肥胖的风险与平板运动心电图诊断(综述)

通过文献资料法、实践观察法等研究方法研究了肥胖引起的合并症、肥胖患者在运动中存在的风险、以及肥胖的治疗和预防。研究结果发现,近年来肥胖的现象在全球越来越普遍,由于生活习惯等因素的改变,出现很大一部分超重或者肥胖的人群。这些人群可能出现冠心病、Ⅱ型糖尿病、胰岛素抵抗、高胰岛素血症、脂肪肝等各种合并症,并且在运动中存在潜在危险。平板运动心电图试验是诊断冠心病、评价心功能和运动耐力的简便有效的方法,通过试验可以诱发心律失常状况,或加重心血管疾病的某些症状,从而发现具有运动风险的人群,并对其运动负荷和持续时间提供指导。治疗和预防肥胖需要家庭、学校、工作场所、社区等多方面的支持。     

Calpain 10基因与新疆维吾尔族2型糖尿病遗传易感性研究

研究Calpain 10基因单核苷酸多态性（SNP）43G-A和63C-T两个位点与新疆地区维吾尔族人群2型糖尿病（Type 2 diabetes mellitus,T2DM）之间的关系。采用1∶1病例——对照研究方法,以聚合酶链式反应——限制性内切酶长度多态性（PCR-RFLP）技术,对120例T2DM患者和120例正常对照者Calpain 10基因SNP43、SNP63多态性位点进行基因分型。SNP43多态性位点的基因型和等位基因频率在病例组和正常对照组中的分布存在差异,T2DM组中GG基因型和等位基因频率均低于对照组,但是A等位基因频率高于对照组,差异有统计学意义（P〈0.005）;SNP63多态性位点的基因型频率和等位基因频率在病例组和正常对照组中的分布无显著差异,（P〉0.005）。结果表明：（1）Calpain 10基因SNP43多态性位点与新疆地区维吾尔族人群T2DM有明显相关性;（2）SNP63多态性位点与新疆地区维吾尔族人群T2DM无明显相关性。     

Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2

Adipocyte fatty-acid-binding protein, aP2 (FABP4) is expressed in adipocytes and macrophages, and integrates inflammatory and metabolic responses. Studies in aP2-deficient mice have shown that this lipid chaperone has a significant role in several aspects of metabolic syndrome, including type 2 diabetes and atherosclerosis. Here we demonstrate that an orally active small-molecule inhibitor of aP2 is an effective therapeutic agent against severe atherosclerosis and type 2 diabetes in mouse models. In macrophage and adipocyte cell lines with or without aP2, we also show the target specificity of this chemical intervention and its mechanisms of action on metabolic and inflammatory pathways. Our findings demonstrate that targeting aP2 with small-molecule inhibitors is possible and can lead to a new class of powerful therapeutic agents to prevent and treat metabolic diseases such as type 2 diabetes and atherosclerosis.     

消费者的时尚生活方式对于顾客忠诚度的影响

在不同的细分方法下,影响顾客忠诚度的要素及差异是最近市场营销领域研究的热点.本研究将讨论如何使用时尚生活方式对消费者细分以及时尚生活方式对于顾客忠诚度的影响.采用问卷调查法收集数据,对时尚生活方式量表的信度和效度进行检验,并进一步验证时尚生活方式的属性对于顾客忠诚度的影响.结果表明在全球市场中存在着跨国界的市场细分方法;消费者购买时尚产品时考虑的产品属性以及他们对于时尚产品的忠诚度均存在显著差异;时尚生活方式对于顾客的忠诚度有着显著的直接影响.     

Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes

In obesity and type 2 diabetes, expression of the GLUT4 glucose transporter is decreased selectively in adipocytes. Adipose-specific Glut4 (also known as Slc2a4) knockout (adipose-Glut4(-/-)) mice show insulin resistance secondarily in muscle and liver. Here we show, using DNA arrays, that expression of retinol binding protein-4 (RBP4) is elevated in adipose tissue of adipose-Glut4(-/-) mice. We show that serum RBP4 levels are elevated in insulin-resistant mice and humans with obesity and type 2 diabetes. RBP4 levels are normalized by rosiglitazone, an insulin-sensitizing drug. Transgenic overexpression of human RBP4 or injection of recombinant RBP4 in normal mice causes insulin resistance. Conversely, genetic deletion of Rbp4 enhances insulin sensitivity. Fenretinide, a synthetic retinoid that increases urinary excretion of RBP4, normalizes serum RBP4 levels and improves insulin resistance and glucose intolerance in mice with obesity induced by a high-fat diet. Increasing serum RBP4 induces hepatic expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) and impairs insulin signalling in muscle. Thus, RBP4 is an adipocyte-derived 'signal' that may contribute to the pathogenesis of type 2 diabetes. Lowering RBP4 could be a new strategy for treating type 2 diabetes.     

Insulin signalling and the regulation of glucose and lipid metabolism.

The epidemic of type 2 diabetes and impaired glucose tolerance is one of the main causes of morbidity and mortality worldwide. In both disorders, tissues such as muscle, fat and liver become less responsive or resistant to insulin. This state is also linked to other common health problems, such as obesity, polycystic ovarian disease, hyperlipidaemia, hypertension and atherosclerosis. The pathophysiology of insulin resistance involves a complex network of signalling pathways, activated by the insulin receptor, which regulates intermediary metabolism and its organization in cells. But recent studies have shown that numerous other hormones and signalling events attenuate insulin action, and are important in type 2 diabetes.     

运动对2型糖尿病胰岛素抵抗相关因子的影响研究

通过分析运动对2型糖尿病胰岛素抵抗的相关因子的影响,发现2型糖尿病主要是胰岛素抵抗和胰岛素分泌受损所导致.因此,只要了解胰腺β细胞的胰岛素抵抗程度,就可以加以弥补,使葡萄糖耐受性维持正常.     

高糖诱导ADTIQ的生成和多巴胺的代谢失衡

 2 型糖尿病患者比正常人更容易患帕金森病(PD),而新内源性神经毒素1-乙酰基-6, 7-二羟基-1, 2, 3,4-四氢异喹啉(ADTIQ)可能成为2 型糖尿病并发PD 的一个关键因素,ADTIQ 是由丙酮醛与多巴胺反应合成,但是其在多巴胺能神经元中的生成条件,以及在糖尿病情况下ADTIQ 的生成是否影响多巴胺代谢尚不清楚。本研究以SH-SY5Y 细胞为模型,研究ADTIQ 在细胞模型中的生成条件,发现ADTIQ 是在葡萄糖代谢旺盛的条件下,丙酮醛内源性产生与神经元内的多巴胺反应生成。研究揭示,高糖条件下,SH-SY5Y 细胞和2 型糖尿病的大鼠模型中外周多巴胺的质量浓度减少,而与多巴胺合成和转运相关的酪氨酸羟化酶和多巴胺转运体合成增加。可见,高糖能诱导SH-SY5Y 细胞内ADTIQ 的生成和多巴胺代谢的失衡,ADTIQ 的生成可能成为糖尿病并发PD 的关键因素。     

Diabetes mellitus and genetically programmed defects in beta-cell function.

The pathways that control insulin secretion and regulate pancreatic beta-cell mass are crucial in the development of diabetes mellitus. Maturity-onset diabetes of the young comprises a number of single-gene disorders affecting pancreatic beta-cell function, and the consequences of mutations in these genes are so serious that diabetes develops in childhood or adolescence. A genetic basis for the more common form of type 2 diabetes, which affects 10-20% of adults in many developed countries, is less clear cut. It is also characterized by abnormal beta-cell function, but other tissues are involved as well. However, in both forms identification of causative and susceptibility genes are providing new insight into the control of insulin action and secretion, as well as suggesting new treatments for diabetes.     

蛋白酪氨酸磷酸酶-1B抑制剂研究进展

 蛋白酪氨酸磷酸酶-1B(PTP-1B)在胰岛素信号转导中起负调节作用,是治疗2型糖尿病和肥胖症的一个新靶点。PTP-1B抑制剂可有效治疗2型糖尿病和肥胖症。本文综述了近年来PTP-1B抑制剂的研究进展,重点归纳了通过化学合成方法得到了多种PTP-1B抑制剂,如钒酸盐类化合物、磷酸酯类化合物、肽类化合物等。     

血管紧张素转换酶基因多态性与糖尿病的相关性研究

为了研究血管紧张素转换酶(ACE)基因的插入(I)/缺失(D)多态性是否与糖尿病(DM)的易感性相关,对108例糖尿病患者和196例正常人进行了ACE基因多态性分析.发现DM患者基因型DD基因型频率为22%,χ2=4.7,P>0.05(其中,Ⅰ型糖尿病患者相应频率为21%,χ2=4.9,P>0.05;Ⅱ型糖尿病患者为23%,χ2=2.1,P>0.05),而对照组DD基因型频率为16%;DM患者D等位基因频率为38%,χ2=0.0048,P>0.05(其中,Ⅰ型糖尿病患者相应频率为34%,χ2=0.62,P>0.05;Ⅱ型糖尿病患者为41%,χ2=0.25,P>0.05),而对照组相应频率分别为38%.糖尿病患者与对照组之间ACE基因I/D多态性频率存在差异,但不显著.这一结果表明ACE基因的多态性与糖尿病的易感性可能无关.     

54例2型糖尿病并高压病的临床分析

为弄清2型糖尿病并高血压病的临床特点,提高其防治水平,对54例2型糖尿病并高血压病的临床资料进行了回顾性分析。结果表明,2型糖尿病并高血压病可同时或相继发生,而且具备以下特点：嗜咽酒,高热量饮食,体力活动力,肥胖超重,血脂异常,年龄高;胰岛素抵抗综合征是2型糖尿病并高血压病共同的环境背景和发病机制,通过生活调节及药物干预,可防止病情的发展,降低死亡率。     

305例2型糖尿病维医异常体液分型的量化诊断入选项专家咨询研究

 为了建立2型糖尿病维医异常体液分型诊断标准,以非疾病诊断临床相关信息为依据,对诊断明确的305例2型糖尿病患者进行了量化诊断入选项专家咨询研究。入选的证候要素进行多分类Logistic回归分析、共线性诊断及主成分分析,使用主成分改进的多分类Logistic回归分析方法确立各证候要素对证候的贡献度,根据OR值区分2型糖尿病各异常体液主症、次症。研究结果显示,2型糖尿病异常黑胆质型主症为心神不宁,口干,舌苔为薄白苔,舌质紫暗,口味苦涩;次症为唇色青紫,舌体胖、短,小便青色。2型糖尿病异常血液质型主症为皮肤较热,脉象粗、有力,目光乏神,结膜稍红;次症为舌质色暗、舌苔光滑,面色发红,皮肤略粗。2型糖尿病异常黏液质型主症为唇色淡白,精神疲惫,口黏,舌苔白腻;次症为面色晄白,结膜发白,睡眠较多,脉象沉、缓。2型糖尿病异常胆液质型主症为心烦,脉象细,面色黄白,唇色淡不润,结膜发黄,皮肤较热;次症为面色无华,目光乏神,舌苔色黄,皮肤粗糙。经过对量化诊断入选项专家咨询所得到的临床信息的统计分析,认为研究结果与临床实际比较符合,可靠性高。由此得出结论：2型糖尿病维医异常体液分型诊断标准的建立为开展2型糖尿病维医临床疗效标准研究奠定了基础,同时此标准的建立也为方法学提供了参考。     

强化教育对新诊断的2型糖尿病患者糖代谢的影响

探讨结构化强化教育项目在新诊断的2型糖尿病门诊患者血糖控制中的作用。新诊断的2型糖尿病门诊患者74例随机分为强化教育组和对照组,对照组接受医院常规指导;教育组接受为期3天的强化教育项目,研究时间共12个月。经重复测量方差分析,两组患者教育前后空腹血糖（FBG）、糖化血红蛋白（GHbA1c）测量值差异有统计学意义（P〈0.05）;强化教育组在教育后6、12个月末各指标改善明显优于对照组（P〈0.05或P〈0.01）。结果表明,结构化糖尿病教育有助于新诊断的2型糖尿病门诊患者血糖的控制。     

2型糖尿病合并冠心病患者的血脂异常分析

目的探讨2型糖尿病合并冠心病与血脂异常的关系。方法收集常熟市中医院老年康复中心2004年3月至2005年10月住院病人中2型糖尿病合并冠心病患者共77例,从本中心健康体检者中选取35例作为正常对照组(Ⅲ组),测定血脂水平并进行比较。结果Ⅰ组糖尿病合并心肌梗死组血浆甘油三酯(TG)、血浆总胆固醇(TC)、载脂蛋白B(ApoB)、低密度脂蛋白(LDL)明显升高,高密度脂蛋白(HDL)、载脂蛋白A(ApoA)显著降低,与Ⅱ组无心肌梗死组相比,差异显著(P<0.01),与Ⅲ组正常对照组相比较血TG水平升高,HDL降低(P<0.01)。结论TG升高及HDL的降低是2型糖尿病合并冠心病等心血管疾病发生、发展的主要危险因素。     

beta-Cell death during progression to diabetes.

The hallmark of type 1 diabetes is specific destruction of pancreatic islet beta-cells. Apoptosis of beta-cells may be crucial at several points during disease progression, initiating leukocyte invasion of the islets and terminating the production of insulin in islet cells. beta-Cell apoptosis may also be involved in the occasional evolution of type 2 into type 1 diabetes.     

胰岛炎症导致的2型糖尿病发病过程的动力学模型及治疗策略

为了揭示胰岛炎症导致2型糖尿病发生发展的机制, 建立胰岛β细胞和巨噬细胞相互作用的数学模型, 包括IL-1β的产生和巨噬细胞的浸润过程, 研究高浓度葡萄糖和游离脂肪酸对IL-1β的共同作用, 揭示胰岛炎症在2型糖尿病进程中的动力学机理。通过对模型中动力学参数的敏感性分析, 提出针对不同患病情况的可能的优化治疗策略。     

2型糖尿病力量运动处方研究进展

和传统耐力运动处方相比,糖尿病患者的力量练习更有利于改善糖尿病人的糖代谢、脂代谢及相关并发症.目前,对2型糖尿病患者的运动处方一般采用有氧运动和力量练习结合的方式进行,被证明是安全有效的,对2型糖尿病力量运动处方相关研究进展进行了综述.     

Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity

A subset of neurons in the brain, known as 'glucose-excited' neurons, depolarize and increase their firing rate in response to increases in extracellular glucose. Similar to insulin secretion by pancreatic beta-cells, glucose excitation of neurons is driven by ATP-mediated closure of ATP-sensitive potassium (K(ATP)) channels. Although beta-cell-like glucose sensing in neurons is well established, its physiological relevance and contribution to disease states such as type 2 diabetes remain unknown. To address these issues, we disrupted glucose sensing in glucose-excited pro-opiomelanocortin (POMC) neurons via transgenic expression of a mutant Kir6.2 subunit (encoded by the Kcnj11 gene) that prevents ATP-mediated closure of K(ATP) channels. Here we show that this genetic manipulation impaired the whole-body response to a systemic glucose load, demonstrating a role for glucose sensing by POMC neurons in the overall physiological control of blood glucose. We also found that glucose sensing by POMC neurons became defective in obese mice on a high-fat diet, suggesting that loss of glucose sensing by neurons has a role in the development of type 2 diabetes. The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production. UCP2 negatively regulates glucose sensing in POMC neurons. We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing, and that acute pharmacological inhibition of UCP2 reverses loss of glucose sensing. We conclude that obesity-induced, UCP2-mediated loss of glucose sensing in glucose-excited neurons might have a pathogenic role in the development of type 2 diabetes.     

PI-3K转导通路在Ⅱ型糖尿病发病机制中作用的研究进展

胰岛素是通过胰岛素信号的转导通路来发挥其调节血糖并且促进其代谢合成的,其中磷脂酰肌醇-3激酶（PI-3K）在胰岛素信号转导中起关键性作用,而胰岛素信号转导通路障碍所引起的胰岛素抵抗在Ⅱ型糖尿病治疗中有着至关重要的作用．从胰岛素抵抗的发病机制、影响PI-3K的因素等几个方面综述了PI-3K在Ⅱ型糖尿病发病机制中的作用．