肥胖糖友应用胰岛素更要讲究方式方法

肥胖患者该怎样选择药物治疗 从糖尿病发病机制上考虑 糖尿病的主要发病机制有胰岛功能减退和胰岛素抵抗.肥胖患者的胰岛素抵抗相对严重于消瘦患者.而能够改善胰岛素抵抗的经典降糖药物是噻唑烷二酮类和二甲双胍.     

2型糖尿病患者治疗前后内脂素与内皮素及胰岛素抵抗的关系

探讨2型糖尿病发病机制中内脂素与内皮素及胰岛素抵抗的关系.比较治疗前后内皮素、内脂素等指标.治疗后内脂素水平降低,内皮素与空腹胰岛素、稳态模型评估的胰岛素抵抗指数(HOMA-IR)、稳态模型评估的胰岛β细胞功能(HOMA-β)、内脂素正相关,内脂素与内皮素、HbA1c、空腹胰岛素、HOMA-IR正相关,HOMA-IR是血浆内脂素的独立相关因素.内脂素与内皮素、胰岛索抵抗有关,可能与2型糖尿病及胰岛素抵抗的发病机制密切相关.     

甘油三酯代谢异常与胰岛素抵抗关系的研究进展

高甘油三酯血症以及甘油三酯的异位沉积是引起胰岛素抵抗的危险因素,阐明甘油三酯代谢的调控因素是深入研究胰岛素抵抗相关疾病发病机制、寻找有效治疗方法的基础.     

甘油三酯代谢异常与胰岛素抵抗关系的研究进展

高甘油三酯血症以及甘油三酯的异位沉积是引起胰岛素抵抗的危险因素,阐明甘油三酯代谢的调控因素是深入研究胰岛素抵抗相关疾病发病机制、寻找有效治疗方法的基础.     

胰岛素受体底物及其在支气管哮喘发病机制中的作用

支气管哮喘(简称哮喘)是由多种因素引起的疾病,目前公认的发病机制是气道炎症假说.近来研究表明,胰岛素受体底物(insulin receptor substrate,IRS)在哮喘发病中也起很大作用,通过探索IRS如IRS-1、IRS-2和SHc(SHc是含有SH结构域的基因编码的蛋白产物),尤其是SHc在哮喘中的作用机制,将有望在哮喘治疗上提出新的治疗方向.     

胰岛素抵抗与高血压的关系

研究表明胰岛素抵抗与高血压密切相关,胰岛素抵抗是高血压的一个独立危险因子,二者存在理论上的因果关系.胰岛素抵抗在高血压的发病机制中起至关重要的作用,而高血压也可影响胰岛素的代谢,造成胰岛素抵抗,两者相辅相成,导致一系列严重慢性并发症的发生.同时,多种降压药物可通过影响糖代谢从而改善胰岛素抵抗,另一方面,部分改善胰岛素抵抗的药物可用于治疗原发性高血压.因此,了解胰岛素抵抗与高血 压之间的关系对于胰岛素抵抗及高血压的防治有重要意义.     

X综合征的研究现状及进展

X综合征即胰岛素抵抗综合征是近年提出的一个概念 ,认为胰岛素抵抗是糖耐量异常、肥胖、高血脂、高血压等一系列代谢异常的共同发病基础 ,而这些代谢异常与冠心病发病密切相关 ,本文对胰岛素抵抗的基本概念、发生机制、检测方法、流行病学研究和治疗等进行综述     

2型糖尿病合并肌少症的发病机制、药物治疗及健康管理研究进展

2型糖尿病(T2DM)是临床常见内分泌疾病,以血糖异常及胰岛素抵抗为主要特征;肌少症则是以骨骼肌质量及力量减少为特征的症候群.两者在发病机制上存在着共同点,临床也常合并出现.T2 DM合并肌少症的发病机制主要涉及骨骼肌代谢平衡紊乱、线粒体损伤、氧化应激及胰岛素抵抗.T2 DM合并肌少症的治疗方法是通过补充外源性胰岛素,...     

激素抵抗型哮喘中糖皮质激素受体β亚单位的表达

支气管哮喘的本质是气道慢性炎症 ,糖皮质激素是目前临床上治疗哮喘的首选药物。但部分哮喘患者对激素治疗不敏感 ,称为糖皮质激素抵抗型哮喘。近年来 ,大量证据表明激素抵抗型哮喘与糖皮质激素受体结构和功能的改变有关 ,尤其是受体 β亚单位的异常表达成为研究的热点。为进一步探讨激素抵抗型哮喘的发病机制 ,现将糖皮质激素受体 β亚单位的表达在激素抵抗型哮喘中的意义作一综述。     

非酒精性脂肪性肝病的胰岛素抵抗与丝氨酸磷酸化

胰岛素抵抗与非酒精性脂肪性肝病的发生发展关系密切,但其发病机制尚未完全明确,可能与胰岛素受体底物的丝氨酸磷酸化有关.通过对引起丝氨酸磷酸化因素的研究,可能有助于找到与胰岛素抵抗相关的治疗靶点.     

Asthma and insulin resistance in morbidly obese children and adolescents.

BACKGROUND: Obesity is well recognized as a state of increased insulin resistance and has been implicated as a significant risk factor for both asthma prevalence and asthma severity in children and adolescents. However, little is known about the specific factors that relate asthma and obesity. Recently, the pro-inflammatory state in obesity and its association with insulin resistance have been recognized. We hypothesize that the effect of morbid obesity on asthma is related to insulin resistance. METHODS: The patient cohort in the obesity management program at the Children's Hospital of Wisconsin was retrospectively reviewed. Variables were collected from the program data base and chart review was done for missing variables. Patients were considered to have asthma if the evaluating physician confirmed the diagnosis through history and/or the patient had been on inhaled corticosteroids. Insulin resistance (IR) was calculated using a homeostasis model assessment (HOMA). Multivariate logistic regression was performed to identify variables that were significantly related to the odds of having asthma. RESULTS: Of the 415 patients included in the study, 146 (35%) were asthmatic and 269 (65%) were non-asthmatic. The asthma (AG) and non-asthma (NAG) groups were similar with respect to mean age (11.3 vs. 11.5 years), gender (45% vs. 43% males), mean body mass index (BMI) (36.4 vs. 34.9), and exposure to smoking (43% vs. 42%). Fhx of asthma was significantly higher in AG (71%) compared to NAG (40%). IR level+/-SD was 8.5+/-9.7 in AG compared to 5.3+/-6.7 in NAG (p<0.0001). Multivariate regression analysis found the following variables to be associated with having asthma: younger age (p<0.05), smoking exposure (p<0.05), positive Fhx of asthma (p<0.0001, odds ratio of 3.1), and IR (p<0.0001, odds ratio of 4.1). CONCLUSION: Morbidly obese asthma patients have a higher degree of insulin resistance compared to morbidly obese non-asthma patients. We speculate that the pro-inflammatory state of insulin resistance may contribute to the pathogenesis of asthma in obese patients. Future prospective studies should address insulin resistance as a possible risk factor for asthma in obese children and adolescents.     

线粒体功能紊乱与胰岛素抵抗

胰岛素抵抗是2型糖尿病的重要发病机制,而骨骼肌线粒体功能紊乱与胰岛素抵抗密切相关,遗传、环境、衰老以及氧化应激可以导致线粒体功能紊乱.胰岛素抵抗者伴有线粒体功能下降,通过运动或减重等手段改善胰岛素敏感性的同时,线粒体功能也得以改善,其机制可能与线粒体功能异常通过抑制胰岛素受体底物-l活性、干扰胰岛素信号转导系统有关.     

Visfatin与胰岛素抵抗及非酒精性脂肪肝

Visfatin是新发现的一种脂肪细胞因子,能够影响糖和脂肪代谢.研究发现,血浆visfatin水平降低在胰岛素抵抗的形成过程中起重要作用;胰岛素抵抗者会出现血浆visfatin水平显著升高.非洒精性脂肪肝的主要发病机制是胰岛素抵抗,另外在疾病的不同病理阶段,随着病情轻重的不同visfatin的表达不同.因此,visfatin可能与非酒精性脂肪肝的发病有关.     

20-Hydroxyeicosatetraenoic acid is not associated with circulating insulin in lean to overweight humans

Hypertension is often associated with insulin resistance or hyperinsulinemia. Metabolism of arachidonic acid by cytochrome P450 to the vasoconstrictor 20-HETE is thought to be involved in the pathogenesis of hypertension, but the relationship of 20-HETE with insulin resistance is not clearly understood. Obesity is a major determinant of insulin resistance, and we have previously demonstrated a positive relationship between BMI and 20-HETE in untreated hypertensive and normotensive individuals. The present analysis sought to determine if this relationship was related to insulin levels or insulin resistance (HOMA). We analysed 24h urinary excretion of 20-HETE, serum insulin levels and insulin resistance in 66 lean to overweight untreated hypertensive and normotensive individuals. There was a significant positive association between 20-HETE and BMI (p<0.001), and serum insulin and BMI (p=0.003). There were no associations between 20-HETE excretion and either serum insulin or insulin resistance, before or after adjustment for age, gender, BMI and BP, or when hypertensive and normotensive individuals were considered separately. The results of the present study suggest that the observed positive association between urinary 20-HETE excretion and BMI may not be related to circulating insulin levels or insulin resistance.     

Relationship of nocturnal bronchoconstriction to sleep stages

The possible role of sleep stages in the pathogenesis of nocturnal asthmatic attacks is still under debate because previous studies suffered methodologic limitations that prevented the possibility of providing a clear-cut answer to the question. To evaluate the relationship of nocturnal asthma to sleep, eight asthmatics with unstable asthma (seven with history of nocturnal wheeze) and four reference subjects were submitted to all-night polysomnography, including the continuous evaluation of esophageal and supraglottic pressure (with two catheters) as well as of airflow (with a face mask), so as to derive total lung resistance, supraglottic resistance, and, by subtraction lower respiratory resistance (Rlr). Stage 3-4 was characterized by the highest peaks in Rlr and by longer episodes of bronchoconstriction; conversely, neither the onset nor the remission of the latter were specifically related to any sleep stage. Considering episodes remitted with an awakening. Stage 3-4 was marked by higher Rlr peaks than during REM sleep. We conclude that sleep plays a contributory role in the multifactorial pathogenesis of nocturnal asthma, with a higher susceptibility during slow-wave sleep, probably related to a decreased responsivity to resistive loads.     

RAS与胰岛素抵抗——代谢综合征新的治疗靶点

代谢综合征(M etS)是多种心血管危险因素的组合,以胰岛素抵抗、腹型肥胖、高三酰甘油(TG)血症、低高密度脂蛋白(HDL)胆固醇血症、高血压和空腹血糖受损为其临床特征[1]。尽管代谢综合征的发病机制尚不十分清楚,但胰岛素抵抗在其发生、发展中起关键作用的观点被学术界一致认可[1,2]。因此,M etS被认为是机体正常代谢与2型糖尿病的中间代谢状态。大量新近研究证据表明,肾素-血管紧张素系统(RAS)的激活与胰岛抵抗的发生间存在相互促进作用[1]。故对激活的RAS进行干预应成为代谢综合征的重要治疗靶点,进而改善胰岛素抵抗和降低心血管事件的发生。现就近年来有关RAS激活与胰岛素抵抗的发生机制、RAS被阻断后胰岛素抵抗的改善和临床上心血管事件减少的基础和临床证据及其意义综述如下。     

胰升血糖素与肝源性胰岛素抵抗

肝源性IR是T2DM重要发病基础之一,机制主要为受体缺陷及信号转导异常。作为对抗胰岛素的重要激素,胰升血糖素在糖尿病发病中起重要作用。与健康人群比,糖尿病患者或动物存在胰岛素异常分泌,也存在胰升血糖素异常高分泌。胰升血糖素在肝源性IR中的作用主要为抑制肝糖原合成及糖酵解,促进肝糖原分解、糖异生及脂肪分解。     

Hepatitis C,insulin resistance,and steatosis

Chronic hepatitis C (CHC) and nonalcoholic fatty liver disease (NAFLD) are two frequently identified liver diseases worldwide. NAFLD is related to obesity and insulin resistance, which may also be a preexisting condition in patients with CHC. The complex relationship among obesity, steatosis, and insulin resistance as it pertains to the pathogenesis, treatment, and outcomes in CHC is discussed in this article.     

Adipose tissue dysfunction and the pathogenesis of metabolic syndrome

Metabolic syndrome is a growing research area. The underlying mechanisms of metabolic syndrome are still not very clear. Insulin resistance, obesity, inflammation and oxidative stress may play an important role in the pathogenesis of metabolic syndrome. The role of adipose tissue dysfunction is emphasized during the development of obesity. Adipose tissue is identified as a complex endocrine organ and its metabolic functions extend well beyond the classical actions of thermoregulation and of storage and release of fatty acids. Chronic low-grade inflammation activated by the immune system in adipose tissue is a key contributing factor to type 2 diabetes mellitus and cardiovascular diseases. Visceral obesity results in cell autonomous impairment in insulin signaling that leads to insulin resistance. Chronic inflammation in adipose tissue has gained acceptance as a lead promoter of insulin resistance in obesity. Furthermore, obesity creates oxidative stress conditions in adipose tissue that not only correlates with insulin resistance but is also causative in its development. Oxidative stress may be a mechanistic link between several components of metabolic syndrome and cardiovascular diseases, through its role in inflammation and its ability to disrupt insulin-signaling. The study around adipose tissue dysfunction will help to understand the pathogenesis of metabolic syndrome and may bring effective therapy in treatment of metabolic syndrome related diseases. Therefore, this review mainly focuses on the roles of adipose tissue dysfunction in inflammation, insulin resistance, and oxidative stress in the pathogenesis of metabolic syndrome.