAB807 and reference product Prolia® in healthy males. However, the efficacy and safety of CMAB807 in postmenopausal women with osteoporosis were unknown. To compare the efficacy and safety of CMAB807 and Prolia® in Chinese postmenopausal women with osteoporosis. This randomized, double-blind, active-controlled study enrolled Chinese postmenopausal women with osteoporosis. Participants received either CMAB807 or Prolia® 60 mg every 6 months for 12 months. The primary endpoint was the percentage change in BMD at lumbar spine (LS) from baseline to month 12. Secondary endpoints included BMD changes at LS at month 6, total hip (TH) and femoral neck (FN) at month 6 and 12. Additionally, bone turnover markers (BTMs) and incidence of new fragility fractures were evaluated. Safety assessments were also included. A total of 284 women were enrolled, with 276 (97.2

AIMS:This study aimed to investigate the efficacy and safety of finerenone in the treatment of diabetic kidney disease (DKD) in the real-world medical setting and explore the underlying mechanism of its kidney-protecting effects from the perspective of the inflammatory response. MATERIALS AND METHODS:Forty-eight DKD patients were selected and completed a 6-month finerenone treatment. Renal parameters, inflammatory cytokines, other related indicators and adverse effects were collected at every visit. Additionally, subgroup analysis was conducted on the microalbuminuria group (baseline urinary albumin/creatinine ratio (UACR) 30 - < 300 mg/g) and the macroalbuminuria group (baseline UACR ≥ 300 mg/g). RESULTS:After finerenone treatment, the levels of UACR, urinary β2-microglobulin (β2-MG) and proinflammatory cytokines in patients decreased compared with the pretreatment levels. Moreover, the rates of decrease in the UACR levels in the macroalbuminuria group were significantly greater than those in the microalbuminuria group. In the initial stage of treatment, the patient's estimated glomerular filtration rate (eGFR) level decreased and serum potassium level increased compared to before, but with prolongation of the treatment time, both eGFR and serum potassium levels remained stable. CONCLUSIONS:With the assistance of RAS inhibitors, SGLT2 inhibitors, and GLP-1 receptor agonists, finerenone effectively reduces urinary protein and improves the inflammatory response, demonstrating relatively manageable safety in real-world DKD treatment. The patients with macroalbuminuria may experience greater benefits.

BACKGROUND:Type 2 diabetes mellitus (T2DM) is closely associated with both environmental and genetic factors, involving multi-gene inheritance. This study examined the association between the polymorphic locus rs10757278 in long non-coding RNA ANRIL and T2DM. METHODS:Polymerase chain reaction (PCR) was used to detect the rs10757278 polymorphism in the ANRIL gene. RT-qPCR measured ANRIL expression levels, and logistic regression identified independent risk factors for T2DM. Furthermore, the receiver operating characteristic (ROC) curve was constructed to evaluate the clinical diagnostic value of serum ANRIL levels in diagnosing T2DM. RESULTS:The rs10757278 polymorphism of the ANRIL was associated with the development of T2DM. Specifically, the G allele increases the risk of T2DM, and individuals carrying the GG genotype have a higher risk of developing the disease. Significant differences were found in low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), and glycated hemoglobin (HbA1c) among T2DM patients with different genotypes of ANRIL rs10757278. The relative FPG and HbA1c levels were relatively lower in individuals with the AA genotype and higher in those with the GG genotype. Moreover, serum ANRIL levels in the T2DM group were lower than in the control group. Body mass index (BMI), the rs10757278 locus, and serum ANRIL levels were independent risk factors for the development of T2DM. The ROC curve showed that serum ANRIL levels have significant clinical diagnostic value for the diagnosis of T2DM. CONCLUSION:The rs10757278 polymorphism in ANRIL was strongly associated with the genetic predisposition to T2DM.

This study evaluated the effects of sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) on glycemic control, islet cell function, and insulin resistance in type 2 diabetes mellitus (T2DM) patients with T1-stage renal cell carcinoma (RCC). A retrospective cohort of 175 patients was divided into a control group receiving SGLT2i monotherapy (n = 84) and an observation group receiving combination therapy with SGLT2i and GLP-1RA (n = 91). Propensity score matching (PSM) was employed to balance baseline characteristics, resulting in 35 patients per group. After treatment, the observation group showed significant improvements in fasting plasma glucose (FPG), 2-hour postprandial glucose (2hPG), and glycated hemoglobin (HbA1c) compared to the control group (P < 0.001). Islet cell function markers, including fasting insulin and HOMA-IR, also improved significantly (P < 0.001). Renal function markers, such as serum creatinine, blood urea nitrogen, and urinary albumin excretion rate, were better in the observation group (P < 0.05). Multivariate analysis identified older age (OR = 7.434, P = 0.025), higher BMI (OR = 6.812, P = 0.003), and high-fat diet (OR = 0.044, P = 0.005) as independent risk factors for insulin resistance. The combined use of SGLT2i and GLP-1RA demonstrated superior efficacy in improving glycemic variability, insulin sensitivity, and renal function, highlighting its potential as an effective strategy for managing patients with T2DM and RCC.

Abstract Aims/Introduction Mitochondrial damage caused by oxidative stress is a main driver of pancreatic β‐cell dysfunction in the pathogenesis of type 2 diabetes mellitus. Prohibitin2 (PHB2) is a vital inner mitochondrial membrane protein that participates in mitophagy to remove the damaged mitochondria. This study aimed to investigate the role and mechanisms of PHB2‐mediated mitophagy in oxidative stress‐induced pancreatic β‐cell dysfunction. Materials and Methods PHB2 and mitophagy‐related protein expression were analyzed by real‐time polymerase chain reaction and western blotting in RINm5F cells treated with H2O2 and islets of diabetic rats. Mitophagy was observed by mitochondrial and lysosome colocalization. RINm5F cells were transfected by phb2 siRNA or overexpression plasmid to explore the role of PHB2 in mitophagy of RINm5F cells. The mechanism of Nrf2 regulating PHB2 was explored by Nrf2 inhibitor and agonist. Results The expression of PHB2, mitophagy related protein PINK1, and Parkin were decreased in RINm5F cells incubated with H2O2 and in islets of diabetic rats. Overexpression of PHB2 protected β‐cells from oxidative stress by promoting mitophagy and inhibiting cell apoptosis, whereas transfection with PHB2 siRNA suppressed mitophagy. Furthermore, PHB2‐mediated mitophagy induced by oxidative stress was through the Nrf2/PHB2 pathway in β‐cells. Antioxidant NAC alleviated oxidative stress injury by promoting PHB2‐mediated mitophagy. Conclusion Our study suggested that PHB2‐mediated mitophagy can protect β‐cells from apoptosis via the Nrf2/PHB2 pathway under oxidative stress. Antioxidants may protect β‐cell from oxidative stress by prompting PHB2‐mediated mitophagy. PHB2‐mediated mitophagy as a potential mechanism takes part in the oxidative stress induced β‐cell injury.

ObjectiveThis study examined the potential of combining Doppler ultrasound (DUS) and CT angiography (CTA) for early detection and intervention of lower extremity arterial disease (LEAD) in diabetes.Concurrently, risk factors influencing LEAD progression were analyzed.Methods106 Type-2 diabetes patients with LEAD, having undergone DUS and CTA, were divided into four stages according to Fontaine stage. Results of DUS and CTA were compared across stages and potential risk factors were analyzed.ResultsPositive detection rates of LEAD differed between DUS and CTA for Fontaine stages I and II (P < 0.05), with no significant difference for stages III and IV (P > 0.05). CTA identified subgroups with mild to moderate stenosis and severe stenosis or occlusion, with positive rates on DUS of 17.95% and 89.9% respectively. Hypertension was found as an independent risk factor affecting LEAD progression.ConclusionCTA should be performed early for LEAD in diabetes patients at Fontaine stages I and II, regardless of DUS results. For diabetes patients with LEAD, stringent blood pressure control is crucial to delay disease progression.

目的 观察利拉鲁肽联合延续性护理对老年慢性心力衰竭(CHF)伴糖尿病患者心功能的影响,探讨CHF伴糖尿病患者院外治疗策略.方法 选择2017年1—12月就诊于河北医科大学第一医院的老年CHF伴糖尿病患者120例,随机分为对照组、利拉鲁肽组和利拉鲁肽护理组,3组分别有37例、37例和39例完成研究.对照组维持原治疗方案,利拉鲁肽组给予利拉鲁肽干预,利拉鲁肽护理组给予利拉鲁肽联合延续性护理干预,观察12个月.分别于干预前及干预3,6,12个月后测定糖化血红蛋白(HbA1c)、左室射血分数(LVEF)、B型利钠肽(BNP)、左心室舒张末期内径(LVEDd)、6 min步行试验、明尼苏达心力衰竭生活质量量表评分.结果 干预后,利拉鲁肽组和利拉鲁肽护理组LVEDd、LVEF、6 min步行试验、BNP、HbA1 c和生活质量评分均逐渐改善(P均<0.05),利拉鲁肽护理组LVEDd、LVEF、6 min步行试验、BNP、HbA1 c、生活质量评分和利拉鲁肽组LVEF、6 min步行试验、HbA1 c、生活质量评分改善持续至实验结束(P均<0.05),利拉鲁肽组LVEDd和BNP改善持续至6个月时(P均<0.05).干预3个月后,利拉鲁肽组BNP、LVEF和利拉鲁肽护理组BNP、LVEF、HbA1 c、生活质量评分改善情况均明显优于对照组(P均<0.05),利拉鲁肽护理组BNP、LVEF和生活质量评分改善情况均明显优于利拉鲁肽组(P均<0.05);干预6个月和12个月后,利拉鲁肽组和利拉鲁肽护理组LVEDd、BNP、LVEF、6 min步行试验、HbA1 c、生活质量评分改善情况均优于对照组(P均<0.05);干预6个月后利拉鲁肽护理组BNP、LVEF和生活质量评分改善情况均优于利拉鲁肽组(P均<0.05),12个月后利拉鲁肽护理组LVEDd、BNP、LVEF、HbA1c和生活质量评分改善情况均优于利拉鲁肽组(P均<0.05).结论 利拉鲁肽联合延续性护理治疗老年CHF伴糖尿病患者,可更好地改善心功能和控制血糖平稳,并可改善患者生活质量,可作为老年CHF伴糖尿病患者优选院外治疗及护理策略.

目的 探讨双心医学模式下的延续性护理在慢性心力衰竭伴2型糖尿病患者中的应用效果.方法 按照不同护理方式将2017年5—10月在河北医科大学第一医院住院的60例慢性心力衰竭伴2型糖尿病患者分为对照组和观察组,每组30例.对照组患者出院后给予常规延续性护理;观察组在常规延续性护理的基础上实施双心医学模式下的延续性护理.观察2组患者出院时及出院3个月、出院6个月希望水平量表评分,评估2组患者出院时及出院6个月心功能情况[6 min步行试验(6MWT)、左室射血分数(LVEF)、血浆氨基末端B型利钠肽(NT-proBNP)],统计2组患者出院6个月内不良事件发生情况.结果 观察组患者出院3个月、6个月各项评分均明显高于出院时及同期对照组(P均<0.05),且出院6个月采取的积极行动评分、与他人保持亲密的关系评分及总评分均显著高于出院3个月(P均<0.05);对照组患者出院3个月、6个月各项评分与出院时比较差异均无统计学意义(P均>0.05).观察组出院6个月6MWT明显高于出院时及对照组(P均<0.05),NT-proBNP水平明显低于出院时及对照组(P<0.05),2组出院6个月LVEF与出院时比较及2组间出院6个月比较差异均无统计学意义(P均>0.05).2组患者均无严重低血糖和急性心力衰竭事件发生,2组6个月内再住院率比较差异无统计学意义(P>0.05).结论 在双心医学模式下实施延续性护理能及时调整慢性心力衰竭伴2型糖尿病患者心理状态,提高患者希望水平,促使患者采取积极健康行为,有效改善患者心功能.

目的 探讨解耦联蛋白(UCP)-2、活性氧(ROS)表达水平对老年2型糖尿病患者血管内皮功能障碍的调控作用及其机制.方法 选取老年2型糖尿病患者30例;老年2型糖尿病合并内皮功能障碍患者30例及门诊进行体检的健康人群30例,分为糖尿病组、共病组及健康组.分析3组UCP-2、ROS水平表达.结果 3组年龄、性别、体重指数(BIM)、高密度脂蛋白胆固醇(HDL-C)比较差异无统计学意义(P>0.05);与健康组比较,糖尿病组和共病组中三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)水平明显升高(P<0.05);与糖尿病组比较,共病组TG、LDL-C水平显著更高(P<0.05);糖尿病组和共病组糖化血红蛋白(HbA1c)、空腹血糖(FPG)、血清空腹胰岛素(FINS)及胰岛素抵抗指数(HOMA-IR)均显著高于健康组(P<0.05);共病组与糖尿病组各项指标比较差异无统计学意义(P>0.05).与健康组比较糖尿病组、共病组UCP-2显著下降(P<0.05);与糖尿病组比较,共病组UCP-2表达明显下降(P<0.05).与健康组比较,糖尿病组ROS明显升高(P<0.05);与糖尿病组比较,共病组ROS表达明显升高(P<0.05).健康组的肱动脉内皮依赖性舒张功能、非血管内皮依赖性舒张功能变化率优于糖尿病组,但差异无统计学意义(P>0.05);而健康组的肱动脉内皮依赖性舒张功能、非血管内皮依赖性舒张功能变化率明显优于共病组(P<0.05).健康组的颈动脉内中膜厚度高于糖尿病组,但差异无统计学意义(P>0.05);健康组的颈动脉内中膜厚度明显高于共病组(P<0.05).结论 人体内UCP-2水平对ROS水平的表达具有重要影响作用,其两者的关系呈现负相关,且UCP-2可以通过降低ROS水平对老年内皮功能障碍起到重要改善作用,对此两种指标进行调控可以帮助老年2型糖尿病共病内皮功能障碍患者减轻血管内皮损伤,更好地控制血糖.

目的 探讨利拉鲁肽对2型糖尿病轻度认知功能损害(mild cognitive impairment,MCI)患者蒙特利尔认知评估量表(Montreal Cognitive Assessment,MoCA)评分、尿白蛋白与肌酐比值(albumin-creatinine ratio,ACR)、足细胞标志蛋白(podocyte proteins,PCX)的影响.方法 将80例2型糖尿病MCI患者随机分为对照组(40例)和利拉鲁肽组(40例),对照组给予原治疗方案,利拉鲁肽组改用利拉鲁肽治疗,疗程均为24周.比较治疗前及治疗后24周时2组收缩压(systolic blood pressure,SBP)、舒张压(diastolic blood pressure,DBP)、糖化血红蛋白(hemoglobin A1 c,HbA1 c)、空腹血糖(fasting plasma glucose,FPG)、总胆固醇(total cholesterol,TC)、三酰甘油(triglycerides,TG)、尿ACR、PCX.应用MoCA评估患者认知功能.结果 2组治疗前、治疗后和2组治疗前后FPG、HbA1 c、SBP、DBP、TG、TC差异均无统计学意义(P>0.05).治疗前,2组MoCA评分、尿ACR、PCX差异均无统计学意义(P>0.05);治疗后,对照组MoCA评分、尿ACR、PCX与治疗前差异均无统计学意义(P>0.05),利拉鲁肽组MoCA评分显著高于治疗前,尿ACR、PCX显著低于治疗前,利拉鲁肽组MoCA评分显著高于对照组(P<0.05),尿ACR、PCX显著低于对照组,差异均有统计学意义(P<0.05).结论 利拉鲁肽可改善 2 型糖尿病MCI 患者认知功能,降低其尿 ACR 和 PCX 水平.

目的 探讨2型糖尿病轻度认知功能障碍(mild cognitive impairment,MCI)患者在二甲双胍基础上加用胰岛素促泌剂、α-糖苷酶抑制剂、二肽基肽酶(dipeptidyl peptidase-4,DPP-4)抑制剂治疗有效性、安全性的区别.方法 将2型糖尿病MCI患者120例随机分为阿格列汀组、阿卡波糖组和瑞格列奈组各40例.阿格列汀组加用阿格列汀,阿卡波糖组加用阿卡波糖,瑞格列奈组加用瑞格列奈.疗程24周.测定糖化血红蛋白(hemoglobin A1c,HbA1 c)、空腹血糖(fasting plasma glucose,FPG)、餐后2h血糖(2 h postprandial blod glucose,2 hPBG)、总胆固醇(total cholesterol,TC)、三酰甘油(triglycerides,TG),记录所有低血糖事件、胃肠道反应及HbA1c达标率.结果 与治疗前比较,3组HbA1c、FPG、2 hPBG均显著下降(P＜0.01),TG、TC无显著变化(P＞0.05).同一时间点各组间HbA1c、FPG、2 hPBG、TG和TC差异均无统计学意义(P＞0.05).治疗结束时,阿格列汀组血糖达标率最高74.36％(x2 =6.496,P＜0.01),胃肠道反应发生率最低0.00％(x2=37.853,P＜0.01),低血糖发生率最低2.56％(x2=16.955,P＜0.01).结论 阿格列汀治疗2型糖尿病MCI患者,降糖效果不劣于阿卡波糖和瑞格列奈,低血糖发生率、胃肠道反应发生率更低.

目的 探讨阿格列汀和瑞格列奈对2型糖尿病轻度认知功能障碍患者血糖、血脂及认知功能的影响.方法 纳入2017年2月—2018年2月于河北医科大学第一医院内分泌科就诊的2型糖尿病轻度认知功能障碍患者80例,将患者按随机数字表法分为2组,阿格列汀组40例给予阿格列汀联合二甲双胍治疗,瑞格列奈组40例给予瑞格列奈联合二甲双胍治疗,疗程均为24周.观察2组治疗前及治疗12周、24周糖化血红蛋白(HbA1 c)、空腹血糖(FPG)、餐后2 h血糖(2hPG)、总胆固醇(TC)、三酰甘油(TG)及蒙特利尔认知评估评分(MoCA评分,评估认知功能)变化情况,记录2组治疗结束时血糖达标率和治疗过程中低血糖及其他不良反应发生情况.结果 阿格列汀组37例、瑞格列奈组38例完成研究.治疗前2组HbA1 c、FPG、2 hPG、TG、TC、MoCA评分比较差异均无统计学意义(P均>0.05).治疗12周、24周后,2组TG、TC以及瑞格列奈组MoCA评分与治疗前比较差异均无统计学意义(P均>0.05),2组HbA1 c、FPG、2 hPG均较治疗前显著降低(P均<0.05);治疗24周后,阿格列汀组HbA1c显著低于瑞格列奈组(P<0.05),MoCA评分显著高于瑞格列奈组(P<0.05);治疗结束时,瑞格列奈组血糖达标率为71.1％(27/38),阿格列汀组血糖达标率为78.4％(29/37),2组间比较差异无统计学意义(P>0.05);瑞格列奈组低血糖发生率为31.6％(12/38),阿格列汀组低血糖发生率为10.8％(4/37),阿格列汀组低血糖发生率显著低于瑞格列奈组(P<0.05).结论 阿格列汀联合二甲双胍与瑞格列奈联合二甲双胍的降糖效果相当,对血脂均无明显影响,但阿格列汀可改善2型糖尿病轻度认知功能障碍患者认知功能,且低血糖发生率更低.

目的 观察沙格列汀联合阿卡波糖治疗初诊老年2型糖尿病疗效.方法 样本选取时间2015年1月—2017年12月,研究目标为99例2型糖尿病患者,根据治疗措施的差异性随机分为观察组(n=50)和对照组(n=49),对照组予以阿卡波糖治疗,观察组予以沙格列汀+阿卡波糖治疗.治疗12周后对比两组患者血糖控制情况、体质指数、空腹胰岛素、胰岛β细胞功能以及不良反应发生情况.结果 观察组空腹血糖、餐后2h血糖、糖化血红蛋白、体质指数、空腹胰岛素、胰岛β细胞功能分别为(6.81±1.62)mmol/L、(10.03±4.13)mmol/L、(7.28±0.94)％、(26.63±1.25)kg/m2、(9.96±1.24)mIU/L、(38.24±19.36)％,对照组分别为(8.93±2.21)mmol/L、(14.29±5.38)mmol/L、(8.05±1.33)％、(28.31±1.52)kg/m2、(9.01±1.27)mIU/L、(45.97±18.55)％,(t=5.4514、4.4247、3.3318、6.0117、3.7658、2.0278,P<0.05);观察组不良反应发生率为2.00％,低于对照组12.24％,(x2=3.9530,P=0.0467).结论 沙格列汀联合阿卡波糖治疗初诊老年2型糖尿病疗效极佳,在临床治疗过程中可以作为首选措施.

Objective To investigate the changes of urinary podocalyxin (PCX) and vascular endothelial growth factor (VEGF) in the patients with diabetic nephropathy (DN) at stage Ⅲ and the effect of alpha-lipoic acid (ALA) on them. Methods According to the uriary albumin excretion rate (UAER), 182 participants were divided into three groups as: simple diabetes mellitus group (SDM, n = 62), DN at stage Ⅲ group (NA, n = 60), and normal control group (NC, n = 60). Then the NA group was randomly divided into ALA treatment group (NA Ⅰ, n = 30) and conventional treatment group (NA Ⅱ, n = 30). The levels of MDA, SOD, GSH-px, urinary PCX and serum VEGF were determined at baseline and 2 weeks after treatment. Results The level of MDA after ALA treatment was lower than that before ALA treatment in the NA Ⅰ group (P < 0.05). The levels of SOD and GSH-px were higher than those before treatment (P < 0.05). The levels of urinary PCX and serum VEGF were lower after treament (P < 0.05). Conclusions ALA can provide some protection against glomerular podocyte injury, which may be related to its effect in alleviating enhanced oxidative stress in DN at stage Ⅲ.

Objective It is to observe the effects of urine albumin-creatinine ratio (UACR) on cognitive function in patients with type 2 diabetes mellitus,and explore its relationship.Methods 180 patients with type 2 diabetes mellitus were collected and divided into normoalbuminuria group (NAU group),microalbuminuria group (MIAU group)and macroalbuminuria group (MAAU group) according to the UACR,each group had 60 patients.The fasting blood glucose (FBG),hemoglobin A 1c (HbA1c),systolic blood pressure (SBP),diastolic blood pressure (DBP),triglyceride (TG),total cholesterol (TC),low density lipoprotein (LDL),high-density lipoprotein (HDL) were measured,and the score of MoCA was assessed.Results The score of MoCA (P ＜ 0.05),delay recall ability (P ＜ 0.05) and orientation ability (P ＜ 0.05) in MIAU group and MAAU group were reduced gradually,while the attention ability(P ＜ 0.05),abstract ability(P ＜ 0.05),language ability(P ＜0.05) in MIAU group and visual space and executive function(P ＜ 0.05),naming ability(P ＜ 0.05) in MAAU group were significantly lower than NAU group.The scores of MoCA and sub-items were inversely associated with the UACR (P ＜ 0.05).Conclusion The UACR was closely related to the cognitive function of type 2 diabetes mellitus,and the impairment of the attention ability,language ability,abstract ability,delay recall ability and orientation ability may occur during the early-stage diabetic nephropathy in type 2 diabetes mellitus,and the impairment of visual space and executive function and naming ability may occur during the later-stage.