目的 探讨miRNA-126对高糖诱导的内皮细胞自噬与凋亡的影响及分子机制.方法 采用高糖(HG)诱导HUVECs模型,随机分为4组,即正常葡萄糖(5.5 mmo/L)对照组,HG模型组,miRNA-126-5p mimics组(转染miRNA-126-5p mmics组),miRNA-126-5p inhibitor组(转染miRNA-126 inhibitor组).HG模型组即终浓度为33.3 mmol/L的葡萄糖诱导24 h,miRNA-126-5p mimics组是miRNA-126-5p mimics转染至HUVECs细胞,48 h后在培养基中加入33.3 mmol/L(终浓度)葡萄糖,培养24 h.miRNA-126-5p inhibitor组是miRNA-126-5p inhibitor转染至HUVECs细胞,48 h后在培养基中加入33.3 mmol/L(终浓度)的葡萄糖,培养24 h.再利用miRNA-126-5p mimics组模型,分别予自噬抑制剂3-甲基腺嘌呤(3-methyl adenine,3-MA)5 mmol/L、ERK通路抑制剂(U-0126)10 mmol/L干预24 h.RT-qPCR检测细胞中miRNA-126-5p的表达水平,CCK-8检测细胞活性,划痕实验检测细胞迁移能力,Westernblot检测细胞培养液中血管内皮生长因子(VEGF)和肝细胞生长因子(HGF),p-ERK、ERK蛋白,p-AKT、AKT蛋白,Bax、Bcl-2蛋白,cleaved-caspase-3蛋白,Beclin-1和Lc3蛋白含量.结果 与正常组比较,HG模型细胞中miRNA-126水平,p-ERK/ERK蛋白水平低于正常对照组(P<0.05);与HG模型组相比较,miRNA-126-5p mimics组细胞中miRNA-126、p-ERK/ERK蛋白表达明显升高(P<0.01),细胞中Bax/Bcl-2蛋白,cleaved caspase-3蛋白表达下降(P<0.05),Beclin-1和Lc3蛋白的表达水平升高(P<0.01),细胞活性增强(P<0.01),细胞迁移率提高(P<0.01),VEGF水平升高(P<0.05);与miRNA-126-5p inhibitor组比较,miRNA-126-5p mimics组细胞中miRNA-126、pERK/ERK蛋白表达升高(P<0.01),细胞中Bax/Bcl-2蛋白,cleaved caspase-3蛋白表达下降(P<0.05),Beclin-1和Lc3蛋白表达水平升高(P<0.01),细胞活性增强(P<0.05),细胞迁移率提高(P<0.05),VEGF水平升高(P<0.01);在miRNA-126-5p mimics组中加入3-MA后凋亡蛋白表达明显下降(P<0.01),加入ERK抑制剂后,自噬蛋白表达明显下降(P<0.01).结论 miRNA-126可通过激活ERK信号通路促进细胞的自噬并抑制细胞凋亡,减轻HG诱导的内皮细胞损伤.

目的:研究重组人脑钠肽(rhBNP)对高糖环境下人脐静脉内皮细胞(HUVECs)的作用和机制.方法:利用高糖诱导HUVECs凋亡模型,给予rhBNP、rhBNP+自噬抑制剂3-甲基腺嘌呤(3-MA)或rhBNP+ERK通路抑制剂U0126干预,观察rhBNP对高糖诱导下HUVECs自噬、凋亡及其相关信号通路的影响.结果:体外高糖诱导HUVECs,细胞活力被抑制,细胞凋亡增加,自噬相关蛋白beclin-1表达水平和LC3-II/LC3-I比值均显著降低,ERK信号通路活性显著减弱(P<0.05或P<0.01).1 mg/L rhBNP干预后细胞活力和迁移能力显著增强(P<0.01),LC3-II/LC3-I比值提高(P<0.05),beclin-1表达增加(P<0.01),Bax/Bcl-2比值和cleaved caspase-3蛋白水平降低,ERK蛋白水平增加(P<0.05).加入ERK抑制剂后,beclin-1自噬蛋白表达减弱(P<0.05),提示rhBNP可能通过激活ERK信号通路促进自噬蛋白表达进而调节HUVECs的生物学活性.结论:高糖抑制ERK信号通路,自噬降低,凋亡增加;rhBNP通过激活ERK信号通路,促进自噬发生,减少细胞凋亡,保护细胞.

Autoimmune deficiency and destruction in either β-cell mass or function can cause insufficient insulin levels and, as a result, hyperglycemia and diabetes. Thus, promoting β-cell proliferation could be one approach toward diabetes intervention. In this report we describe the discovery of a potent and selective DYRK1A inhibitor GNF2133, which was identified through optimization of a 6-azaindole screening hit. In vitro, GNF2133 is able to proliferate both rodent and human β-cells. In vivo, GNF2133 demonstrated significant dose-dependent glucose disposal capacity and insulin secretion in response to glucose-potentiated arginine-induced insulin secretion (GPAIS) challenge in rat insulin promoter and diphtheria toxin A (RIP-DTA) mice. The work described here provides new avenues to disease altering therapeutic interventions in the treatment of type 1 diabetes (T1D).

Loss of beta-cell mass and function can lead to insufficient insulin levels and ultimately to hyperglycemia and diabetes mellitus. The mainstream treatment approach involves regulation of insulin levels; however, approaches intended to increase beta-cell mass are less developed. Promoting beta-cell proliferation with low-molecular-weight inhibitors of dual-specificity tyrosine-regulated kinase 1A (DYRK1A) offers the potential to treat diabetes with oral therapies by restoring beta-cell mass, insulin content and glycemic control. GNF4877, a potent dual inhibitor of DYRK1A and glycogen synthase kinase 3 beta (GSK3 beta) was previously reported to induce primary human beta-cell proliferationin vitroandin vivo. Herein, we describe the lead optimization that lead to the identification of GNF4877 from an aminopyrazine hit identified in a phenotypic high-throughput screening campaign measuring beta-cell proliferation.

Autophagy,a self-protecting response of eukaryotic cells,has important physiological functions.There is few research about autophagy during the course of diabetic vasculopathy and the protective effect of autophagy on vascular endothelial cell injury.It has been indicated that the basis of autophagy in endothelial cell is a survival mechanism in diabetes,while autophagy can protect cells from excessive stimulation,especially in the case of high glucose,hyperinsulinemia,hyperlipidemia,oxidative stress and inflammation.However,excessive autophagy can damage endothelial cells,leading to autophagic death of cells.Therefore,a comprehensive study of the characteristics and mechanisms of autophagy in endothelial cells under different conditions might provide novel strategies for the prevention and treatment of diabetes and its vascular complications.

To the Editor: Fish bone is a kind of common ingested foreign body. In most cases, it may pass through the gastrointestinal tract or retain upper digestive tract such as the oral cavity, esophagus.[1] However, ascending colon perforation by huge fish body is rare, which can cause several complications.[2] There are only few case of colon perforation by foreign body in the literature.[3] Here, we presented an unusual case due to the size of the fish bone, its location of the digestive tract, and successful diagnosis and treatment. In July 2016, a 60-year-old man was presented with complaints of persistent dull ache in the right upper quadrant without nausea and vomiting for a week. A history of eating fish food 10 days ago was present. On physical examination, the patient had tenderness localized to the right upper abdomen without rebound tenderness, and Rovsing's sign was questionable positive. Blood investigations showed hemoglobin was 112 g/L, and white blood cells count was 8.59 × 109/L. Cholecystitis, gastritis, and perforation of colon caused by foreign bodies were considered. Abdominal ultrasound was performed, which showed a 37-mm foreign body in the area of ascending colon without peritoneal effusion [Figure 1a]. A three-dimensional (3D) reconstruction abdominal computed tomography (CT) scan was performed, and a hyperdense linear object was seen in the abdominal cavity [Figure 1b]. Therefore, the patient was diagnosed as perforation of colon caused by foreign bodies.Figure 1: (a) The picture of abdominal ultrasound; (b) the picture of three-dimensional reconstruction computed tomography (the white arrow indicates the foreign body); (c) the picture of intraoperative colonoscopy examination (the white arrow indicates fistula into the ascending colon wall); (d) the fish bone after retrieval.There was no foreign body seen using intraoperative colonoscopy while an acutely inflamed ascending colon near hepatic region and a fistula with blood was observed [Figure 1c]. The decision of exploratory laparotomy was taken with diagnosis of ascending colon perforation. On exploration, a protruding foreign body was found through the perforation in the ascending colon [Figure 1d]. That was identified as a thin, curvilinear fish bone, approximately 37 mm in length and 2 mm in width. The surgery was successful, and the patient was discharged 5 days after the operation without any unexpected event. The ascending colon perforation by fish bone is extremely uncommon, with few cases reported.[4] The most common perforation site of the digestive tract is the esophagus because of its anatomical nature. Fish bones can not only cause pathology in the part of digestive tract but also involve adjacent organs. The clinical presentation may vary and can mimic a diverse entity of clinical conditions. In our case, the patient complained of pain in the abdomen that was similar to gastritis. Sometimes, difficulties arose in diagnosis from fish bone ingestion. There are three tools available to diagnose fish bone in the digestive tract. The 3D CT reconstruction is a feasible and effective method of detecting the fish bone. It also could directly show the relationships between the foreign body and surrounding tissues. Ultrasound may be a high sensitivity in detecting hyper-reflective foreign bodies. However, it is not always reliant due to some factors such as wrapped by tissues nearby and the operator's performance. The third one is plain abdominal radiograph. That is most often negative and considered as an ineffective at diagnosing fish bone ingestion. Early diagnosis and timely treatment is the key to a fair prognosis. If there is a lack of peritoneal irritation, intraoperative colonoscopy can be employed as assessing the location of the fish bone in the digestive tract and improving lesion localization. However, if the colon has been confirmed perforation, the decision of exploratory laparotomy needs to be considered. A reference reported delayed massive bleeding caused by an ingested fish bone. Costa et al. pointed out that codfish may cause acute abdomen.[5] In our study, the successful treatment was performed in our patient. Therefore, the operation timing for the removal of a fish bone should be tactically considered, and we should always keep in mind that delayed complications, such as the migration of the foreign body into an adjacent organ. Financial support and sponsorship This work was supported by the National Natural Science Foundation of China (No. 81500760), Zhejiang Provincial Natural Science Foundation of China (No. LQ15H120002), and the Science and Technology Projects of Shaoxing City (No. 2015B70041). Conflicts of interest There are no conflicts of interest.

Our research groups recently described a series of small‐molecule inducers of β‐cell proliferation that could be used to increase β‐cell mass. To mitigate the risk of nonspecific proliferation of other cell types, we devised a delivery strategy built on the tissue specificity observed in the experimental β‐cell imaging agent (+)‐dihydrotetrabenazine (DTBZ). The β‐cell proliferator agent aminopyrazine (AP) was covalently linked with (+)‐DTBZ to afford conjugates that retain both the proliferation activity and binding affinity for vesicular monoamine transporter‐2 (VMAT2). In vivo mouse tissue distribution studies of a prototypical AP–DTBZ conjugate showed 15‐fold pancreas exposure over plasma. Tissue‐to‐plasma ratios in liver and kidneys were two‐ and five‐fold, respectively. This work is the first demonstration of enhanced delivery of β‐cell‐proliferating molecules to the pancreas by leveraging the intrinsic tissue specificity of a β‐cell imaging agent.

Insufficient pancreatic β-cell mass or function results in diabetes mellitus. While significant progress has been made in regulating insulin secretion from β-cells in diabetic patients, no pharmacological agents have been described that increase β-cell replication in humans. Here we report aminopyrazine compounds that stimulate robust β-cell proliferation in adult primary islets, most likely as a result of combined inhibition of DYRK1A and GSK3B. Aminopyrazine-treated human islets retain functionality in vitro and after transplantation into diabetic mice. Oral dosing of these compounds in diabetic mice induces β-cell proliferation, increases β-cell mass and insulin content, and improves glycaemic control. Biochemical, genetic and cell biology data point to Dyrk1a as the key molecular target. This study supports the feasibility of treating diabetes with an oral therapy to restore β-cell mass, and highlights a tractable pathway for future drug discovery efforts.

The effects of brain natriuretic peptide (BNP) on the risk of cardiovascular disease and atherosclerosis have been studied. However, little information is available regarding peripheral arterial disease (PAD), particularly among subjects with type-2 diabetes mellitus (T2DM). The aim of our study was to assess the potential relationship between BNP levels and PAD among T2DM patients.

Background Diabetes mellitus is associated with many kinds of complications. Recent studies have shown that oxidative stress and inflammatory reactions have critical roles in the pathogenesis of diabetic gastroparesis. Curcumin is known to have antioxidant and anti-inflammatory properties. In the present study, we investigated the effect of curcumin on diabetic gastric motility in a Sprague Dawley rat model of type 1 diabetes mellitus. Methods Male SD rats were divided into a control group, a control group receiving curcumin, a diabetic group, and a diabetic group receiving curcumin. Diabetes was induced by intraperitoneal injection of streptozotocin. Curcumin (150 mg/kg) was given intragastrically for 6 weeks, and blood glucose levels and body weights were measured. Stomachs were excised for analysis of gastric emptying rates, and levels of oxidative stress. NF-κB, I-κB, and stem cell factor (SCF)/c-kit protein levels were assessed by western blot analysis, while the apoptosis of interstitial cells of Cajal (ICCs) was assessed by TUNEL staining. Results Curcumin-treated diabetic rats showed significantly improved gastric emptying rates [(59.4 ± 7.5)%] compared with diabetic rats [(44.3 ± 5.7)%], as well as decreased levels of MDA [21.4 ± 1.8 (nmol/mg) vs 27.9 ± 2.1 (nmol/mg)], and increased SOD activity [126.2 ± 8.8 (units/mg) vs 107.9 ± 7.5 (units/mg)]. On the other hand, the gastric emptying level in the control group was not significantly different from that in the control group receiving curcumin treatment. In addition, curcumin-treated diabetic rats showed significantly increased levels of SCF/c-kit protein in stomach tissues, inhibited I-κB degradation and NF-κB activation, and reduced ICC apoptosis index [(26.2 ± 4.1)% vs (47.5 ± 6.2)%], compared with the diabetic group. Conclusion Curcumin treatment improved gastric emptying by blocking the production of oxidative stress, abolishing NF-κB signal transduction and enhancing expression of SCF/c-kit in rats with diabetic gastroparesis.

Background Plasma galectin-3, a mediator of fibrogenesis and inflammation, its potential to associate with type 2 diabetes (T2DM) is poorly investigated. Here, we explored its interaction with the serum galectin-3 and vascular complications. Methods We conducted a population-based cross-sectional survey in Zhejiang, China involving 165 men and 119 women (age range, 43-84 years), investigating the relationship between serum galectin-3 and vascular disease in patients with T2DM. Results Serum galectin-3 was higher in subjects with T2DM than that in control participants (27.4 vs. 17.6 ng/ml, P <0.001). Compared with subjects with galectin-3 values in the lowest quartile, those with values in the highest quartile had an increased likelihood of vascular complications (4th quartile odds ratio ( OR ) 2.52, 95% confidence interval ( CI ), 1.25–4.07). Increased risk of micro- or macrovascular complications corrrelated with serum galectin-3 concentration ( ORs 11.4 and 8.5, respectively). An increased number of vascular complications was associated with high serum galectin-3 levels ( P <0.05). Patients with serum galectin-3 levels >25 ng/ml had an elevated risk of diabetes relative to patients with levels <10 ng/ml ( OR for any vascular complication 2.64, for heart failure 3.97, for nephropathy 4.09, for peripheral arterial disease (PAD) 4.18; all P <0.05). Complication risk was higher in patients with neurogenic, stroke, or retinopathy complications, but this difference was not significant after risk factor adjustment. Serum galectin-3 levels correlated with diabetes duration, C-reactive protein (CRP) levels, and albuminuria. Conclusion High galectin-3 values were associated with increased odds of developing heart failure, nephropathy, and peripheral arterial disease in patients with T2DM.

Background Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are thought to be associated with increased mortality in elderly patients. Low retinol-binding protein-4 (RBP4) is associated with a high risk of respiratory infections in the general population. Therefore, we hypothesized that low RBP4 levels are associated with an increased risk of AECOPD and can be used as a biomarker for AECOPD in elderly patients. Methods Enzyme-linked immunosorbent assays were used to assess RBP4 levels in elderly with AECOPD within the first 24 hours after intensive care unit admission. Forty-six elderly patients with stable COPD in outpatient clinics and 50 healthy elderly persons who had physical examinations as outpatients were controls. Results In AECOPD patients, RBP4 levels were lower than those in stable COPD patients and healthy controls (59.7 vs 91.2 and 113.6 mg/L, p < 0.001). RBP4 levels were decreased by 30.6% in non-survivors compared with survivors (51.5 vs 74.2 mg/L, p < 0.001). A higher Acute Physiology and Chronic Health Enquiry II (APACHE II) score and Simplified Acute Physiology score (SAPS II) were associated with lower RBP4 levels (r = −0.692, p = 0.024 and r = −0.670, p = 0.015, respectively). RBP4 was positively correlated with creatinine and body mass index, and negatively correlated with C-reactive protein and Global Initiative for Chronic Obstructive Lung Disease stage. Multivariate logistic regression showed that RBP4 was an independent mortality predictor of AECOPD (odds ratio: 0.926, p = 0.007). Analysis of the area under the receiver operating characteristic (AUC) curve showed that RBP4 showed good discrimination (AUC: 0.88; 95% confidence interval: 0.78–0.94; p = 0.008) in predicting mortality. RBP4 improved the prognostic accuracy of mortality for the APACHE II and SAPS II scores. Conclusions Serum RBP4 levels are significantly reduced in elderly AECOPD patients. RBP4 might be a good predictive biomarker for mortality in elderly AECOPD patients in the intensive care unit.

The identification of factors that promote β cell proliferation could ultimately move type 1 diabetes treatment away from insulin injection therapy and toward a cure. We have performed high-throughput, cell-based screens using rodent β cell lines to identify molecules that induce proliferation of β cells. Herein we report the discovery and characterization of WS6, a novel small molecule that promotes β cell proliferation in rodent and human primary islets. In the RIP-DTA mouse model of β cell ablation, WS6 normalized blood glucose and induced concomitant increases in β cell proliferation and β cell number. Affinity pulldown and kinase profiling studies implicate Erb3 binding protein-1 and the IκB kinase pathway in the mechanism of action of WS6.

Excessive caloric intake is a contributing risk factor for human metabolic disorders. Caloric restriction may prolong a person's life by lowering the incidence of deadly diseases. Reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMC) have been associated with the biochemical basis of the relationship between caloric intake and pathophysiologic processes. Polymorphisms associated with ROS generation genes are being increasingly implicated in inter-individual responses to daily caloric intake alterations. In the current study, a single nucleotide polymorphism, rs1836882, in the nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) gene's promoter region was found to modulate associations between dietary caloric intake and ROS levels in PBMC. Based on rs1836882, 656 Chinese Han participants were classified into CC, CT and TT genotypes. ROS levels in PBMC were significantly higher in the CC or CT genotypes compared with the TT genotype with the same increases in daily caloric intake. Using an electrophoretic mobility shift assay, NOX4 promoter region with rs1836882 (T) was observed to have a higher affinity for hepatocyte nuclear factor gamma (HNF3γ) protein than rs1836882 (C). HNF3γ protein over-expression decreased NOX4 gene transcriptional activity in the TT genotype more than in the CC genotype (5.68% vs. 2.12%, P<0.05) in a dual luciferase reporter assay. By silencing the NOX4 gene using small interfering RNA or over-expressing HNF3γ using an expression plasmid, serum from high dietary caloric intake participants decreased ROS levels in PBMC of the TT genotype more than in the CC or CT genotype via HNF3γ down-regulating the NOX4 gene expression signaling pathway. This is the first study to report on the functions of phenotypes of rs1836882 in the NOX4 gene, and it suggests rs1836882 as a candidate gene for interpreting inter-individual ROS levels differences in PBMC induced by alterations in daily caloric intake.

糖尿病足(diabetic foot,DF)是糖尿病病人常见的慢性并发症之一,据流行病学资料显示,糖尿病病人的DF患病率为4%～10%.目前认为糖尿病引起的氧化应激损伤是慢性并发症发生的共同通路和致病原因,抗氧化治疗糖尿病各种并发症的疗法也应运而生.α-硫辛酸(Alpha lipoic acid,ALA)作为一种强力的抗氧化剂,目前已用于糖尿病神经病变的治疗有显著疗效,但国内对DF方面的临床研究甚少.

AIM:To investigate the changes of oxidative stress in the stomach tissues and their roles in gastric motility and interstitial cells of Cajal(ICC) in diabetic rats.METHODS: Thirty-eight SD rats(8-week-old,male) were intraperitoneally injected with streptozotocin(STZ).Diabetes was successfully induced in 36 of them.The diabetes rats were randomly divided into untreated diabetes group and treated diabetes group.Eighteen healthy SD rats(8-week-old,male) served as controls.The body weight and the levels of blood glucose and glycosylated hemoglobin were measured.At the end of week 1 and week 10,9 rats were sacrificed in each group.The gastric emptying rate and the levels of malondialdehyde(MDA),superoxide dismutase(SOD),tumor necrosis factor α(TNF-α),tyrosine kinase receptor c-Kit and stem cell factor(SCF) in gastric smooth muscle were analyzed.The apoptosis of ICC in gastric tissues was detected by the methods of immunocytochemistry and TUNEL.RESULTS: Compared with control group,gastric motility and SOD activity in untreated diabetes group were significantly weakened,the levels of MDA and TNF-α increased,the levels of c-Kit and SCF decreased,and apoptosis of ICC enhanced.In treated diabetes group,the oxidative stress level was attenuated,antioxidant capacity was enhanced,the levels of c-Kit and SCF were significantly increased,and the ICC apoptosis was reduced.Gastric motility was significantly improved after antioxidant therapy.CONCLUSION: Hyperglycemia affects the expression of antioxidant enzymes in the stomachs of diabetic rats.Oxidative stress is caused by hyperglycemia and is an important factor in the etiology of gastric motility dysfunction in diabetic rats,which may be correlated with the augmentation of ICC apoptosis resulting from oxidative stress-induced c-Kit/SCF damage.

目的 观察血糖波动对在体大鼠胰岛β细胞凋亡的影响以及核因子(NF)-кB在其中的作用.方法 通过高脂饲料及注射小剂量链脲佐菌素(STZ)20mg/kg的方法制造糖尿病(DM)大鼠模型,小剂量高糖(25%的葡萄糖溶液10mg/g体重)每日3次腹腔注射制造持续高糖(SHG)组模型,在SHG组基础上高糖注射后0.5h皮下注射诺和锐1U/100g,造成每日血糖波动3次的血糖波动(IHG)大鼠模型.根据血糖、血糖波动分正常(N)组、DM组、SHG组、IHG组4组.实验14d结束并检测胰腺组织氧化应激指标丙二醛(MDA)、超氧化物歧化酶(SOD),酶标记免疫吸附测定(ELISA)方法检测炎症指标肿瘤坏死因子(TNF)-α、环氧酶(COX)-2以及凋亡基因Bax、Bcl-2,NF-кB等.原位末端转移酶标记技术(TUNEL)法观察胰岛细胞凋亡指数.结果 DM组、SHG组、IHG组较N组MDA 、TNF-α、COX-2、Bax含量升高,SOD、Bcl-2含量减少,NF-кB含量升高,胰岛细胞凋亡指数增多.与DM组比较,SHG组和IHG组MDA、Bax、NF-кB含量升高以及胰岛细胞凋亡指数升高.与SHG组比较,IHG组NF-кB含量最高、Bcl-2/Bax值最低,胰岛细胞凋亡指数最高.偏相关分析提示,Bcl-2/Bax与NF-κB之间具有相关性(r=-0.239,P＜0.05).结论 血糖波动明显增加β胰岛细胞凋亡,可能与血糖波动增加氧化应激、炎症反应,激活并放大了NF-кB活性,NF-кB通过调节炎症及下游凋亡基因而促进胰岛细胞凋亡.

Ninty-eight patients with newly diagnosed type 2 diabetes mellitus were divided into atherosclerosis(AS) group and non-AS group.Fasting plasma cystatin C level( CysC ) was determined.The results showed that there existed a significant correlation between CysC level and the number of carotid arteries plaque ( r =0.432,P＜0.01 ).CysC was an independent risk factor( OR =2.21,95％ CI 1.88-3.02 ) of carotid artery intimamedia thickening in patients with type 2 diabetes.

OBJECTIVE To explore the relationship between sleep quality and glucose level, diabetic complications in elderly type 2 diabetes mellitus. METHODS A total of 130 hospitalized elderly type 2 diabetes in our hospital were included in the study. Questionnaires and other related clinical data were collected within one week after admission. Patients were divided into two groups: poor-sleeper group and good-sleeper group according to Pittsburgh Sleep Quality Index (PSQI). RESULTS Sixty percent (78/130) of these patients were poor sleepers. The following parameters differed in the two groups: the duration of diabetes [(7.9 ± 1.8) years vs (7.2 ± 1.5) years, t = 2.318], systolic blood pressure [(148 ± 30) mm Hg (1 mm Hg = 0.133 kPa) vs (138 ± 23) mm Hg, t = 2.037], fasting plasma glucose (FPG) [(10.7 ± 2.2) mmol/L vs (9.8 ± 1.9) mmol/L, t = 2.410], hemoglobin A1c (HbA1c) [(8.6 ± 2.2)% vs (7.8 ± 2.1)%, t = 2.068], high-sensitive C-reactive protein (hs-CRP) [(5.27 ± 2.34) mg/L vs (4.44 ± 1.76) mg/L, t = 2.179], ratio of diabetic complications (61% vs 32%, χ(2) = 4.257), percentage of depression (20% vs 8%, χ(2) = 3.722), score of life quality [(98 ± 19) scores vs (89 ± 13) scores, t = 2.980], and proportion of patients treated with insulin (32% vs 12%, χ(2) = 4.489). All the above parameters were significantly higher in poor-sleeper group than the good-sleeper group (all P value < 0.05). Multiple correlation analysis showed that the factors affecting sleep quality were FPG, HbA1c, duration of diabetes, diabetic complications, depression, life quality and insulin application (r = 0.213, 0.257, 0.223, 0.335, 0.422, 0.3451, 0.231, respectively; all P value < 0.05). By multivariate logistic regression analysis, the followings were found: FPG (β = 1.29, P < 0.05) and PSQI (β = 1.07, P < 0.05) were found to be correlated with HbA1c. With increasing of PSQI, FPG, HbA1c, diabetic complications and life quality were changed significantly (all P value < 0.05). The independent risk factors of diabetic complications were duration of diabetes (OR = 1.32, 95%CI 1.01 - 2.01), HbA1c (OR = 2.01, 95%CI 1.63 - 2.67), hs-CRP (OR = 1.12, 95%CI 1.08 - 1.21) and PSQI (OR = 1.71, 95%CI 1.58 - 2.02). CONCLUSIONS Elderly type 2 diabetes mellitus are usually poor sleepers. Sleep quality probably affects blood glucose regulation, and is closely correlated with the occurrence of complications. In addition, poor sleep quality results in poor life quality.