C反应蛋白与2型糖尿病及其血管并发症

2型糖尿病的主要病理生理改变为从以胰岛素抵抗(IR)为主伴胰岛素分泌不足到以胰岛素分泌不足为主伴胰岛素抵抗.目前研究认为IR是一种系统性慢性炎性反应,C反应蛋白(CRP)作为非特异性急性期反应蛋白,在IR各阶段普遍升高.升高的CRP又加重糖、脂代谢紊乱,加重内皮功能失调,促进动脉粥样硬化形成,从而促进2型糖尿病及其并发症的发生、发展.因此,研究CRP与2型糖尿病的关系有助于糖尿病并发症的预测及治疗.     

C反应蛋白与2型糖尿病及其血管并发症

2型糖尿病的主要病理生理改变为从以胰岛素抵抗(IR)为主伴胰岛素分泌不足到以胰岛素分泌不足为主伴胰岛素抵抗.目前研究认为IR是一种系统性慢性炎性反应,C反应蛋白(CRP)作为非特异性急性期反应蛋白,在IR各阶段普遍升高.升高的CRP又加重糖、脂代谢紊乱,加重内皮功能失调,促进动脉粥样硬化形成,从而促进2型糖尿病及其并发症的发生、发展.因此,研究CRP与2型糖尿病的关系有助于糖尿病并发症的预测及治疗.     

糖尿病伴径动脉粥祥硬化Hs-CRP水平及罗格列酮疗效探讨

目的:探讨超敏c反应蛋白(Hs-CRP)、颈动脉内膜中层厚度(IMT)、胰岛素抵抗指数(HOMA-IR)之间的关系及罗格列酮对H,CRP水平,颈动脉内膜中层厚度疗效.方法:将2型糖尿病患者分为2组:2型糖尿扁伴颈动脉硬化组、单纯2型糖尿病组,并测定超敏反应蛋白、颈动脉内膜中层厚度,血糖、胰岛素等.结果:2型糖尿病伴颈动脉硬化组的Hs-CRP明显高于单纯2型糖尿病组,对2型糖尿病患者进行线性相关分析表明2型糖尿病患者hg.CRP与胰岛素抵抗指数、糖化血红蛋白、颈动脉IMT都有极显著的相关性(P相似文献   

脐血干细胞经微创介入下胰腺血管插管移植治疗Ⅱ型糖尿病1例

Ⅱ型糖尿病多见于成年人,尤其是40岁以上的人群,常并发血管并发症(尤其是动脉粥样硬化性心、腩血管病),其占糖尿病群体的大多数(95%),主要病理生理改变为从以胰岛素抵抗为主伴胰岛素分泌不足到以胰岛素分泌不足为主伴胰岛素抵抗.我院开展了干细胞移植,治疗Ⅱ型糖尿病1例后已取得了良好的近期疗效.现结合患者情况进行文献讨论.     

2型糖尿病患者血清白细胞介素18、C反应蛋白水平与胰岛素抵抗相关

探讨2型糖尿病患者血清白细胞介素18(IL-18)、C反应蛋白(CRP)水平与胰岛素抵抗关系.2型糖尿病患者血IL-18和CRP升高,提示2型糖尿病为慢性炎症性疾病,且二者水平可反映胰岛素抵抗程度.     

老年2型糖尿病患者甘精胰岛素治疗的护理

2型糖尿病以胰岛素抵抗为主伴有胰岛素分泌不足,或以胰岛素分泌不足为主伴或不伴胰岛素抵抗,约占糖尿病患者的90％以上,病因为多基因遗传背景加之环境因素影响,多为中老年发病。2型糖尿病是一种慢性进展性疾病,可导致多种严重并发症。随着糖尿病病程的进展,很多老年2型糖尿病患者血糖控制不理想,需要应用胰岛素治疗。     

慢性炎症与2型糖尿病

2型糖尿病的发病机制主要是胰岛素抵抗（IR）和胰岛素分泌不足。但近年来的研究显示2型糖尿病是一种慢性炎症疾病，许多炎症因子，如TNF-α、IL-6、CRP、PAI-1不但直接参与胰岛素抵抗，而且与糖尿病大血管并发症的危险性联系紧密，在2型糖尿病的发生发展进程中起着重要作用。     

脂肪肝与糖尿病相关关系及临床对策

2型糖尿病(type 2 diabetes mellitus,T2DM)是从以胰岛素抵抗为主伴胰岛素进行性分泌不足,到以胰岛素进行性分泌不足为主伴胰岛素抵抗的以慢性高血糖为特征的代谢性疾病。非酒精性脂肪性肝病(non-alcoholic fatty liver idsease NAFLD)是指除外酒精和其他明确的肝损害因素所致的、与胰岛素抵抗和遗传易感密切相关的代谢应激性肝脏     

甘精胰岛素与格列美脲联合治疗口服降糖药控制不佳2型糖尿病的疗效

糖尿病由多种病因引起的以慢性高血糖为特征的代谢紊乱,伴有因胰岛素分泌绝对或作用缺陷引起的糖、脂肪和蛋白质代谢异常.病因与胰岛素抵抗和胰岛素分泌不足有关[1].2型糖尿病以胰岛素抵抗为主,伴胰岛素分泌或相对不足,目前,2型糖尿病多通过控制饮食、口服降糖药物、注射胰岛素等治疗[2,3].本研究主要探讨甘精胰岛素与格列美脲联合应用治疗口服降糖药控制不佳的2型糖尿病的临床效果.     

罗格列酮联合中药治疗肥胖性2型糖尿病临床观察

2型糖尿病是以胰岛素抵抗为主伴胰岛素分泌不足 ,或以胰岛素分泌不足为主伴胰岛素抵抗并导致高血糖为特征的疾病[1] 。在临床工作中常见的 2型糖尿病病人又多伴全身肥胖及(或 )体脂分布异常 ,后者中尤其为腹型肥胖。罗格列酮 (文迪雅 )由葛兰素史克投资有限公司提供 ,为新一代噻唑烷二酮类胰岛素增敏剂 ,国内外的大量研究均证实该药具有针对胰岛素抵抗、长期稳定血糖、减少大血管、微血管病变及延缓糖尿病进程的作用。笔者从 2 0 0 2年 2月至 2 0 0 3年 2月采用文迪雅联合中药治疗肥胖性 2型糖尿病 ,取得较好疗效 ,现总结报告如下。1　资料…     

Adiponectin and C-reactive protein in obesity, type 2 diabetes, and monodrug therapy

To learn more about the factors that regulate adipokines in diabetes, we examined fasting plasma concentrations of adiponectin and C-reactive protein (CRP) in well-characterized groups of age-matched individuals classified as: (1) type 2 diabetes; (2) impaired fasting glucose or mild diabetes (IFG/mild DM); (3) obese, matched for body mass index (BMI); and (4) non-obese. Diabetic subjects were also studied on no phamacologic treatment, after 3 months randomization to metformin or glyburide, and after 3 months crossover to the opposite drug. CRP decreased and adiponectin increased progressively between subjects in groups 1 through 4. CRP was significantly associated with percent (r = 0.45) and total (r = 0.50) fat, insulin sensitivity as S(I) (r = -0.39) or homeostasis model assessment of insulin resistance [HOMA (IR)] (r = -0.36), and hemoglobin A(1c) (HbA(1c)) (r = 0.41). The relationship of CRP to percent fat appeared to be logarithmic and log CRP varied with percent fat independent of gender. Adiponectin concentration was significantly associated with insulin sensitivity as S(I) (r = 0.55) or HOMA (IR) (r = -0.46). Adiponectin concentrations were higher among women overall (all groups included) but not in women classified as type 2 diabetes. Although mean adiponectin was higher in subjects classified as non-obese compared to obese, adiponectin, in sharp contrast to leptin (previously reported data) and to CRP, varied markedly when expressed as a function of adiposity. Multiple regression models confirmed the strong relationship of adiponectin to insulin sensitivity, as well as the relationships of CRP to adiposity and insulin sensitivity. Glyburide treatment of diabetes decreased CRP and did so even though body weight increased. We conclude that both CRP and adiponectin correlate strongly to S(I). CRP, in contrast to adiponectin, is far more dependent on adiposity. The relationship between CRP (like leptin) and gender depends on how CRP is expressed relative to adiposity. Our data raise the possibility that gender differences in adiponectin may be lost in diabetes. Finally, pharmacologic treatment of diabetes may modulate CRP independent of adiposity.     

白脂素与2型糖尿病及其血管并发症的研究进展

白脂素(asprosin)是一种新型葡萄糖调控蛋白激素,其主要由白色脂肪细胞合成分泌。Asprosin可通过增强胰岛素抵抗、调节胰岛素分泌、影响食欲参与糖脂代谢,从而调节血糖稳态。此外,研究发现Asprosin与糖尿病大血管并发症及糖尿病微血管并发症存在较多联系,但具体机制尚不清楚。深入探讨Asprosin与糖尿病及其...     

Toll样受体4与2型糖尿病及其并发症

介导先天免疫和炎性反应的Toll样受体(TLR)4参与了炎性反应性疾病的发病.炎性反应在2型糖尿病(T2DM)及其并发症的发生、发展中具有重要作用.TLR4信号通路的激活与胰岛素抵抗(IR)有关,而IR是T2DM及其大血管病变的重要病理生理基础,TLR4信号通路激活后炎性反应因子释放增加,与糖尿病微血管病变及神经病变密切相关.抑制TLR4信号通路的激活可能会防治T2DM及其并发症的发生、发展.     

Pre-diabetes,insulin resistance,inflammation and CVD risk

There is accumulating evidence that insulin resistance in the pre-diabetic state is associated with the presence of additional cardiovascular risk factors and increased incidence of cardiovascular disease (CVD). There is also accumulating evidence indicating that chronic sub-clinical inflammation as measured by such inflammatory markers as C-reactive protein (CRP) is associated with insulin resistance and other features of the insulin resistance syndrome, increased risk of development of type 2 diabetes and increased cardiovascular event risk. Insulin-sensitizing agents may have greater effects in reducing cardiovascular risk than secretagogues in the pre-diabetic state, and glitazones have been found to decrease CRP levels in patients with diabetes. Statins also reduce CRP levels. Efforts to reduce CVD should include increased emphasis on improving glycaemic control, preventing development of diabetes and addressing cardiovascular risk factors in the pre-diabetic state.     

Effects of rosiglitazone and aspirin on experimental model of induced type 2 diabetes in rats: focus on insulin resistance and inflammatory markers

Both insulin resistance and decreased insulin secretion are major features of the pathophysiology of type 2 diabetes. Inflammatory pathways are found to be critical in mechanisms underlying insulin resistance, which is a major determinant of increased risk of cardiovascular complications in type 2 diabetes, and so, it is a potential therapeutic target. Thiazolidinediones (e.g., rosiglitazone) act primarily as insulin sensitizers and were discovered to have anti-inflammatory effects leading to reevaluation of their potential use in treatment of diabetes. Acetyl salicylic acid (aspirin), which is currently recommended for cardiovascular disease (CVD) or even CVD risk factors, is shown to ameliorate diabetic process. This work aimed to study correlation between homeostasis model assessment estimate of insulin resistance (HOMA-IR) with serum levels of inflammatory markers tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), C-reactive protein (CRP), and free fatty acids (FFAs) in experimental model of induced type 2 diabetes in rats, with evaluation of effects of rosiglitazone and aspirin (low or high dose), alone or in combination. There is significant elevation of insulin resistance and serum levels of fasting glucose, insulin, TNF-α, IL-6, CRP, and FFAs in the diabetic group when compared to the normal group, with positive significant correlation between levels of each of TNF-α, IL-6, CRP, and FFAs with insulin resistance (HOMA-IR). Administration of rosiglitazone, low-dose aspirin, or high-dose aspirin to diabetic rats caused nonsignificant lowering in insulin level with significant reduction of levels of other parameters when compared to the diabetic group. Also, there is no significant difference in the measured parameters between diabetic rats administered a combination of rosiglitazone with high-dose aspirin and those administered a combination of rosiglitazone with low-dose aspirin. It was concluded that aspirin and rosiglitazone offer unique approaches for treatment of type 2 diabetes due to their insulin-sensitizing and anti-inflammatory properties, and their combination was found to provide augmented beneficial effects. Also, in view of the potential dose-dependent adverse effects of aspirin, with no achievement of further benefit by high dose in this study, it is strongly recommended to use low-dose aspirin as a safe and effective medication for diabetes.     

Presence of impaired insulin secretion and insulin resistance in normoglycemic male subjects with family history of type 2 diabetes

In order to demonstrate the effect of family history (FH) coexisting with obesity in insulin resistance (IR) and secretion in subjects at risk for type 2 diabetes, fasting and 2 h post-glucose load serum glucose and insulin concentrations were measured in 143 individuals, 66 men and 77 women, ages ranging from 18 to 68 years, who were considered at risk but were normoglycemic following ADA criteria. Insulin resistance was estimated using HOMA(IR), basal hyperinsulinemia and I(0)/G(0) ratio. Insulin secretion was estimated by means of HOMA(beta-cell), DeltaI(30-0)/DeltaG(30-0) ratio and the insulin concentration at 30 min post-glucose load (I(30)). Disposition index (DI) was calculated to verify if insulin secretion compensate IR. Obesity in males produced an increase in all the parameters indicative of IR in both groups of individuals, with (FH(+)) or without (FH(-)) family history of diabetes, increase that was more pronounced in those FH(-). This effect was not observed in women. The parameters indicative of insulin secretion showed that only in males the presence of FH(+) was responsible for a significant decrease in insulin secretion, mainly expressed as lower values of HOMA(beta-cell) in obese as well as in non-obese. The I(30) and the ratio DeltaI(30-0)/DeltaG(30-0), although lower, did not reach statistical significance. The DI showed that only when obesity and FH were associated the decrease in insulin secretion was not a compensatory response to the IR present in those individuals. In conclusion, normoglycemic obese and non-obese male subjects of Hispanic (Latinos) origin with a family history of type 2 diabetes present not only IR but impaired insulin secretion, having the obese FH(+) and additional risk like low DI.     

Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes

In both type 1 and type 2 diabetes, the late diabetic complications in nerve, vascular endothelium, and kidney arise from chronic elevations of glucose and possibly other metabolites including free fatty acids (FFA). Recent evidence suggests that common stress-activated signaling pathways such as nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases underlie the development of these late diabetic complications. In addition, in type 2 diabetes, there is evidence that the activation of these same stress pathways by glucose and possibly FFA leads to both insulin resistance and impaired insulin secretion. Thus, we propose a unifying hypothesis whereby hyperglycemia and FFA-induced activation of the nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases stress pathways, along with the activation of the advanced glycosylation end-products/receptor for advanced glycosylation end-products, protein kinase C, and sorbitol stress pathways, plays a key role in causing late complications in type 1 and type 2 diabetes, along with insulin resistance and impaired insulin secretion in type 2 diabetes. Studies with antioxidants such as vitamin E, alpha-lipoic acid, and N-acetylcysteine suggest that new strategies may become available to treat these conditions.     

Increased LDL cholesterol and CRP in infants of mothers with type 1 diabetes

BACKGROUND: Proatherogenic stimuli during foetal life may predispose to development of atherosclerosis in adulthood. Elevated plasma low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP) expression is associated with increased risk of atherosclerosis. METHODS AND RESULTS: In this study, we examined how maternal type 1 diabetes affects foetal plasma LDL cholesterol and CRP. In comparison with healthy mothers, the plasma LDL cholesterol was not increased in the mothers with diabetes, however, the umbilical-cord plasma LDL cholesterol was increased in their infants. CRP was increased in infants of mothers with diabetes and high haemoglobin A1c (HbA1c, >/= 6.2%). Human placenta expresses microsomal triglyceride transfer protein (MTP), which facilitates secretion of apolipoprotein B-containing lipoproteins. Microsomal triglyceride transfer activity was slightly higher (11%) in placentas from mothers with diabetes and HbA1c >/= 6.2% compared with the controls. CONCLUSION: The results suggest that maternal type 1 diabetes increases the foetal plasma LDL cholesterol and CRP concentration and thus might predispose the offspring to development of atherosclerosis. Copyright (c) 2008 John Wiley & Sons, Ltd.