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Procalcific phenotypic drift of circulating progenitor cells in type 2 diabetes with coronary artery disease. 2型糖尿病合并冠状动脉疾病患者循环祖细胞的钙原表型漂移
Pub Date : 2012-01-01 Epub Date: 2012-02-28 DOI: 10.1155/2012/921685
Gian Paolo Fadini, Mattia Albiero, Lisa Menegazzo, Elisa Boscaro, Carlo Agostini, Saula Vigili de Kreutzenberg, Marcello Rattazzi, Angelo Avogaro

Diabetes mellitus (DM) alters circulating progenitor cells relevant for the pathophysiology of coronary artery disease (CAD). While endothelial progenitor cells (EPCs) are reduced, there is no data on procalcific polarization of circulating progenitors, which may contribute to vascular calcification in these patients. In a cohort of 107 subjects with and without DM and CAD, we analyzed the pro-calcific versus endothelial differentiation status of circulating CD34+ progenitor cells. Endothelial commitment was determined by expression of VEGFR-2 (KDR) and pro-calcific polarization by expression of osteocalcin (OC) and bone alkaline phosphatase (BAP). We found that DM patients had significantly higher expression of OC and BAP on circulating CD34+ cells than control subjects, especially in the presence of CAD. In patients with DM and CAD, the ratio of OC/KDR, BAP/KDR, and OC+BAP/KDR was about 3-fold increased than in other groups. EPCs cultured from DM patients with CAD occasionally formed structures highly suggestive of calcified nodules, and the expression of osteogenic markers by EPCs from control subjects was significantly increased in response to the toll-like receptor agonist LPS. In conclusion, circulating progenitor cells of diabetic patients show a phenotypic drift toward a pro-calcific phenotype that may be driven by inflammatory signals.

糖尿病(DM)改变与冠状动脉疾病(CAD)病理生理相关的循环祖细胞。虽然内皮祖细胞(EPCs)减少,但没有关于循环祖细胞钙原极化的数据,这可能有助于这些患者的血管钙化。在107名患有和不患有糖尿病和冠心病的受试者中,我们分析了循环CD34+祖细胞的促钙化和内皮分化状态。内皮承诺是通过VEGFR-2 (KDR)的表达和骨钙素(OC)和骨碱性磷酸酶(BAP)的表达来决定的。我们发现,与对照组相比,DM患者循环CD34+细胞中OC和BAP的表达明显更高,尤其是在存在CAD的情况下。在DM和CAD患者中,OC/KDR、BAP/KDR和OC+BAP/KDR的比值比其他组增加了约3倍。从患有CAD的糖尿病患者培养的EPCs偶尔会形成高度提示钙化结节的结构,对照受试者的EPCs对toll样受体激动剂LPS的反应显著增加了成骨标志物的表达。总之,糖尿病患者的循环祖细胞表现出可能由炎症信号驱动的表型向前钙化表型漂移。
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引用次数: 45
Diabetes mellitus increased mortality rates more in gender-specific than in nongender-specific cancer patients: a retrospective study of 149,491 patients. 一项对149,491例患者的回顾性研究表明,糖尿病在性别特异性癌症患者中的死亡率高于非性别特异性癌症患者。
Pub Date : 2012-01-01 Epub Date: 2012-06-03 DOI: 10.1155/2012/701643
Wen-Ko Chiou, Jawl-Shan Hwang, Kuang-Hung Hsu, Jen-Der Lin

Aims: Hyperinsulinemia in overweight status, obesity, and type 2 diabetes mellitus (DM) is often accompanied by cancer. Gender is important in cancer epidemiology, clinical presentation, and response to therapy in different histological types of malignancy. Insufficient information is available concerning gender differences in DM with organ-specific and nonorgan-specific cancers. This study aimed to analyze gender differences in hospitalized cancer patients with or without type 2 DM.

Methods: We retrospectively reviewed ten years of patients hospitalized in one institution, enrolling 36,457 female and 50,004 male cancer patients of which 5,992 females and 8,345 males were diagnosed as type 2 DM.

Results: Statistically significant increases in incidence of type 2 DM were found in patients of both genders with pancreatic, liver, and urinary tract cancer. Increased incidence of type 2 DM was found in lung and hematologic malignancies in females and prostate cancer in males. Increases in mortality rates of females with type 2 DM (2.98%) were higher than those in males. DM increased mortality rates in gender-specific cancers from 1.91% (uterus, HR: 1.33) to 5.04% (ovary, HR: 1.49).

Conclusion: Type 2 DM increased mortality of cancer patients of both genders, with higher increases in gender-specific than in nongender-specific cancers.

目的:超重、肥胖和2型糖尿病(DM)患者的高胰岛素血症常伴有癌症。性别在不同组织学类型的恶性肿瘤的流行病学、临床表现和治疗反应中很重要。关于糖尿病伴器官特异性和非器官特异性癌症的性别差异的信息不足。本研究旨在分析伴有或不伴有2型糖尿病的住院癌症患者的性别差异。方法:我们回顾性分析了一家机构10年来住院的36,457名女性和50,004名男性癌症患者,其中诊断为2型糖尿病的女性为5,992名,男性为8,345名。结果:胰腺、肝脏和泌尿道癌患者的2型糖尿病发病率均有统计学意义的增加。女性肺部和血液恶性肿瘤以及男性前列腺癌中2型糖尿病的发病率增加。2型糖尿病女性的死亡率(2.98%)高于男性。糖尿病使性别特异性癌症的死亡率从1.91%(子宫癌,风险比1.33)增加到5.04%(卵巢癌,风险比1.49)。结论:2型糖尿病增加了男女癌症患者的死亡率,性别特异性癌症的死亡率高于非性别特异性癌症的死亡率。
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引用次数: 17
A comparison of inflammatory and oxidative stress markers in adipose tissue from weight-matched obese male and female mice. 体重匹配的肥胖雌雄小鼠脂肪组织中炎症和氧化应激标志物的比较。
Pub Date : 2012-01-01 Epub Date: 2012-06-14 DOI: 10.1155/2012/859395
Karen J Nickelson, Kelly L Stromsdorfer, R Taylor Pickering, Tzu-Wen Liu, Laura C Ortinau, Aileen F Keating, James W Perfield

Expansion of intra-abdominal adipose tissue and the accompanying inflammatory response has been put forward as a unifying link between obesity and the development of chronic diseases. However, an apparent sexual dimorphism exists between obesity and chronic disease risk due to differences in the distribution and abundance of adipose tissue. A range of experimental protocols have been employed to demonstrate the role of estrogen in regulating health benefits; however, most studies are confounded by significant differences in body weight and adiposity. Therefore, the purpose of this study was to compare weight-matched obese male and female mice to determine if the sex-dependent health benefits remain when body weight is similar. The development of obesity in female mice receiving a high-fat diet was delayed; however, subsequent comparisons of weight-matched obese mice revealed greater adiposity in obese female mice. Despite excess adiposity and enlarged adipocyte size, obese females remained more glucose tolerant than weight-matched male mice, and this benefit was associated with increased expression of adiponectin and reductions in immune cell infiltration and oxidative stress in adipose tissue. Therefore, the protective benefits of estrogen persist in the obese state and appear to improve the metabolic phenotype of adipose tissue and the individual.

腹腔内脂肪组织的扩张及其伴随的炎症反应被认为是肥胖与慢性疾病发展之间的统一联系。然而,由于脂肪组织分布和丰度的差异,肥胖和慢性疾病风险之间存在明显的性别二态性。已经采用了一系列实验方案来证明雌激素在调节健康益处中的作用;然而,大多数研究都被体重和肥胖的显著差异所混淆。因此,本研究的目的是比较体重匹配的肥胖雄性和雌性小鼠,以确定当体重相似时,性别依赖的健康益处是否仍然存在。在接受高脂肪饮食的雌性小鼠中,肥胖的发展被推迟;然而,随后对体重匹配的肥胖小鼠的比较显示,肥胖的雌性小鼠肥胖程度更高。尽管过度肥胖和脂肪细胞大小增大,肥胖的雌性小鼠仍然比体重匹配的雄性小鼠具有更高的葡萄糖耐受性,这种益处与脂联素表达增加、脂肪组织中免疫细胞浸润和氧化应激减少有关。因此,雌激素的保护作用在肥胖状态下持续存在,似乎可以改善脂肪组织和个体的代谢表型。
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引用次数: 56
Relation of adiponectin to glucose tolerance status, adiposity, and cardiovascular risk factor load. 脂联素与糖耐量状态、肥胖和心血管危险因子负荷的关系。
Pub Date : 2012-01-01 Epub Date: 2011-12-27 DOI: 10.1155/2012/250621
N Wolfson, D Gavish, Z Matas, M Boaz, M Shargorodsky

Objective: Adiponectin has anti-atherogenic and anti-inflammatory properties. We investigated the influence of adiponectin on glucose tolerance status, adiposity and cardiovascular risk factors (CVRFs).

Design and patients: Study consisted of 107 subjects: 55 with normal glucose tolerance (NGT) and 52 with impaired glucose regulation (IGR) who were divided into two groups: 24 subjects with impaired fasting glucose (IFG Group) and 28 patients with type 2 diabetes mellitus (DM Group). In additional analysis, study participants were divided into two groups, according to CVRFs: low and high risk.

Measurements: Patients were evaluated for glucose, HbA1C, insulin, lipids, CRP, HOMA-IR and adiponectin.

Results: Adiponectin was significantly higher in NGT group than in IFG (P = 0.003) and DM (P = 0.01) groups. Adiponectin was significantly, positively associated with HDL and inversely associated with glucose, HbA1c, ALT, AST, TG, HOMA-IR. Patients with higher CVRFs load have lesser adiponectin compared to patients with low cardiovascular risk P < 0.0001). Adiponectin was inversely associated with the number of risk factors (r = -0.430, P = 0.0001).

Conclusions: Circulating adiponectin was significantly lower in subjects with different degree of IGR compared to subjects with normal glucose homeostasis. Adiponectin was significantly lower in high risk group than low risk group and decreased concurrently with increased number of CVRFs.

目的:脂联素具有抗动脉粥样硬化和抗炎作用。我们研究了脂联素对糖耐量状态、肥胖和心血管危险因素(CVRFs)的影响。设计与患者:研究共纳入107例受试者,其中55例糖耐量正常(NGT), 52例糖调节功能受损(IGR),分为两组:24例空腹血糖受损(IFG组)和28例2型糖尿病(DM组)。在进一步的分析中,根据cvrf,研究参与者被分为两组:低风险和高风险。测量:评估患者的血糖、糖化血红蛋白、胰岛素、血脂、CRP、HOMA-IR和脂联素。结果:NGT组脂联素水平明显高于IFG组(P = 0.003)和DM组(P = 0.01)。脂联素与HDL呈显著正相关,与葡萄糖、HbA1c、ALT、AST、TG、HOMA-IR呈显著负相关。与心血管风险较低的患者相比,cvrf负荷较高的患者脂联素含量较低(P < 0.0001)。脂联素与危险因素数量呈负相关(r = -0.430, P = 0.0001)。结论:不同IGR程度的受试者循环脂联素明显低于正常血糖稳态的受试者。脂联素在高危组明显低于低危组,且随cvrf数的增加而降低。
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引用次数: 27
Acute hyperglycemia does not impair microvascular reactivity and endothelial function during hyperinsulinemic isoglycemic and hyperglycemic clamp in type 1 diabetic patients. 1型糖尿病患者急性高血糖不损害微血管反应性和内皮功能。
Pub Date : 2012-01-01 Epub Date: 2012-01-04 DOI: 10.1155/2012/851487
Eva Horová, Jiří Mazoch, Jiřina Hiigertová, Jan Kvasnička, Jan Skrha, Jan Soupal, Martin Prázný

Aims: The aim of this study was to evaluate the effect of acute glycemia increase on microvasculature and endothelium in Type 1 diabetes during hyperinsulinemic clamp.

Patients and methods: Sixteen patients (51 ± 7 yrs) without complications were examined during iso- and hyperglycemic clamp (glucose increase 5.5 mmol·L(-1)). Insulin, lipid parameters, cell adhesion molecules and fibrinogen were analyzed. Microvascular reactivity (MVR) was measured by laser Doppler flowmetry.

Results: Maximum perfusion and the velocity of perfusion increase during PORH were higher in hyperglycemia compared to baseline (47 ± 16 versus 40 ± 16 PU, P < 0.01, and 10.4 ± 16.5 versus 2.6 ± 1.5 PU·s(-1), P < 0.05, resp.). Time to the maximum perfusion during TH was shorter and velocity of perfusion increase during TH higher at hyperglycemia compared to isoglycemic phase (69 ± 15 versus 77 ± 16 s, P < 0.05, and 1.4 ± 0.8 versus 1.2 ± 0.7 PU·s(-1), P < 0.05, resp.). An inverse relationship was found between insulinemia and the time to maximum perfusion during PORH (r = -0.70, P = 0.007).

Conclusion: Acute glycemia did not impair microvascular reactivity in this clamp study in Type 1 diabetic patients. Our results suggest that insulin may play a significant role in the regulation of microvascular perfusion in patients with Type 1 diabetes through its vasodilation effect and can counteract the effect of acute glucose fluctuations.

目的:探讨高胰岛素钳夹术中急性血糖升高对1型糖尿病微血管和内皮的影响。患者与方法:16例患者(51±7岁)在等高血糖钳夹术中(血糖升高5.5 mmol·L(-1))检查无并发症。分析胰岛素、脂质参数、细胞粘附分子及纤维蛋白原。用激光多普勒血流仪测定微血管反应性(MVR)。结果:与基线相比,高血糖时PORH的最大灌注和灌注增加速度更高(47±16比40±16 PU, P < 0.01; 10.4±16.5比2.6±1.5 PU·s(-1), P < 0.05,均有统计学意义)。与等糖期相比,高血糖期TH至最大灌注时间更短,灌注速度更快(69±15 vs 77±16 s, P < 0.05, 1.4±0.8 vs 1.2±0.7 PU·s, P < 0.05,均为P < 0.05)。胰岛素血症与PORH期间达到最大灌注时间呈负相关(r = -0.70, P = 0.007)。结论:在钳形研究中,急性血糖没有损害1型糖尿病患者的微血管反应性。我们的研究结果表明胰岛素可能通过其血管扩张作用在1型糖尿病患者微血管灌注的调节中发挥重要作用,并可以抵消急性血糖波动的影响。
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引用次数: 3
Sex differences in the association between level of childhood interleukin-6 and insulin resistance in adolescence. 儿童白细胞介素-6水平与青春期胰岛素抵抗之间的性别差异。
Pub Date : 2012-01-01 Epub Date: 2012-01-05 DOI: 10.1155/2012/859186
Anna Bugge, Bianca El-Naaman, Robert G McMurray, Karsten Froberg, Claus Henrik Nielsen, Klaus Müller, Lars Bo Andersen

The purpose of this study was to determine whether levels of interleukin-6 (IL-6) in childhood are related to insulin resistance in adolescence. Further, to explore how fatness and cardiorespiratory fitness (VO(2peak)) moderate this relationship. Methods. 292 nine-year-old children (n = 292) were followed for 4 years. Anthropometrics and VO(2peak) were measured. Fasting blood samples were analyzed for IL-6, insulin, and glucose. Homeostasis model assessment (HOMA-IR) was used as a measure of insulin resistance. Results. For girls but not boys, levels of IL-6 at age 9 yrs correlated with HOMA-IR at age 13 yrs: r = 0.223, P = 0.008. Girls with IL-6 levels within the highest quartile at age 9 yrs had an odds ratio of 3.68 (CI = 1.58-8.57) being in the highest quartile of HOMA-IR four years later. Conclusion. In this cohort, IL-6 levels in childhood were related to insulin resistance in adolescence, but only for girls.

本研究的目的是确定儿童时期的白细胞介素-6 (IL-6)水平是否与青春期的胰岛素抵抗有关。进一步,探讨肥胖和心肺健康(VO(2peak))如何调节这种关系。方法:对292名9岁儿童(n = 292)进行为期4年的随访。测量人体测量和VO(2peak)。空腹血液样本分析IL-6、胰岛素和葡萄糖。体内平衡模型评估(HOMA-IR)被用来衡量胰岛素抵抗。结果。女孩9岁时IL-6水平与男孩13岁时HOMA-IR相关:r = 0.223, P = 0.008。在9岁时IL-6水平处于最高四分位数的女孩在4年后HOMA-IR处于最高四分位数的优势比为3.68 (CI = 1.58-8.57)。结论。在这个队列中,儿童时期的IL-6水平与青春期的胰岛素抵抗有关,但仅适用于女孩。
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引用次数: 7
Cardiovascular benefits of GLP-1-based herapies in patients with diabetes mellitus type 2: effects on endothelial and vascular dysfunction beyond glycemic control. 2型糖尿病患者glp -1治疗的心血管益处:对血糖控制以外的内皮和血管功能障碍的影响
Pub Date : 2012-01-01 Epub Date: 2012-04-17 DOI: 10.1155/2012/635472
Thomas Forst, Matthias M Weber, Andreas Pfützner

Type 2 diabetes mellitus (T2DM) is a progressive multisystemic disease accompanied by vascular dysfunction and a tremendous increase in cardiovascular mortality. Numerous adipose-tissue-derived factors and beta cell dysfunction contribute to the increased cardiovascular risk in patients with T2DM. Nowadays, numerous pharmacological interventions are available to lower blood glucose levels in patients with type 2 diabetes. Beside more or less comparable glucose lowering efficacy, some of them have shown limited or probably even unfavorable effects on the cardiovascular system and overall mortality. Recently, incretin-based therapies (GLP-1 receptor agonists and DPP-IV inhibitors) have been introduced in the treatment of T2DM. Beside the effects of GLP-1 on insulin secretion, glucagon secretion, and gastrointestinal motility, recent studies suggested a couple of direct cardiovascular effects of GLP-1-based therapies. The goal of this paper is to provide an overview about the current knowledge of direct GLP-1 effects on endothelial and vascular function and potential consequences on the cardiovascular outcome in patients with T2DM treated with GLP-1 receptor agonists or DPP-IV inhibitors.

2型糖尿病(T2DM)是一种进行性多系统疾病,伴有血管功能障碍,心血管疾病死亡率急剧增加。许多脂肪组织源性因素和β细胞功能障碍导致T2DM患者心血管风险增加。目前,许多药物干预可用于降低2型糖尿病患者的血糖水平。除了或多或少具有类似的降血糖效果外,其中一些药物对心血管系统和总体死亡率的影响有限,甚至可能是不利的。最近,以肠促胰岛素为基础的治疗(GLP-1受体激动剂和DPP-IV抑制剂)已被引入治疗T2DM。除了GLP-1对胰岛素分泌、胰高血糖素分泌和胃肠道运动的影响外,最近的研究表明,GLP-1为基础的治疗还有一些直接的心血管作用。本文的目的是概述目前GLP-1对内皮和血管功能的直接影响,以及GLP-1受体激动剂或DPP-IV抑制剂对T2DM患者心血管结局的潜在影响。
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引用次数: 38
Effects of glucagon-like peptide-1 receptor agonists on body weight: a meta-analysis. 胰高血糖素样肽-1受体激动剂对体重的影响:一项meta分析。
Pub Date : 2012-01-01 Epub Date: 2012-05-20 DOI: 10.1155/2012/672658
Matteo Monami, Ilaria Dicembrini, Niccolò Marchionni, Carlo M Rotella, Edoardo Mannucci

Glucagon-Like Peptide-1 receptor agonists (GLP-1RAs), approved as glucose-lowering drugs for the treatment of type 2 diabetes, have also been shown to reduce body weight. An extensive Medline, Cochrane database, and Embase search for "exenatide," "liraglutide," "albiglutide," "semaglutide," and "lixisenatide" was performed, collecting all randomized clinical trials on humans up to December 15, 2011, with a duration of at least 24 weeks, comparing GLP-1 receptor agonists with either placebo or active drugs. Twenty two (7,859 patients) and 7 (2,416 patients) trials with available results on body weight at 6 and 12 months, respectively, were included. When compared with placebo, GLP-1RAs determine a reduction of BMI at 6 months of -1.0 [-1.3; -0.6] kg/m(2). Considering the average BMI at baseline (32.4 kg/m(2)) these data means a weight reduction of about 3% at 6 months. This result could seem modest from a clinical standpoint; however, it could be affected by many factors contributing to an underestimation of the effect of GLP-1RA on body weight, such as non adequate doses, inclusion criteria, efficacy of GLP-1RA on reducing glycosuria, and association to non-pharmacological interventions not specifically aimed to weight reduction.

胰高血糖素样肽-1受体激动剂(GLP-1RAs)被批准为治疗2型糖尿病的降糖药物,也被证明可以减轻体重。广泛的Medline、Cochrane数据库和Embase搜索“艾塞那肽”、“利拉鲁肽”、“阿比鲁肽”、“semaglutide”和“利昔那肽”,收集截至2011年12月15日的所有人类随机临床试验,持续时间至少24周,将GLP-1受体激动剂与安慰剂或活性药物进行比较。纳入了22项(7859例患者)和7项(2416例患者)试验,分别获得了6个月和12个月体重的可用结果。与安慰剂相比,GLP-1RAs确定6个月时BMI降低-1.0 [-1.3;-0.6公斤/米(2)。考虑到基线时的平均BMI (32.4 kg/m(2)),这些数据意味着6个月时体重减轻了约3%。从临床的角度来看,这一结果似乎是适度的;然而,它可能受到许多因素的影响,导致GLP-1RA对体重的影响被低估,如剂量不足、纳入标准、GLP-1RA降低糖尿的功效,以及与非专门针对减肥的非药物干预的关联。
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引用次数: 97
Ca+2/calmodulin-dependent protein kinase mediates glucose toxicity-induced cardiomyocyte contractile dysfunction. Ca+2/钙调素依赖性蛋白激酶介导葡萄糖毒性诱导的心肌细胞收缩功能障碍。
Pub Date : 2012-01-01 Epub Date: 2012-06-18 DOI: 10.1155/2012/829758
Rong-Huai Zhang, Haitao Guo, Machender R Kandadi, Xiao-Ming Wang, Jun Ren

(1) Hyperglycemia leads to cytotoxicity in the heart. Although several theories are postulated for glucose toxicity-induced cardiomyocyte dysfunction, the precise mechanism still remains unclear. (2) This study was designed to evaluate the impact of elevated extracellular Ca(2+) on glucose toxicity-induced cardiac contractile and intracellular Ca(2+) anomalies as well as the mechanism(s) involved with a focus on Ca(2+)/calmodulin (CaM)-dependent kinase. Isolated adult rat cardiomyocytes were maintained in normal (NG, 5.5 mM) or high glucose (HG, 25.5 mM) media for 6-12 hours. Contractile indices were measured including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time-to-PS (TPS), and time-to-90% relengthening (TR(90)). (3) Cardiomyocytes maintained with HG displayed abnormal mechanical function including reduced PS, ±dL/dt, and prolonged TPS, TR(90) and intracellular Ca(2+) clearance. Expression of intracellular Ca(2+) regulatory proteins including SERCA2a, phospholamban and Na(+)-Ca(2+) exchanger were unaffected whereas SERCA activity was inhibited by HG. Interestingly, the HG-induced mechanical anomalies were abolished by elevated extracellular Ca(2+) (from 1.0 to 2.7 mM). Interestingly, the high extracellular Ca(2+)-induced beneficial effect against HG was abolished by the CaM kinase inhibitor KN93. (4) These data suggest that elevated extracellular Ca(2+) protects against glucose toxicity-induced cardiomyocyte contractile defects through a mechanism associated with CaM kinase.

(1)高血糖导致心脏细胞毒性。虽然有几种理论假设了葡萄糖毒性诱导的心肌细胞功能障碍,但其确切机制仍不清楚。(2)本研究旨在评估细胞外Ca(2+)升高对葡萄糖毒性诱导的心脏收缩和细胞内Ca(2+)异常的影响,以及与Ca(2+)/钙调蛋白(CaM)依赖性激酶相关的机制。分离的成年大鼠心肌细胞在正常(NG, 5.5 mM)或高糖(HG, 25.5 mM)培养基中维持6-12小时。测量收缩指标包括峰值缩短(PS)、最大缩短/再延长速度(±dL/dt)、至PS时间(TPS)和至90%再延长时间(TR(90))。(3) HG维持心肌细胞表现出异常的机械功能,包括PS、±dL/dt降低,TPS、TR(90)和细胞内Ca(2+)清除率延长。细胞内Ca(2+)调节蛋白(包括SERCA2a、磷蛋白和Na(+)-Ca(2+)交换器)的表达不受影响,而SERCA活性被HG抑制。有趣的是,HG诱导的机械异常被细胞外Ca(2+)升高(从1.0 mM增加到2.7 mM)所消除。有趣的是,高细胞外Ca(2+)诱导的抗HG的有益作用被CaM激酶抑制剂KN93所消除。(4)这些数据表明,升高的细胞外Ca(2+)通过与CaM激酶相关的机制保护葡萄糖毒性诱导的心肌细胞收缩缺陷。
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引用次数: 6
Prostate carcinogenesis with diabetes and androgen-deprivation-therapy-related diabetes: an update. 前列腺癌与糖尿病和雄激素剥夺治疗相关的糖尿病:最新进展。
Pub Date : 2012-01-01 Epub Date: 2012-06-26 DOI: 10.1155/2012/801610
Noboru Hara

Prostate cancer and the androgen deprivation therapy (ADT) thereof are involved in diabetes in terms of diabetes-associated carcinogenesis and ADT-related metabolic disorder, respectively. The aim of this study is to systematically review relevant literature. About 218,000 men are estimated to be newly diagnosed with prostate cancer every year in the United States. Approximately 10% of them are still found with metastasis, and in addition to them, about 30% of patients with nonmetastatic prostate cancer recently experience ADT. Population-based studies have shown that dissimilar to other malignancies, type 2 diabetes is associated with a lower incidence of prostate cancer, whereas recent large cohort studies have reported the association of diabetes with advanced high-grade prostate cancer. Although the reason for the lower prevalence of prostate cancer among diabetic men remains unknown, the lower serum testosterone and PSA levels in them can account for the increased risk of advanced disease at diagnosis. Meanwhile, insulin resistance already appears in 25-60% of the patients 3 months after the introduction of ADT, and long-term ADT leads to a higher incidence of diabetes (reported hazard ratio of 1.28-1.44). Although the possible relevance of cytokines such as Il-6 and TNF-α to ADT-related diabetes has been suggested, its mechanism is poorly understood.

前列腺癌及其雄激素剥夺治疗(ADT)分别在糖尿病相关癌变和ADT相关代谢紊乱方面涉及糖尿病。本研究的目的是系统地回顾相关文献。据估计,美国每年约有218,000名男性新诊断患有前列腺癌。其中约10%仍发现有转移,此外,约30%的非转移性前列腺癌患者最近经历了ADT。基于人群的研究表明,与其他恶性肿瘤不同,2型糖尿病与前列腺癌的发病率较低相关,而最近的大型队列研究报道了糖尿病与晚期高级别前列腺癌的关联。虽然糖尿病男性前列腺癌患病率较低的原因尚不清楚,但他们体内较低的血清睾酮和PSA水平可以解释诊断时晚期疾病风险增加的原因。同时,25-60%的患者在ADT应用3个月后已出现胰岛素抵抗,长期ADT导致糖尿病的发病率升高(报道危险比为1.28-1.44)。虽然已经提出细胞因子如Il-6和TNF-α与adt相关性糖尿病的可能相关性,但其机制尚不清楚。
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引用次数: 11
期刊
Experimental Diabetes Research
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