胰岛素抵抗患者的血脂代谢紊乱

目的探讨胰岛素抵抗患者的血脂代谢紊乱.方法空腹及口服葡萄糖后1小时、2小时、3小时分别抽静脉血,测定血糖、胰岛素、C肽、血脂.结果胰岛素抵抗患者的血脂代谢有明显紊乱,以总胆固醇、甘油三脂增高最多见为特征.结论胰岛素抵抗患者有明显血脂代谢紊乱,此对早期预防及诊断动脉粥样硬化、2型糖尿病可能存在重要价值.     

胰岛素抵抗患者的血脂代谢紊乱

目的　探讨胰岛素抵抗患者的血脂代谢紊乱 .方法　空腹及口服葡萄糖后 1小时、2小时、3小时分别抽静脉血 ,测定血糖、胰岛素、C肽、血脂 .结果　胰岛素抵抗患者的血脂代谢有明显紊乱 ,以总胆固醇、甘油三脂增高最多见为特征 .结论　胰岛素抵抗患者有明显血脂代谢紊乱 ,此对早期预防及诊断动脉粥样硬化、2型糖尿病可能存在重要价值 .     

胰岛素在某些心血管病中的作用

组织细胞对胰岛素的反应缺陷一胰岛素抵抗，促使胰岛代偿世分泌增多，导致高胰岛素血症，随之引起代谢紊乱和某些心血管疾病。治疗时如不考虑胰岛素的敏感性，则有可能加重代谢紊乱、高血压和动脉粥样硬化等。     

糖调节受损合并高胰岛素血症患者的胰岛功能评估及其影响因素分析

目的 评价糖调节受损合并高胰岛素血症患者的胰岛功能,分析其影响因素.方法 选取北京地区中老年男性共计547例,行75g口服葡萄糖耐量(OGTF)试验,根据美国糖尿病协会(ADA) 2003年标准分为三组:空腹血糖受损(IFG)325例、糖耐量减低(IGT)126例和空腹血糖受损合并糖耐量减低(IFG/IGT) 96例;各组根据胰岛素测定结果再分为高胰岛素血症组(HINS)以及非高胰岛素血症组(非HINS),对比各组间的代谢特征、胰岛素抵抗和胰岛β细胞分泌功能,评估合并代谢综合征相关疾病的差异.结果 ①高胰岛素血症患者IFG组和IFG/IGT组的胰岛素抵抗指数(HOMA-IR)分别是IGT组的1.42倍和1.41倍(P＜0.05);非HINS人群胰岛素抵抗情况与之类似:②高胰岛素血症患者胰岛分泌功能IFG/IGT组受损最为严重,其HOMAβ细胞功能指数(HBCI)分别是IGT和IFG组的74.04％和80.98％ (P ＜0.05);经HOMA-IR校正后,与IGT组的显著性差异更加明显,而与IFG组的差异消失;③三组糖调节受损-高胰岛素血症组合并代谢异常疾病的构成比均较相应非HINS组明显升高;IFG/ IGT组合并肥胖、高血压和高脂血症的构成比最高.结论 ①高胰岛素合并IFG主要的病理机制为肝脏的胰岛素抵抗;②高胰岛素血症合并IGT基础状态的胰岛分泌功能优于合并IFG者;③高胰岛素血症更易合并多种代谢紊乱,尤其是IFG/IGT患者,需要综合干预.     

糖耐量减低患者内皮功能、C反应蛋白、胰岛素抵抗水平分析

目的探讨糖耐量减低患者胰岛素抵抗指数、血浆内皮素、一氧化氮、C反应蛋白水平变化。方法口服75g葡萄糖耐量试验筛查出糖耐量减低患者192例和糖耐量正常的体检健康者18例,测定两组人群血浆内皮素、一氧化氮、C反应蛋白水平及胰岛素抵抗指数(HOMA-IR)和胰岛素敏感指数(IAI)。结果糖耐量减低组血浆内皮素、C反应蛋白升高,一氧化氮下降,HOMA-IR升高,IAI下降,与糖耐量正常组比较,差异有统计学意义（P＜0．01）。结论在糖耐量减低阶段已存在血管内皮功能紊乱,轻度炎症进程和胰岛素抵抗。     

妊娠高血压疾病与胰岛素抵抗的关系及其远期影响

妊娠期高胰岛素血症可通过抑制前列腺素的合成增加血管外周阻力使血压增高,通过脂代谢紊乱导致内皮细胞紊乱,从而引起妊娠高血压疾病一系列临床表现及产后心血管疾病发病风险的增加。     

胰岛素作用与糖尿病视网膜病变患者的治疗原则

临床实践证明,对有胰岛素抵抗的NIDDM患者,用胰岛素控制血糖只有暂时和表面现象,并不能纠正机体的代谢紊乱,相反可能会因长期胰岛素积蓄导致代谢紊乱.     

胰岛素抵抗标志物在动脉粥样硬化发病中的研究进展

胰岛素抵抗(IR)是连接代谢紊乱和动脉粥样硬化(AS)的关键枢纽。它在AS的启动和进展中发挥重要作用,其潜在机制涉及复杂的病理生理过程,包括内皮损伤、炎性反应激活及氧化应激。IR标志物显示了代谢风险和AS之间存在的潜在关联,检测IR标志物有利于心血管疾病的管理。     

高血压病胰岛素抵抗与内皮依赖性血管舒张功能的关系

目的 :探讨高血压病胰岛素抵抗与内皮依赖性血管舒张功能的关系。方法 :测定 42例高血压病病人血糖、胰岛素 ,以评价胰岛素敏感性。观测了毛细血管压、毛细血管密度、输入枝口径及NO等生化 ,并做相关分析。结果 :高血压病病人空腹胰岛素及血糖、胰岛素曲线下面积增加 ,比例缩小 (P <0 .0 5～ 0 .0 1) ,即胰岛素抵抗 ;毛细血管压升高 (P <0 .0 1) ;毛细血管密度、口径变小 (P <0 .0 5～ 0 .0 1) ;NO降低、ET/NO升高 (P <0 .0 5 ) ;伴胰岛素抵抗者NO、PGI2 降低 ,ET、TXB2 、TXB2 /PGI2 、ET/NO显著升高 (P <0 .0 5～ 0 .0 1)。且NO与毛细血管压呈负相关 ,与毛细血管密度、口径、胰岛素敏感性呈正相关 (P <0 .0 5 )。结论 :高血压病人存在高胰岛素血症、胰岛素抵抗 ,与内皮功能紊乱、微循环障碍 ,尤其是EDRF/NO功能减退致微动脉痉挛收缩、毛细血管闭塞减少有关。     

妊娠高血压疾病胰岛素抵抗与凝血功能异常的关系

目的：研究妊娠高血压疾病（PIH）胰岛素抵抗（IR）与凝血功能异常的关系。方法以38例妊高症患者为研究对象,并以同期正常孕妇32例为对照组。检测各组空腹血糖（FBG）、胰岛素（FINS）、凝血酶原时间（PT）、活化部分凝血活酶时间（APTT）及纤维蛋白原（Fbg）的含量,用HOMA指数做胰岛素抵抗指标。结果妊娠期高血压疾病组与正常妊娠组相比,其HOMA指数、Fbg含量显著升高,PT、APTT水平显著降低。HOMA指数与凝血功能各指标间具有显著相关性。结论妊高症患者存在胰岛素抵抗与凝血功能异常,并且两者具有相关性。     

TRIB3参与血管动脉粥样硬化机制的探讨

正常内皮细胞功能的障碍首先表现为细胞信号蛋白表达的改变或缺陷,引起相应细胞的生物学功能降低,从而加速相关疾病的发生与进展.TRIB3是肥胖、糖尿病和动脉粥样硬化等代谢性疾病的关键枢纽蛋白,通过胰岛素抵抗、内质网应激、脂质代谢等一系列途径,加速血管动脉粥样硬化的形成与进展.因此,本文旨在探讨TRIB3如何调控机体中血脂水平、血糖代谢、血管活性,加速血管动脉粥样硬化形成的机制所在.     

Chronic complications of polycystic ovary syndrome. Review

In addition to neuroendocrine abnormalities, women with polycystic ovary syndrome have insulin resistance and beta-cell dysfunction associated with a high frequency of metabolic syndrome components, such as glucose intolerance, type 2 diabetes mellitus (DM-2), dyslipidemia and a higher risk for endothelial dysfunction, haemostatic abnormalities, hypertension and cardiovascular disease. Obesity, a common finding in this disorder, plays an important role in the development of metabolic and cardiovascular disorders. Early identification of patients and prompt initiation of insulin sensitizing therapy by pharmacological agents or changes in life style such diet and exercise might improve the metabolic and endocrine abnormalities and reduce the risk of DM-2 and cardiovascular disease in these patients.     

Inhibition of postprandial hyperglycemia by acarbose is a promising therapeutic strategy for the treatment of patients with the metabolic syndrome

The metabolic syndrome is strongly associated with insulin resistance and has been recognized as a cluster of risk factors for cardiovascular diseases such as visceral obesity, hypertension, diabetes, and atherogenic dyslipidemia. Recently, insulin resistance in the absence of overt diabetes or the metabolic syndrome itself has been associated with endothelial dysfunction, one of the initial steps in the process of atherosclerosis. Postprandial hyperglycemia, one of the characteristic features of insulin resistance, induces oxidative stress generation and elicits vascular inflammation and platelet activation, thus being involved in the pathogenesis of atherosclerosis. A recent multicenter, placebo-controlled randomized trial, STOP-NIDDM trial, revealed that acarbose (Glucobay R), an alpha-glucosidase inhibitor, improved postprandial hyperglycemia and subsequently reduced the risk of development of type 2 diabetes in patients with impaired glucose tolerance (IGT). In this study, acarbose treatment was also found to slow the progression of intima-media thickness of the carotid arteries, a surrogate marker for atherosclerosis, and to reduce the incidence of cardiovascular diseases and newly diagnosed hypertension in subjects with IGT. Acarbose significantly reduced body mass index and waist circumference in these patients over 3 years. Furthermore, a meta-analysis of seven long-term studies has also shown that intervention with acarbose prevents myocardial infarction and cardiovascular diseases in type 2 diabetic patients. In this analysis, glycemic control, triglyceride levels, body weight and systolic blood pressure was also significantly improved during acarbose treatment. These observations suggest that prevention of postprandial hyperglycemia by acarbose may be a promising therapeutic strategy for reducing the increased risk for diabetes, hypertension, dyslipidemia, obesity, and cardiovascular diseases in patients with the metabolic syndrome. Acarbose improves postprandial hyperglycemia by delaying the release of glucose from complex carbohydrates in the absence of an increase in insulin secretion. Therefore, we would like to hypothesize here that this improvement in glucose metabolism could be associated with amelioration in insulin sensitivity, thus explaining the above-mentioned beneficial cardiometabolic actions of acarbose. Large clinical trials will provide us with more definite information whether acarbose treatment can improve insulin sensitivity and resultantly reduce the risk of diabetes, hypertension and cardiovascular diseases in patients with the metabolic syndrome.     

Asthma Phenotype with Metabolic Dysfunction

Asthma is chronic eosinophilic bronchitis with the dominancy of T helper 2 (Th2) inflammation. However, patients with asthma and metabolic dysfunction have pathogenic and pathological differences from those with Th2 inflammation. Metabolic dysfunction, typically presented as metabolic syndrome, has several important clinical components including central obesity, insulin resistance or glucose intolerance, dyslipidemia, and vitamin D deficiency. Data from large epidemiological studies support the significance of these components in the control of asthma and their contribution to airway remodeling, suggesting the presence of an asthma phenotype with metabolic dysfunction. These components are quite interactive with each other, so it is difficult to reveal the individual role of each. It is well known that asthma is difficult to treat in patients with obesity, due in part to inadequate response to inhaled corticosteroids. Additionally, vitamin D deficiency and insulin resistance have been regarded as aggravating factors of asthma control and airway remodeling. Recent clinical and in vivo studies have revealed the specific mechanisms of these components, which may aggravate asthma control and airway remodeling. In this review article, I summarize the recent studies and unmet needs for patients with asthma and metabolic dysfunction.     

代谢综合征和胰岛素抵抗的认识进展

代谢综合征是一组复杂的代谢紊乱症候群,是导致糖尿病、心脑血管疾病的危险因素,胰岛素抵抗在其发病机制中可能起重要作用。至今对它认识争议颇多,本文就MS的定义、发病机制和治疗以及对IR认识方面的进展作简要介绍。     

Oxygenation of adipose tissue: A human perspective

Obesity is a complex disorder of excessive adiposity, and is associated with adverse health effects such as cardiometabolic complications, which are to a large extent attributable to dysfunctional white adipose tissue. Adipose tissue dysfunction is characterized by adipocyte hypertrophy, impaired adipokine secretion, a chronic low‐grade inflammatory status, hormonal resistance and altered metabolic responses, together contributing to insulin resistance and related chronic diseases. Adipose tissue hypoxia, defined as a relative oxygen deficit, in obesity has been proposed as a potential contributor to adipose tissue dysfunction, but studies in humans have yielded conflicting results. Here, we will review the role of adipose tissue oxygenation in the pathophysiology of obesity‐related complications, with a specific focus on human studies. We will provide an overview of the determinants of adipose tissue oxygenation, as well as the role of adipose tissue oxygenation in glucose homeostasis, lipid metabolism and inflammation. Finally, we will discuss the putative effects of physiological and experimental hypoxia on adipose tissue biology and whole‐body metabolism in humans. We conclude that several lines of evidence suggest that alteration of adipose tissue oxygenation may impact metabolic homeostasis, thereby providing a novel strategy to combat chronic metabolic diseases in obese humans.     

Mitochondrial biogenesis in the metabolic syndrome and cardiovascular disease

The metabolic syndrome is a constellation of metabolic disorders including obesity, hypertension, and insulin resistance, components which are risk factors for the development of diabetes, hypertension, cardiovascular, and renal disease. Pathophysiological abnormalities that contribute to the development of the metabolic syndrome include impaired mitochondrial oxidative phosphorylation and mitochondrial biogenesis, dampened insulin metabolic signaling, endothelial dysfunction, and associated myocardial functional abnormalities. Recent evidence suggests that impaired myocardial mitochondrial biogenesis, fatty acid metabolism, and antioxidant defense mechanisms lead to diminished cardiac substrate flexibility, decreased cardiac energetic efficiency, and diastolic dysfunction. In addition, enhanced activation of the renin–angiotensin–aldosterone system and associated increases in oxidative stress can lead to mitochondrial apoptosis and degradation, altered bioenergetics, and accumulation of lipids in the heart. In addition to impairments in metabolic signaling and oxidative stress, genetic and environmental factors, aging, and hyperglycemia all contribute to reduced mitochondrial biogenesis and mitochondrial dysfunction. These mitochondrial abnormalities can predispose a metabolic cardiomyopathy characterized by diastolic dysfunction. Mitochondrial dysfunction and resulting lipid accumulation in skeletal muscle, liver, and pancreas also impede insulin metabolic signaling and glucose metabolism, ultimately leading to a further increase in mitochondrial dysfunction. Interventions to improve mitochondrial function have been shown to correct insulin metabolic signaling and other metabolic and cardiovascular abnormalities. This review explores mechanisms of mitochondrial dysfunction with a focus on impaired oxidative phosphorylation and mitochondrial biogenesis in the pathophysiology of metabolic heart disease.     

Obesity, blood vessels and metabolic syndrome

Obesity is rising worldwide at an alarming rate and so is the incidence of obesity-related disorders, such as the metabolic syndrome, type 2 diabetes and cardiovascular diseases. The obesity-dependent vascular damage appears to be derived from a variety of changes in the adipose tissue, leading to a chronic inflammatory state and dysregulation of adipocyte-derived factors. This, in turn, impairs vascular homeostasis by determining an unbalance between the protective effect of the nitric oxide pathway and the unfavourable action of the endothelin-1 system. In addition, hyperinsulinemia and insulin resistance contribute to vascular dysfunction because the opposing endothelium-dependent vasodilating and vasoconstrictor effects of insulin are shifted towards a predominant vasoconstriction in patients with obesity. Importantly, emerging evidence suggests that the vascular dysfunction of obesity is not only limited to the endothelium but also involves the other layers of the vessel wall. In particular, obesity-related changes in vascular smooth muscle seem to disrupt the physiological facilitatory action of insulin on the responsiveness to vasodilator stimuli, whereas the adventitia and the perivascular fat appear to be a source of proinflammatory and vasoactive factors that may contribute to endothelial and smooth muscle cell dysfunction and to the pathogenesis of vascular disease.     

Obesity, insulin resistance and cancer risk

Obesity is a known cause of metabolic syndrome which includes Type II diabetes, hypertension, and dyslipidemia. It is well documented that insulin resistance contributes to the mortality and the incidence of metabolic syndromes including central obesity, dyslipidemia, hyperglycemia and hypertension. Both obesity and diabetes are emerging topics for researchers to consider as having a possible causal association with cancer since the two factors have been viewed as risk factors for cancer. The present paper introduced the hypothesis of a possible causal relationship between obesity, insulin resistance and cancer and reviews relevant existing studies in this area. More efforts and studies are needed to clarify the mechanisms and the common risk factors which might be incorporated into interventions to prevent cancer and cardiovascular diseases as top causes of death.     

Acarbose is a promising therapeutic strategy for the treatment of patients with nonalcoholic steatohepatitis (NASH)

The metabolic syndrome is strongly associated with insulin resistance and has been recognized as a cluster of risk factors for cardiovascular diseases such as visceral obesity, hypertension, and diabetes. There is a growing body of evidence to show that nonalcoholic steatohepatitis (NASH) is the hepatic manifestation of insulin resistant patients with the metabolic syndrome. Indeed, insulin resistance increases adipocyte lipolysis and subsequently elevates circulating free fatty acids, thus stimulating the accumulation of fatty acids in the liver (hepatic steatosis). Fatty acids elicit reactive oxygen species generation, thereby promoting disease progression to NASH by both lipid peroxidation and inflammatory cytokine production. Postprandial hyperglycemia, one of the characteristic features of insulin resistance, also induces oxidative stress generation, being involved in dysfunction of pancreatic beta cells and vascular wall cells in the metabolic syndrome. Recently, STOP-NIDDM trial revealed that acarbose (Glucobay), an alpha-glucosidase inhibitor, improved postprandial hyperglycemia and subsequently reduced the risk of development of type 2 diabetes and newly diagnosed hypertension in patients with impaired glucose tolerance. In this study, acarbose treatment was also found to reduce body mass index and waist circumference in these patients. Furthermore, a meta-analysis of seven long-term studies has also shown that intervention with acarbose improved triglyceride levels, body weight and systolic blood pressure and subsequently prevented myocardial infarction in type 2 diabetic patients. Since acarbose improves postprandial hyperglycemia by delaying the release of glucose from complex carbohydrates in the absence of an increase in insulin secretion, the beneficial aspects of acarbose could be ascribed to improvement of insulin sensitivity in these patients. Given the pathological link between NASH and insulin resistance, we would like to hypothesize here that acarbose may become a promising therapeutic strategy for the treatment of patients with NASH. Does acarbose treatment improve steatohepatitis histologically? Is the extent of histological improvement by acarbose parallel to that of insulin sensitivity in these patients? Large clinical trials will provide us with more definite information whether acarbose treatment can improve insulin sensitivity and resultantly reduce the risk of progression of liver diseases in patients with NASH.