老年糖尿病人的病理生理特色

老年病人构成了2型糖尿病的主体,因此,明确老年糖尿病人的病理生理学特点对总体控制糖尿病至关重要.引起老年人糖尿病高发的因素:(1)与年龄相关的胰岛素分泌受损及胰岛素抵抗;(2)肥胖;(3)体力活动减少;(4)药物影响;(5)遗传因素;(6)伴发的其他疾病等.     

肝硬化患者糖代谢异常的临床观察

由于存在胰岛素抵抗 ,同时肝脏储备及合成糖原的能力受损 ,肝硬化病人普遍存在糖代谢异常。我们比较分析了肝硬化所致肝源性糖尿病患者、肝硬化合并原发性 2型糖尿病患者与单纯原发性 2型糖尿病患者的血糖、胰岛素、Ｃ肽水平及胰岛素敏感性 ,以指导临床治疗。对象与方法1.对象 :( 1)具有慢性病毒性肝病病史 ,否认长期饮酒史 ,具有肝功能失代偿的临床表现 ,同时影像学检查符合肝硬化 ;( 2 )ＯＧＴＴ检测 (糖耐量试验 ,口服葡萄糖粉 75 ｇ) ,结果提示糖尿病或糖耐量异常 ;( 3)慢性肝病病史 >糖耐量异常 (包括糖尿病 )病史至少 2年。将 47例患…     

糖尿病人血浆肿瘤坏死因子α变化及其相关因素研究

肿瘤坏死因子 (TNF-α)在 2型糖尿病的胰岛素抵抗 (IR)发生机理中的作用是近年来研究的热点问题之一。我们用EL ISA法测定了 1型和 2型糖尿病人外周血的 TNF- α水平 ,并分析其与作用相关因素的关系 ,旨在了解其对胰岛素抵抗成因的影响。一、对象与方法1 .研究对象 :全部研究对象均为我院糖尿病研究中心的健康体检者和住院病人。两型糖尿病人的诊断均符合美国糖尿病学会 1 997年标准 ,所有对象均排除感染、肿瘤、昏迷以及其他系统性疾病。2 .研究方法 :整个研究分两批完成。第一批选择正常对照组 1 2例 (男 6,女 6) ,平均年龄 46± 1 …     

关于召开第二次国际分子糖尿病学讨论会征文通知

研讨会主题 :肥胖、胰岛素抵抗与 2型糖尿病 :从分子到临床(1)体脂恒定调控网络 ;(2 )瘦素 :基础与临床 ;(3)ＰＰＡＲγ与脂肪细胞 ;(4 )肥胖突变 /易感基因 ;(5 )中国人肥胖的流行病学 ;(6 )全身及局部肥胖估测方法 ;(7)细胞内胰岛素信号传递系统 ;(8)胰岛素抵抗状态的评估 :临床与研究 ;(9)胰岛素受体基因突变与疾病 ;(10 )全身及局部体脂与糖尿病 ;(11)代谢综合征 :中国人之现状 ;(12 )噻唑烷二酮类药物 ;(13)二甲双胍作用机制新观点 ;(14)肥胖治疗的策略及其靶分子—小肠脂肪酶抑制剂、中枢单胺再摄取抑制剂。会议时间 :2 0 0 0年 9月 8…     

新诊断2型糖尿病患者的短期胰岛素强化治疗意义

研究背景:2型糖尿病的发生与胰岛素分泌不足及胰岛素抵抗密切相关。本文研究新诊断2型糖尿病患者接受初期的胰岛素强化治疗后,对患者长期血糖控制的影响。研究方法:该研究共入选16例新诊断2型糖尿病患者,其治疗前的基本资料包括:年龄(52±2)岁,体重指数(30.8±1.9)kg/m2,空腹血糖(13.3±0.7)mmol/L等。所有患者在接受2～3周的初期胰岛素强化治疗使血糖控制基本达标后停用胰岛素,依据血糖控制状况分别接受饮食、运动治疗(7例)、口服降糖药物(8例)或胰岛素治疗(1例),共随访1年。结果:全部患者在胰岛素强化治疗结束及随访1年后空腹血糖较治疗…     

2型糖尿病与结直肠肿瘤的关系

2型糖尿病可显著增加结直肠肿瘤风险,高胰岛素血症在此过程中起重要作用.胰岛素可增加胰岛素样生长因子-1(IGF-1)的活性,临床、血清学、动物模型、细胞培养等研究显示,IGF-1及胰岛素可促进结直肠肿瘤的发生.流行病学研究发现,糖尿病病程、血糖、糖化血红蛋白、外源性胰岛素及药物治疗、体重指数等均与结直肠肿瘤的风险有关.     

环氧合酶与消化系肿瘤相关性研究

在人体发现环氧和酶(cyclooxygenase,COX)至少存在3种异构体:COX-1、COX-2和COX-3。COX-2呈诱生性表达,在消化系肿瘤发生、发展、分化、转移、预后中起重要作用。现就COX-2与常见消化系肿瘤研究综述如下,为消化系肿瘤的诊治提供依据。     

可乐亭对用胰岛素治疗的糖尿病患者胆囊收缩和小肠转运时间的影响

作者对13例用胰岛素治疗的糖尿病患者8例健康者作比较研究,观察空腹口服可乐亭(0.3mg)对胆囊收缩功能和小肠转运时间的影响。糖尿病组均符合下列条件:(1)胰岛素治疗至少三年;(2)除胰岛素外不用其他药物;(3)超声检查无胆石症:(4)无胃排空延缓的症状和体征;(5)无上腹部手术史。健康组在性别、身高、体重方面与糖尿病组相似。糖尿病组无一例肥胖者。Ⅰ型糖尿病12例,Ⅱ型糖尿病1例,经胰岛素治疗病情控制良好。3例伴有周围神经病变,无自主神经病变。     

胰岛素抵抗激酶

随着人口老年化 ,2型糖尿病的发病率逐年上升。现已清楚 2型糖尿病 (T2 DM)的基本发病机制为胰岛素抵抗 (IR) ,胰岛素抵抗的病理机制包括 :(1)肌肉和脂肪对葡萄糖利用的障碍即对胰岛素的不敏感 [1 ] ;(2 )胰岛β细胞不能分泌足够的胰岛素以满足机体的需要 ,两者之间互为因果 [2 ] 。胰岛素不足或不敏感造成糖和脂质代谢障碍 ,脂质障碍又使上述循环加速。曾有人认为糖尿病是一种与免疫因素有关的炎症性疾病 ,因为在 2型糖尿病的循环中可见到与炎症有关的炎性介质如唾液酸 ,α- 1球蛋白 ,淀粉样多肽 ,C-反应蛋白 ,可的松和白介素 - 6 ,甚至…     

高血糖毒性作用的分子机制

糖尿病的主要危害在于其慢性并发症 ,可广泛累及心、脑、肾、眼、神经系统及皮肤等器官组织。无论是 1型还是 2型糖尿病 ,血管并发症的主要致病因素目前已公认为高血糖的糖毒性作用。对于 2型糖尿病 ,除糖毒性作用外高脂血症及高胰岛素血症也是血管并发症 ,尤其是动脉粥样硬化的协同致病因素 ,在此仅介绍高血糖对血管细胞的毒性作用。高血糖导致血管并发症的分子致病机制目前主要有四种假说 :(1)多元醇通路增多假说 ;(2 )ＤＡＧ ＰＡＣ活化假说 ;(3)非酶促蛋白糖基化假说 ;(4 )氧化还原势能失衡及氧化应激假说。其中多元醇通路增多假说最早…     

Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): similarities between TNF-alpha and interleukin 1.

The role of tumor necrosis factor alpha (TNF-alpha) in the pathogenesis of autoimmune diabetes mellitus was tested in the nonobese mouse (NOD) model system. The effects of TNF-alpha were assessed on three levels: (i) insulitis development, (ii) development of overt diabetes, (iii) adoptive transfer of diabetes by splenic lymphocytes. Spontaneous diabetes mellitus was blocked in NOD mice by long-term treatment with recombinant TNF-alpha. Treatment with TNF-alpha caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Class II major histocompatibility complex Ia expression by islet cells was not up-regulated by TNF-alpha. Moreover, TNF-alpha was able to suppress the induction of diabetes in adoptive transfer of lymphocytes from diabetic female mice to young nondiabetic male NOD mice. These activities of TNF-alpha were shared by interleukin 1 alpha in this system. These studies have implications for the pathogenesis and therapy of autoimmune diabetes mellitus.     

Impact of Diabetes Mellitus and Insulin on Nonalcoholic Fatty Liver Disease in the Morbidly Obese

Introduction and aim. The prevalence of obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease are increasing. Type 2 diabetes mellitus may aggravate non-alcoholic fatty liver disease, increasing the risk of developing cirrhosis and hepatocellular carcinoma. This study aims to determine the effect of type 2 diabetes mellitus and insulin therapy on non-alcoholic fatty liver disease in the patients with morbid obesity. Material and methods. Clinical, anthropometric and laboratory data were analyzed together with intraoperative liver biopsies from morbidly obese patients undergoing bariatric surgery. Results. 219 patients with morbid obesity were evaluated. Systemic arterial hypertension (55.9% vs. 33.8%, p = 0.004) and dyslipidemia (67.1% vs. 39.0%, p < 0.001) were more prevalent in patients with diabetes when compared to patients without diabetes. In multivariate analysis, type 2 diabetes mellitus was an independent risk factor for severe steatosis (RR = 2.04, p = 0.023) and severe fibrosis (RR = 4.57, p = 0.013). Insulin therapy was significantly associated with non-alcoholic steatohepatitis (RR = 1.89, p = 0.001) and fibrosis (RR = 1.75, p = 0.050) when all patients were analysed, but when only patients with diabetes were analysed, insulin therapy was not associated with non-alcoholic steatohepatitis or fibrosis. Conclusion. Type 2 diabetes mellitus plays an important role in the progression of non-alcoholic fatty liver disease as an independent risk factor for severe fibrosis.     

2型糖尿病患者结直肠癌的发生风险和潜在机制

流行病学研究发现,糖尿病与自身免疫性疾病、肿瘤等众多疾病的发生和发展有关,与非糖尿病人群相比,糖尿病人群患肿瘤等疾病的概率更大,症状更重,预后更差。结直肠癌(CRC)是消化系统中常见的恶性肿瘤,也是威胁我国居民生命健康及造成人民生活质量下降的主要癌症之一。近年来,糖尿病尤其是2型糖尿病(T2DM)与结直肠癌的关系受到越来越多的关注。其中受学者最为关注的一点是T2DM可作为CRC的独立影响因素,这可能与胰岛素抵抗、高血糖、炎症反应、外源性胰岛素等有关。本文对2型糖尿病患者结直肠癌的发生风险及潜在机制进行综述。     

海南86例2型糖尿病合并消化系统恶性肿瘤临床特点分析

目的探讨海南地区2型糖尿病合并消化系统恶性肿瘤患者临床特点,提高疾病预防与治疗的认识。方法回顾性收集海南医学院第一附属医院2015年1月—2019年6月期间2型糖尿病合并消化系统恶性肿瘤86例和单纯2型糖尿病100例患者的临床资料,分别作为病例组和对照组。结果①病例组中,男性73例,女性13例,男性发病率84.88%(73/86),女性发病率15.12%(13/86),男性肿瘤发病率明显高于女性。男性以肝癌高发占32.6%。②两组患者年龄、性别、糖尿病病程、舒张压、糖尿病家族史、TC、TG、LDL、HGB、HbA1c、WBC、RBC、NE、LYM水平差异有统计学意义(P<0.05)。两组患者吸烟、饮酒、高血压病史、收缩压、合并心脑血管疾病、BMI、FPG、HDL、PLT水平差异无统计学意义(P>0.05)。③多因素logistic分析显示:糖尿病家族史、NE与T2DM合并消化系统恶性肿瘤存在显著正相关关系,是T2DM合并消化系统恶性肿瘤的独立危险因素(OR=24.085,3.562,P<0.05)。结论2型糖尿病合并消化系统恶性肿瘤患者以男性为主,年龄在43~85岁之间,其中以肝癌高发,依次为结直肠癌、胃癌;糖尿病家族史、NE是T2DM合并恶性肿瘤的独立危险因素。     

Impact of diabetes mellitus on prognosis of patients infected with hepatitis C virus

Diabetes is a risk factor for the progression of liver fibrosis and development of hepatocellular carcinoma in chronic hepatitis C. However, the impact of diabetes on the long-term prognosis and the synergistic interactions of various host factors for diabetes to the progression of liver fibrosis are unknown. In the present study, we examined the host factors associated with the progression of hepatitis C in 68 patients with a posttransfusion hepatitis (PTH) and analyzed the relationships. Multivariate analysis showed that age of PTH, being male, and type 2 diabetes mellitus were risk factors for the progression of liver fibrosis. By the Kaplan-Meier method, the cirrhosis-free survival rates after the onset of PTH were significantly lower in the diabetic group than in the nondiabetic group (P < .01). Diabetes also had a great impact on the long-term prognosis of chronic hepatitis C by reducing the time from PTH to the occurrence of hepatocellular carcinoma (P < .01) and to liver-related death (P < .05). Coexistence of obesity (body mass index > or =25 kg/m(2)) or hypertriglyceridemia (> or =150 mg/dL) with diabetes had a synergistic effect on liver fibrosis progression in patients with chronic hepatitis C. Thus, the treatment of diabetes, obesity, and hypertriglyceridemia may hold the key to improving the prognosis of chronic hepatitis.     

Sex differences in survival after acute myocardial infarction in patients with diabetes mellitus (Worcester Heart Attack Study)

Background

Women with diabetes mellitus are at particularly high risk for coronary heart disease-related morbidity and mortality compared with men with diabetes mellitus. However, recent data comparing hospital and long-term outcomes in women with diabetes mellitus and men hospitalized with acute myocardial infarction (AMI) are scarce. The objectives of our multi-hospital observational study were to examine sex differences and temporal trends (1975-99) in hospital and long-term case-fatality rates (CFRs) in patients with diabetes mellitus and AMI from a population-based perspective.

Methods

A community-wide study of residents of the Worcester, Mass, metropolitan area who were hospitalized with confirmed AMI was conducted. Data were collected in 12 1-year periods between 1975 and 1999. The study sample consisted of 1354 men and 1280 women with diabetes mellitus.

Results

Overall hospital CFRs were significantly greater for women with diabetes mellitus (21.3%) than for men with diabetes mellitus (14.9%). Between 1975 and 1999, hospital CFRs declined from 39.2% to 17.5% for women and from 18.9% to 9.5% in men. In examining long-term survival patterns for as long as 10 years after hospital discharge, there were no significant sex differences in long-term survival rates after adjustment for a limited number of known potentially confounding factors.

Conclusions

Hospital death rates after AMI in men and women with diabetes mellitus have declined in the last 2 decades. The gap in hospital CFRs between men and women with diabetes mellitus has decreased considerably with time, although women have a higher risk of dying after AMI than men. Patients with diabetes mellitus continue to represent a high-risk group who will benefit from enhanced surveillance efforts and increased use of effective cardiac treatments.     

Clinical epidemiological analysis of the relationship between pancreatic cancer and diabetes mellitus: Data from a single institution in China

OBJECTIVE: To investigate the relationship between pancreatic cancer (PC) and diabetes mellitus. METHODS: All PC patients diagnosed and treated at Zhongshan hospital from January 1991 to December 2007 were retrospectively analyzed. During this period, 770 non‐digestive tract, non‐neoplastic and non‐hormone‐related patients matched for sex and age were collected as controls. The incidence of diabetes mellitus between the two groups was compared. RESULTS: Between the PC group and the control group, sex and age of the patients were well matched. The incidence of diabetes mellitus was 34.63% in the PC group and 8.83% in the control group (P < 0.001, RR = 5.19). In the PC group there was no correlation between age, sex, site of the cancer, tumor differentiation, lymph node metastasis, TNM staging and the incidence of diabetes mellitus. In this group with diabetes, 74.56% experienced onset within two years of cancer diagnosis. Of the control patients, 57.35% had had diabetes for under 2 years (P = 0.009, RR = 2.18). In the PC group with diabetes, 5.9% had had diabetes for more than 10 years while compared with 8.8% of the controls (P = 0.42). CONCLUSION: Whether diabetes mellitus is a result of or a risk factor for PC is still unclear. The incidence of diabetes mellitus is much higher in the PC patients. The onset of diabetes mellitus in adults might be an alerting factor that could lead to an early diagnosis of pancreatic cancer.     

十五省市1991—2005年住院糖尿病病人死因调查

目的通过大规模的全国性调查以明确糖尿病（DM）患者的死亡原因。方法选择全国31省市自治区首府各一家三级甲等医院,回顾性收集所有1991—2005年住院患者中伴有DM的死亡患者病历,根据ICD-10确定根本死因。结果共有15个省市2895个病例。T1DM患者根本死亡原因的前五位为DM、心血管疾病（CVD）、呼吸系统疾病（RSD）、消化系统疾病（DSD）和意外事故;T2DM根本死亡原因的前七位分别为CVD、脑血管疾病（BVD）、肿瘤、DM、RSD、DSD和意外事故。结论心脑血管疾病、肿瘤和DM为DM患者的主要死亡原因。     

Pathogenesis of diabetic nephropathy: the role of oxidative stress and protein kinase C

Hyperglycemia, a well recognized pathogenetic factor of long-term complications in diabetes mellitus, not only generates more reactive oxygen species but also attenuates antioxidative mechanisms through glycation of the scavenging enzymes. Therefore, oxidative stress has been considered to be a common pathogenetic factor of the diabetic complications including nephropathy. A causal relationship between oxidative stress and diabetic nephropathy has been established by observations that (1) lipid peroxides and 8-hydroxydeoxyguanosine, indices of oxidative tissue injury, were increased in the kidneys of diabetic rats with albuminuria; (2) high glucose directly increases oxidative stress in glomerular mesangial cells, a target cell of diabetic nephropathy; (3) oxidative stress induces mRNA expression of TGF-beta1 and fibronectin which are the genes implicated in diabetic glomerular injury, and (4) inhibition of oxidative stress ameliorates all the manifestations associated with diabetic nephropathy. Proposed mechanisms involved in oxidative stress associated with hyperglycemia are glucose autooxidation, the formation of advanced glycosylation end products, and metabolic stress resulting from hyperglycemia. Since the inhibition of protein kinase C (PKC) effectively blocks not only phorbol ester-induced but also high glucose- and H2O2-induced fibronectin production, the activation of PKC under diabetic conditions may also have a modulatory role in oxidative stress-induced renal injury in diabetes mellitus.     

Improvement in quality of diabetes control and concentrations of AGE-products in patients with type 1 and insulin-treated type 2 diabetes mellitus studied over a period of 10 years (JEVIN)

Advanced glycation end (AGE)-products, a complex and heterogeneous group of compounds, have been implicated in diabetes-related long-term complications. Up to the present, only few data exist about serum levels of the AGE-proteins N- epsilon -carboxymethyllysine (CML) and pentosidine in selection-free populations of patients with type 1 and insulin-treated type 2 diabetes mellitus. In the present 10-year, population-based trial of patients with insulin-treated diabetes mellitus, serum CML and pentosidine levels were examined in correlation to the patients' quality of diabetes control and the prevalence of diabetes-related long-term complications. Jena's St. Vincent Trial (JEVIN) was started in 1989/1990. At this time, a centralised diabetes care system existed. After the baseline examination of 190 patients (83% of the target population) with insulin-treated diabetes mellitus, follow-up examinations were performed in 1994/1995 and 1999/2000. In 1994/1995, the CML concentration in patients with type 1/type 2 diabetes mellitus was 1096.47+/-405.50/1136.43+/-405.24 ng/ml. In 1999/2000, it was significantly lower (727.49+/-342.91 ng/ml, P=.033/743.76+/-312.47 ng/ml, P<.0001). The same tendency showed the AGE-protein pentosidine (type 1: 1994/1995 203.18+/-118.88 vs. 1999/2000 156.59+/-104.84 pmol/ml [P=.029], type 2: 1994/1995 189.72+/-67.66 vs. 1999/2000 151.54+/-127.73 pmol/ml [P=.020]). Parallel to the decrease in the mean concentration of the AGE-products CML and pentosidine mean HbA1c improved and the prevalence of diabetic long-term complications (retino-, neuro-, and nephropathy) remained comparable 1999/2000-1989/1990. Comparing the data of 1999/2000 with those from 1994/1995, there was not only a substantial improvement in patients' quality of diabetes control but also a decrease in the concentration of AGE-products. In patients with diabetes mellitus, the AGE-products seem to be mainly influenced by the quality of diabetes control. However, the most important parameter reflecting the risk for development and progression of diabetes-related long-term complications seems not to be the AGE-products, but patients' HbA1c.