Diabetic osteoporosis (DOP) is a serious skeletal complication of type 2 diabetes mellitus (T2DM), characterized by deteriorated bone microarchitecture and elevated fracture risk independent of reduced bone mineral density. Emerging evidence indicates that immunometabolic reprogramming of bone marrow immune cells serves as a core driver of DOP pathogenesis. This review focuses on macrophages and CD4+ Th17/Treg cells, the pivotal immune subsets mediating skeletal immune-metabolic homeostasis. We systematically elaborate how hyperglycemia triggers glycolytic predominance, HIF-1α stabilization, and succinate-SUCNR1 axis activation in macrophages, alongside mTORC1-HIF-1α-dependent Th17/Treg imbalance. Bidirectional immunometabolic crosstalk between these immune cells disrupts the RANKL/OPG and Wnt/β-catenin signaling pathways, thereby disturbing bone formation and resorption. Furthermore, we summarize current immunometabolic-targeted modulators for DOP, stratifying their preclinical and clinical evidence, skeletal benefits, and safety limitations. We also highlight existing clinical diagnostic defects and translational bottlenecks in DOP research. Finally, we prospect emerging research directions including spatial immunometabolic profiling, gut-immune-bone axis regulation, and artificial intelligence-assisted precision intervention, aiming to provide mechanistic insights and novel translational strategies for DOP targeted therapy.

Background Cardiovascular risk in patients with type 2 diabetes mellitus (T2DM) with metabolic dysfunction-associated steatotic liver disease (MASLD) may be underestimated when body mass index (BMI) is used as the dominant marker of metabolic severity. Lower BMI does not preclude hepatic fibrosis, vascular injury, kidney dysfunction, or systemic vulnerability. We aimed to develop and internally validate an interpretable multiorgan score for cardiovascular risk stratification in lower-BMI patients with T2DM-MASLD. Methods In this retrospective hospital-based cohort study, adults with T2DM, MASLD, and BMI < 27.0 kg/m² were identified from the hospital information system of Gansu Provincial Hospital, China. Patients were divided before modelling into training and locked internal-validation cohorts at a 7:3 ratio. Candidate predictors were screened within the training cohort only. A parsimonious ridge-logistic model was developed as the primary model, converted into an additive clinical score, and evaluated by discrimination, precision–recall performance, Brier score, calibration, decision-curve analysis, and training-derived risk strata. Results Among 1466 lower-BMI patients with T2DM-MASLD, 240 had documented cardiovascular disease (CVD) by the administrative study cut-off. The training and validation cohorts included 1026 and 440 patients, respectively, with identical CVD rates of 16.4%. The final A2 score retained eight routinely available predictors: diabetes duration, carotid plaque number, mean carotid intima–media thickness, age, fibrosis-4 index, estimated glomerular filtration rate, LDL cholesterol, and albumin. In locked internal validation, A2 achieved an area under the receiver operating characteristic curve of 0.792, average precision of 0.420, Brier score of 0.116, calibration intercept of − 0.307, and calibration slope of 0.849. Training-derived low-, intermediate-, and high-risk strata separated observed CVD burden in validation, with event rates of 2.9%, 12.0%, and 33.3%; corresponding rates in the BMI < 25 kg/m² subgroup were 1.3%, 10.8%, and 36.8%. Conclusions In lower-BMI T2DM-MASLD, cardiovascular burden was not captured by BMI category alone. A routine, interpretable multiorgan score provided stable internal risk stratification and may support earlier cardiovascular evaluation beyond BMI-defined obesity categories, pending external and prospective validation.

Although current guidelines for type 2 diabetes (T2D) underscored the importance of attaining glycemic control and weight management goals, the patient perspectives on achieving these goals remained unclear in China. This study aimed to understand Chinese patients’ perspectives on stringent glycemic control (hemoglobin A1c [HbA1c] ≤ 6.5

BACKGROUND:Papillary thyroid cancer (PTC) is the most common endocrine malignancy, demonstrating the most rapid incidence growth among solid tumors in the past decades. Notably, aggressive variants frequently manifest metastatic potential and therapeutic resistance, substantially compromising poor prognosis. Circular RNAs (circRNAs) have been recognized as pivotal regulators in diverse biological processes across multiple cancer types. However, the molecular mechanism underlying circ_0003997 (circCLMP) in PTC remains largely unexplored. METHODS:The expression levels of circ_0003997, miR-370-3p, and HMGA2 were assessed using real-time quantitative polymerase chain reaction (RT-qPCR). The functions of circ_0003997 were evaluated through CCK-8 assays, wound healing assays, and Transwell assays in PTC cells. Western blotting was used to analyze the expression of key epithelial-mesenchymal transition (EMT) proteins. Tumor development in vivo was assessed using xenograft tumor models. The expression of Ki67 and HMGA2 in tumor tissues was evaluated by immunohistochemical (IHC) assay. Dual-luciferase reporter assays were performed to validate the interactions among circ_0003997, HMGA2, and miR-370-3p. RESULTS:Circ_0003997 demonstrated significant upregulation in PTC tissues and cells. Functional validation experiments revealed that knockdown of circ_0003997 inhibited cell proliferation, migration, invasion, and EMT, while its overexpression promoted PTC progression. Mechanistically, circ_0003997 modulated HMGA2 expression by sponging miR-370-3p. Rescue experiments demonstrated that the oncogenic effects of circ_0003997 could be reversed by miR-370-3p. In vivo data showed that the decreased expression of circ_0003997 significantly suppressed tumor growth of PTC. CONCLUSIONS:We identified a novel biomarker panel consisting of the circ_0003997/miR-370-3p/HMGA2 axis, offering potential diagnostic and therapeutic avenues for PTC.

PurposeThis study was designed with the goal of exploring miR-99a expression in T2DM patients suffering from comorbid MASLD and clarifying the importance of miR-99a in this pathological context.MethodsA total of 137 subjects were included in this study, including 50 T2DM patients with MASLD (T2DM +MASLD group),48 T2DM patients without MASLD (T2DM group), and 39 healthy subjects (Control group). We measured the levels of IL-6, mTOR and SOD in the serum of the subjects by ELISA. The plasma miR-99a levels was detected by RT-PCR. The correlation between serum miR-99a level and other indicators was analyzed.ResultsSerum miR-99a levels (median 0.79 vs 0.16 vs 0.03, P < 0.001) were significantly lower in the T2DM group than the healthy population and further decreased in the T2DM with MASLD patients (P < 0.001). After adjusting for age, gender, illness duration and BMI, spearman correlation analysis showed that TG, HbA1c, FPG, HOMA-IR, Hs-CRP, IL-6, HDL-C, mTOR(P < 0.05) remained independently linked with serum miR-99a. And stepwise linear regression analysis showed that HbA1c, IL-6 and mTOR are independent serum miR-99a correlation variables (P < 0.05). Moreover, the ROC results indicated that serum miR-99a has a high diagnostic value for T2DM with MASLD. In conclusion, serum miR-99a may be utilized as a screening biomarker for T2DM with MASLD.ConclusionsThese data highlight a potential role for miR-99a as a regulator of the comorbid incidence of T2DM and MASLD, suggesting that measuring the levels of miR-99a can effectively predict the risk of MASLD in those with T2DM.

Background/Objectives: Metabolic dysfunction-associated fatty liver disease (MAFLD) is closely associated with type 2 diabetes mellitus (T2DM), where T2DM serves as a crucial driving factor for MAFLD progression. While vitamin D (VD) demonstrates protective effects against MAFLD, the underlying mechanisms through which it influences MAFLD-related liver sinusoidal endothelial cell (LSEC) capillarization remain to be elucidated. This study aimed to explore how vitamin D ameliorates LSEC capillarization in T2DM-associated MAFLD. Methods: Culture human liver sinusoidal endothelial cells (HLSECs) according to the established protocol. After 1,25(OH)2D3 intervention in high glucose (HG)-induced HLSECs, determine the changes in liver sinusoidal capillarization-related proteins (LN, PLVAP), autophagy and pyroptosis levels. Observe the changes in cell lipid accumulation and fenestration structures. After adding Bafilomycin A1, MCC950, compound C and rapamycin to HLSECs, explore the therapeutic mechanism of 1,25(OH)2D3. After supplementing VD to MAFLD model mice, further verify the therapeutic mechanism of VD on MAFLD. Results: HG can induce the capillarization and lipid accumulation of HLSEC, increase the level of pyroptosis, and simultaneously reduce the autophagy level. Vitamin D alleviated high-glucose-induced pyroptosis (by suppressing GSDMD/NLRP3) and autophagic inhibition by activating the AMPK-mTOR axis (upregulating p-AMPK and downregulating mTOR), and improved lipid accumulation and hepatic sinusoidal capillarization. In the mouse model of MAFLD, VD supplementation can induce autophagy, inhibit pyroptosis and capillarization, and improve MAFLD. Conclusions: These results demonstrate, for the first time, that VD mitigates LSEC dysfunction through dual mechanisms: activating AMPK-dependent autophagy and inhibiting pyroptosis, providing a therapeutic rationale for VD in treating MAFLD-related sinusoidal pathology.

The role that vascular smooth muscle cell (VSMC)-derived foam cells play as drivers of atherosclerosis has been a growing focus of recent research interest. Toll-like receptor 4 (TLR4) has been identified as a regulator of the formation of VSMC foam cells, while vitamin D can reportedly suppress macrophage-derived foam cell development. Our aim is to investigate Whether vitamin D can similarly suppress the formation of VSMC foam cells, as does the role that TLR4 plays in this pathogenic context.The impact of vitamin D on VSMC-derived foam cell and atherosclerotic plaque formation was assessed, and the expression of cholesterol transport-related genes and TLR4 was assessed in ApoE-/- mice. The impact of 1,25(OH)2D3 on the ox-LDL-mediated formation of foam cells and the underlying molecular mechanisms were also examined in VSMCs cultured in vitro. Supplemental vitamin D administration resulted in a pronounced reduction in aortic atherosclerotic plaque formation and the development of SMA-a-positive foam cells. Vitamin D further suppressed TLR4, CD36, and SR-A in atherosclerotic plaque lesions while promoting ABCA1, ABCG1, and LXR-α upregulation. 1, 25 (OH)2 D3 significantly reduced Dil-ox-LDL uptake and increased NBD-LDL efflux in VSMCs, in addition to suppressing TLR4, CD36, and SR-A expression, while upregulating ABCA1, ABCG1, and LXR-α. Knocking down TLR4 impaired VSMC foam cell formation, while 1,25(OH)2D3-induced JNK activation suppressed TLR4 signaling and promoted VSMC foam cell development. Our study reveals that Vitamin D can reduce VSMC foam cell formation and protect against atherosclerotic progression through the JNK-TLR4 signaling pathway.

Papillary thyroid cancer (PTC) is the most common type of thyroid malignancy, and its global incidence has been gradually increasing. For advanced PTC, the mortality rates are also increasing yearly. Despite advancements in diagnosis and treatment, some advanced PTC exhibit aggressive behaviors, leading to a poor prognosis. CircRNAs are a class of non-coding RNAs characterized by a covalently closed loop structure. Their stability and abundance have positioned them as promising diagnostic and prognostic biomarkers. Numerous studies have identified dysregulated circRNAs in PTC tissues and cell lines, suggesting their involvement in PTC initiation and progression. In this review, we provide an overview of circRNAs and systematically discuss their role in PTC. CircRNAs affect cancer progression by regulating the Wnt/β-catenin, PI3K/AKT, MAPK pathways, and others. Furthermore, circRNAs have been implicated in PTC metastasis and chemoresistance. We highlight their potential value as diagnostic markers, therapeutic targets, and prognostic indicators. In conclusion, circRNAs play a critical role in PTC, and dysregulated circRNAs influence multiple signaling pathways and cellular processes involved in tumorigenesis and metastasis. It represents a promising avenue for advancing the diagnosis, management, and treatment of PTC.

Insulin degludec (degludec), an ultra-long-acting basal insulin analogue, provides equivalent glycemic control to other basal insulin analogues, with lower risk of hypoglycemia and flexible dosing. Chinese TREsiba AudiT (CN-TREAT) investigated outcomes with degludec in people with type 2 diabetes (T2D) in routine clinical practice in China. This was a retrospective chart review study in adults with T2D initiating or switching to degludec at 50 sites in China between January 2020 and July 2021. The primary endpoint was change in glycated hemoglobin (HbA1c) from baseline to end of study (EOS; week 20). Secondary endpoints included change from baseline to EOS in fasting plasma glucose (FPG), self-measured plasma glucose (SMPG), daily insulin dose, and rate of hypoglycemia. Data from 936 participants were included (499 insulin-naïve; 437 insulin-experienced). Mean (95

Abstract Purpose This study was designed with the goal of exploring miR-99a expression in T2DM patients suffering from comorbid NAFLD and clarifying the importance of miR-99a in this pathological context. Methods A total of 137 subjects were included in this study, including 50 T2DM patients with NAFLD (T2DM + NAFLD group),48 T2DM patients without NAFLD (T2DM group), and 39 healthy subjects (Control group). We measured the levels of IL-6, mTOR and SOD in the serum of the subjects by ELISA. The plasma miR-99a levels was detected by RT-PCR. The correlation between serum miR-99a level and other indicators was analyzed. Results Serum miR-99a levels (median 0.79 vs 0.16 vs 0.03, P < 0.001) were significantly lower in the T2DM group than the healthy population and further decreased in the T2DM with NAFLD patients (P < 0.001). After adjusting for age, gender, illness duration and BMI, spearman correlation analysis showed that TG, HBA1c, FPG, HOMA-IR, Hs-CRP, IL-6, HDL-C, mTOR(P < 0.05) remained independently linked with serum miR-99a. And stepwise linear regression analysis showed that HBA1c, IL-6 and mTOR are independent serum miR-99a correlation variables (P < 0.05). Moreover, the ROC results indicated that serum miR-99a has a high diagnostic value for T2DM with NAFLD. In conclusion, serum miR-99a may be utilized as a screening biomarker for T2DM with NAFLD. Conclusions These data highlight a potential role for miR-99a as a regulator of the comorbid incidence of T2DM and NAFLD, suggesting that measuring the levels of miR-99a can effectively predict the risk of NAFLD in those with T2DM.

Growth factor receptor-bound protein 2 (GRB2) is a key adaptor protein involved in multiple signalling pathways, and its dysregulation is associated with various diseases. Type 2 diabetes is a systemic condition characterized by insulin resistance and impaired β-cell function. The complications of diabetes significantly reduce life expectancy and quality of life, imposing a substantial burden on society. However, the role of GRB2 in diabetes and associated complications is largely unknown. Emerging evidence suggests that GRB2 plays a crucial role in insulin resistance, inflammation, immune activation and the regulation of cellular processes such as cell proliferation, growth, metabolism, angiogenesis, apoptosis and differentiation. Dysregulation of GRB2-mediated pathways contributes to the progression of diabetic neuropathy, cognitive dysfunction, nephropathy, retinopathy and related disorders. This review provides a comprehensive overview of the current understanding of the role of GRB2 in diabetes, diabetes complications and related disorders, alongside recent advances in the development of GRB2-targeted therapies. Elucidating the complex role of GRB2 in these disorders provides valuable insights into potential therapeutic strategies targeting GRB2-mediated pathways.

目的 探讨 2 型糖尿病(T2DM)患者骨钙素(OC)与左心室参数、颈动脉内膜厚度之间的相关性.方法 选取T2DM患者 390 例,询问病史,收集一般资料、实验室指标,超声测量颈动脉内膜厚度(cIMT)、左心室参数,计算左心室质量指数(LVMI).根据是否存在合并症分为 4 组:T2DM组、T2DM亚临床动脉粥样硬化组、T2DM微血管并发症组、T2DM大血管并发症组.比较 4 组相关指标并做相关性分析.结果 与T2DM组相比,其他 3 组中OC含量明显减低(P<0.05).相关性分析显示:OC与LVMI呈负相关;与LVEF、E/A比值呈正相关;与cIMT无相关性.同时OC与FBG、HbA1c、TC、TG、LDL-C、hs-CRP、HOMA-IR呈负相关,与HDL-C呈正相关(P<0.05).结论 OC对T2DM患者的心脏及血管可能具有保护作用.

Objective:To investigate the risk factors of diabetic kidney disease (DKD) in type 2 diabetes mellitus (T2DM) patients in plain-sand areas and loess hilly areas of Gansu province.Methods:A total of 1 599 T2DM patients who participated in chronic disease and risk factors monitoring and basic public health service management were selected by multi-stage stratified random sampling method in the sandy plain areas and loess hilly areas of Gansu province. Questionnaire survey, physical measurement and laboratory tests were performed. Multivariate binary logistic model was used to analyze the influencing factors.Results:The prevalence of DKD was 22.1% (174/787) among T2DM patients in the sandy plain areas and 19.1%(155/812) in the loess hilly area, respectively. Hypertension ( OR=3.022), hyperuricemia ( OR=2.114) and HbA1c≥7%( OR=2.231) were the risk factors for DKD in the plain-sand areas, and the risk of DKD increased with age. In the loess hilly areas, female sex ( OR=0.379) was the protective factor for DKD; while duration of disease≥10 years ( OR=2.476), hyperuricemia ( OR=1.907), HbA1c≥7% ( OR=1.927) were the risk factors for DKD; and the risk of DKD increased with the increase of age, and decreased with the increase of per capita monthly income. Conclusions:The prevalence of DKD and its influencing factors are different between sandy plain areas and loess hilly areas in Gansu province. The prevention and treatment of hypertension should be given more attention in sandy plain areas. In addition, the screening of DKD should be conducted among T2DM patients, particularly for those with old age, hyperuricemia and HbA1c≥7% in both areas of the province.

目的 探讨甘肃省平原风沙与黄土丘陵地区DR的患病率及其影响因素.方法 选取甘肃省慢性病及其危险因素监测和基本公共卫生服务管理的T2DM患者 1739 例,根据眼底检查结果分为单纯T2DM组(n=1328)和DR组(n=411).比较各组一般资料及生化指标,Logistic回归分析DR的影响因素.结果 与T2DM组比较,DR组年龄、DM病程、风沙环境、吸烟史、高强度活动、FPG、HbA1c、SBP、TC、HDL-C升高(P＜0.05),文化程度、人均月收入、食用新鲜水果、食用坚果、步行或骑行比例降低(P＜0.05).Logistics回归分析显示,风沙环境、吸烟史、DM病程、HbA1c、SBP、高强度活动是DR的危险因素,食用坚果、人均月收入是DR的保护性因素.结论 甘肃省平原风沙地区DR患病率高于黄土丘陵地区,除DM病程、HbA1c、SBP、经济水平、文化程度外,环境因素可能增加DR风险.

Hemichorea associated with non-ketotic hyperglycemia（HC-NH）is a rare complication of diabetes mellitus. Early diagnosis and treatment could improve the prognosis. We reported a female patient with hyperglycemia who developed involuntary choreiform movements of right limb,and MRI showed high signal in the contralateral basal ganglia region on T1WI. Hercondition improved after treatment.Clinical understanding needs to be improved because HC-NH is easily misdiagnosed or missed.

The incidence of diabetic patients with non-alcoholic fatty liver disease (NAFLD) is continuously increasing worldwide. However, the specific mechanisms of NAFLD patients with diabetes are still not clear. Recent studies have indicated that integrins play an important role in NAFLD. In this study, we considered the relationship between integrin αv (IGTAV)/FAK pathway and sinusoidal capillarization. We investigated the difference between the expression of IGTAV, laminin (LN), focal adhesion kinase (FAK), and phosphor-FAK protein in human liver sinusoidal endothelial cells (HLSECs) to explore the specific mechanisms of the diseases of NAFLD with diabetes under high glucose. We cultured and identified the HLSECs and constructed the recombinant lentivirus vector with IGTAV shRNA by quantitative real-time PCR (qRT-PCR) to silence the IGTAV gene. Cells were divided into groups of 25 mmol/L glucose and 25 mmol/L mannitol. We measured the protein levels of IGTAV, LN, FAK, and phosphor-FAK by western blot at 2 h, 6 h, and 12 h before and after IGTAV gene silencing. The lentivirus vector was successfully constructed with IGTAV shRNA. The HLSECs under high glucose were observed by scanning electron microscope. SPSS19.0 was used for statistical analysis. High glucose significantly increased the expression of IGTAV, LN, and phosphor-FAK protein in HLSECs; the shRNA IGTAV could effectively inhibit the expression of phosphor-FAK and LN at 2 h and 6 h. Inhibition of the phosphor-FAK could effectively decrease the expression of LN in HLSECs at 2 h and 6 h under high glucose. Inhibition of IGTAV gene of HLSECs under high glucose could improve hepatic sinus capillarization. Inhibition of IGTAV and phosphor-FAK decreased the expression of LN. High glucose led to hepatic sinus capillarization via IGTAV/ FAK pathway.

Objective:To explore the prevalence and influencing factors of diabetic peripheral neuropathy (DPN) in the plain sand and loess hilly area of Gansu Province.Methods:This study was a cross-sectional study. Type 2 diabetes mellitus (T2DM) patients in the plain sand and loess hilly area of Gansu Province were selected as the subjects. Educational level, age, course of diabetes, family history of diabetes and foot chaps were collected. The diagnostic criteria for DPN are based on the Expert Consensus on Diagnosis and Treatment of diabetes Neuropathy (2021 Edition). χ2 test was used to compare the DPN prevalence between patients in plain sandstorm and loess hilly area, and a multivariate logistic regression model was used to analyze the influencing factors of DPN. Results:A total of 1 532 T2DM patients were included in the study, including 729 T2DM patients in the plain sandstorm area and 803 patients in the loess hilly area. The overall prevalence of DPN in the plain sandstorm and loess hilly areas of Gansu Province was 53.7 % (822/1 532). Compared to the loess hilly area, the incidence rate of DPN in the plain sandstorm area was higher, 42.3% (340/803) and 66.1% (482/729), respectively. The logistic regression model showed that high education level (OR=0.218, 95%CI 0.215-0.382, P<0.001) was a protective factor for DPN, and the high-risk risk of DPN increased with age ( χ2=86.671, P<0.001). The course of disease ≥10 years (OR=1.562, 95%CI 1.230-1.984, P<0.001), HbA 1c≥7% (OR=1.300, 95%CI 1.028-1.645, P=0.029), diabetes family history (OR=1.320, 95%CI 1.052-1.654, P=0.016), presence of foot chaps (OR=1.374, 95%CI 1.069-1.766, P=0.013), and high altitude (2 700 m) (OR=2.733, 95%CI 2.172-3.438, P<0.001) were independent risk factors for DPN. Conclusions:The incidence of DPN in the plain sandstorm area of Gansu Province was significantly higher than that in the loess hilly area. In addition to factors such as age, course of disease, education level, and HbA 1c, altitude also increased the risk of DPN occurrence.

目的 探索厄贝沙坦对糖尿病肾病(DN)大鼠肾形态和功能的影响.方法 用高脂饮食联合小剂量链脲佐菌素腹腔注射建立DN大鼠模型,并将造模成功的DN大鼠随机分为模型组和实验组,每组 10 只;另取 10 只标准饲料喂养大鼠作为正常组.实验组给予50 mg·kg-1 厄贝沙坦灌胃;其他2 组均给予等剂量0.9%NaCl灌胃.3 组大鼠均连续给药 22 周.于 22 周末,检测大鼠尿白蛋白/肌酸酐比值(UACR),用实时荧光定量聚合酶链反应法检测肾组织中整合素av和整合素β5 mRNA的表达水平,用免疫组化法检测肾组织中玻连蛋白(VN)、层粘连蛋白(LN)的定位分布和蛋白表达水平.结果 实验组、模型组和正常组的UACR分别为(436.23±96.52)、(698.00±90.38)和(46.56±9.68)mg·g-1,整合素av mRNA相对表达水平分别为 1.52±0.17、2.31±0.28 和0.52±0.04,整合素β5 mRNA相对表达水平分别为 1.76±0.15、2.65±0.23 和 0.68±0.07,VN平均光密度值分别为 430.32±38.46、880.35±63.26 和 160.46±12.37,LN平均光密度值分别为 450.17±36.35、730.42±68.28 和 350.08±36.42.实验组的上述指标与模型组相比较,差异均有统计学意义(均P＜0.05).结论 厄贝沙坦可能通过抑制整合素avβ5 及其相关蛋白的表达,从而发挥肾保护作用.

非酒精性脂肪性肝病(NAFLD)是世界范围内慢性肝病的重要原因,其患病率的持续增高已对人体健康造成严重威胁.维生素D是一种抗纤维化、抗炎和胰岛素增敏分子,参与肠道-脂肪组织-肝轴内的免疫代谢途径.流行病学研究支持维生素D缺乏症与NAFLD有关,在动物实验及体外研究中发现,抑制核苷酸结合寡聚化结构域样受体蛋白3炎症小体和焦亡的激活可以延缓肝脏脂肪变性及纤维化.本研究综述细胞焦亡和维生素D在NAFLD发病中的研究进展,探讨三者的相互关联,为维生素D基于焦亡为靶点治疗NAFLD的可能性提供参考.

目的 探讨综合疗法在勃起功能障碍(ED)合并2型糖尿病(T2DM)吸烟患者中的疗效及影响因素.方法 选取2018年2月-2021年3月甘肃省武威市人民医院内分泌科收治的30-56岁ED合并T2DM吸烟的已婚患者198例,随机分为对照组、治疗组,其中对照组97例,治疗组101例,记录患者一般资料、问询生活习惯后进行国际勃起功能指数(ⅡEF-5)问卷评分,给予综合治疗2周后再次进行ⅡEF-5问卷评分,对比分析综合疗法在ED合并T2DM吸烟患者中的疗效及影响因素.结果 治疗组给予综合治疗后ⅡEF-5总评分和各问题的评分均显著高于对照组,差异有统计学意义(P＜0.05),影响其治疗有效性的常见因素为T2DM病程、年龄及体重指数,是否饮酒、糖化血红蛋白、空腹血糖、24h尿蛋白、治疗后空腹血糖等因素对ED疗效的改善差异无统计学意义(P＞0.05).结论 在吸烟的T2DM患者中ED是常见的合并症.T2DM病程、年龄和体重指数是影响吸烟的T2DM合并ED患者治疗有效性的危险因素.