黄连素的降糖机制及临床应用新进展

黄连素是从中药黄柏、黄连、三棵针等植物药材中提取出来的生物碱。近年来黄连素的药理作用得到了广泛深入的研究,如抗感染、抗心律失常、保护缺血心肌、降血压、抗肿瘤及抗获得性免疫缺陷综合征(HIV)等作用,尤其对其降血糖作用的报道日渐增多,但其降糖作用机制尚不明确。本文就目前黄连素可能的降糖作用机制及临床疗效观察进行综述。     

黄连素对糖尿病及其并发症的作用

本文就黄连素对糖尿病及其并发症的作用作一介绍。1黄连素的特点又名小檗碱，主要存在于小檗属植物黄连、黄柏和三颗针中，是一种季铵化合物，现也可人工合成，临床常制成盐酸黄连素应用。具有较强的抗菌作用。在临床上常用盐酸黄连素治疗菌痢、胃肠炎等疾病。近年来还发现了黄连素的其他作用。①较多报道黄连素的抗心律失常作用，     

黄连素对糖尿病及其并发症的作用

本文就黄连素对糖尿病及其并发症的作用作一介绍。1黄连素的特点又名小檗碱，主要存在于小檗属植物黄连、黄柏和三颗针中，是一种季铵化合物，现也可人工合成，临床常制成盐酸黄连素应用。具有较强的抗菌作用。在临床上常用盐酸黄连素治疗菌痢、胃肠炎等疾病。近年来还发现了黄连素的其他作用。①较多报道黄连素的抗心律失常作用，     

柚皮素与代谢综合征的研究进展

柚皮素属于二氢黄酮类天然化合物,是柚皮苷的苷元,主要存在于蔷薇科、芸香科、柑橘属植物中,具有重要的抗炎、抗菌、抗氧化、抗癌等生物学效应。研究表明,其具有改善肥胖、糖尿病、高血脂、高血压和代谢综合征等作用。本文旨在对柚皮素与代谢综合征的相关研究进行综述,以期为代谢综合征及其相关疾病的防治提供新的理论依据。     

小檗碱在神经系统疾病中的应用前景

<正> 小檗碱(berberine,BBR),又称黄连素,早期多用于抗微生物、抗原虫和利胆。现代药理学研究证实,BBR是结构明确,临床使用安全的中药单体,且药理作用确实可靠,作用机制多样、独特,具有显著的抗心力衰竭、抗心律失常、降压、抑制血管平滑肌增殖、免疫调节、抗血小板、调脂、降糖、改善胰岛素抵抗、抗炎、抗动脉粥样硬化、抗脑缺血、抗精神疾患等作用。高血压、高血糖、高血脂、胰岛素抵抗、血小板聚集     

黄连素的抗心律失常作用及其研究

黄连素(Berberin)是一种季铵化合物,长期以来一直作为抗生素应用于临床。八十年代初,国外动物实验研究表明,它可以防治实验性心律失常。1985年黄伟民等首先报道黄连素治疗人类室性快速心律失常取得较满意疗效。随后的一些动物和临床研究也进一步证实黄连素的确具有抗心律失常的作用,并有较好的临床效果。 1药代动力学黄连素口服仅缓慢吸收少量,血浓度一般在0.1mg/dl左右,吸收入血后迅速进入体内几乎所有组织。它在各组织中贮留的时间甚为短暂,主要通过肝脏代谢,其代谢产物由肾脏排泄。 2血液动力学效应动物实验结果表明,小剂量黄连素(1～5mg/kg)具有正性肌力作用,而大剂量(10～30mg/kg)则抑制心肌,减弱其收缩力。黄连素以负性频率为主;扩张外周血管,也能扩张     

饮酒与代谢综合征

代谢综合征是一组包括超重或腹型肥胖、高血糖、高血压、高甘油三酯及低高密度脂蛋白血症等的代谢紊乱症候群,也是多重心脑血管疾病危险因素聚集的表现。过去20年来的研究发现饮酒对体内多元代谢有着复杂影响,对代谢综合征具有保护和促进的双重矛盾效应。本文从饮酒与代谢综合征中各种组分的关系出发,分析饮酒对代谢综合征的利与弊。     

代谢综合征与冠心病

代谢综合征已成为新世纪,继高血压、糖尿病、肥胖和血脂异常等疾病之后的又一慢性流行性疾病。代谢综合征的成分如肥胖、2型糖尿病、致粥样硬化血脂表型与高血压是冠心病重要的独立危险因素,每一个成分都可直接促进动脉粥样硬化发生。由于代谢综合征是这些独立危险因素的聚集,因此代谢综合征伴有更大比例、更大程度和病变更广泛的冠心病发病率及病死率。但代谢综合征所有组分对心血管危险的确切影响还需进行更深入的研究,今后代谢综合征的研究和防治还需多个学科和专业人才的合理整合。     

脂联素在代谢综合征及心血管疾病中的研究进展

脂联素(APN)由脂肪细胞分泌产生,在代谢综合征和心血管疾病中起重要的保护作用。在肥胖、糖尿病、高血压、冠状动脉硬化性疾病的患者中,APN水平显著降低。APN具有增加胰岛素敏感性、抗炎、抗动脉粥样硬化及保护心肌等作用。本文将对APN及其受体在糖尿病、胰岛素抵抗、代谢综合征及心血管疾病中的作用进行总结概括。     

浙江省瑞安市公务员代谢综合征流行病学趋势调查

<正>代谢综合征(metabolic syndrome,MS)是一种代谢性疾病,主要表现为肥胖、高血压、高血糖和血脂代谢异常等代谢紊乱异常聚集的一组症候群。在过去的10年间有关我国居民代谢综合征的状况,流行病学方面已经做了很多相关研究[1],但基本属于横断研究,缺乏纵向性的MS患病率对照研究。因此,本文就瑞安市公务员这一特殊职业人群关于2007年、2010年及2013年这三年代谢综合征患病情况进行     

功能性食品与代谢综合征

由于代谢综合征在世界范围内日益增多,饮食干预越发受到人们重视.近年来研究发现一些食物或成分(即功能性食品或成分)有希望改善代谢综合征,尤其是肥胖、糖尿病、血脂异常.此文主要从这三方面举例并评估了一些潜在功能性食品或成分.     

Seaweeds as potential therapeutic interventions for the metabolic syndrome

Seaweeds are a characteristic part of the traditional diet in countries such as Japan and Korea; these countries also have a lower prevalence of metabolic syndrome than countries such as the USA and Australia. This suggests that seaweeds may contain compounds that reduce the characteristic signs of obesity, diabetes, hypertension, fatty liver and inflammation in the metabolic syndrome. Potentially bioactive compounds from seaweeds include polysaccharides, peptides, pigments, minerals and omega-3 fatty acids. This review emphasises current research on these compounds in isolated cells, animal models and patients. Key problems for future research include chemical characterisation of the bioactive principles, defining pharmacological responses in all aspects of the metabolic syndrome, determining if a therapeutic dose has been administered, and defining oral bioavailability of the active ingredients.     

2型糖尿病家系一级亲属脂肪细胞因子变化特点及影响因素的研究进展

脂肪细胞因子是脂肪组织产生的一系列具有生物活性的细胞因子,参与体内能量代谢、免疫、内分泌等生理活动,在代谢平衡的调控过程中起到重要作用。2型糖尿病家系一级亲属作为糖尿病的高危人群,常伴有脂肪细胞因子分泌异常,本文就其体内脂肪细胞因子变化特点及影响因素的研究进展作一综述。     

Diabetic cardiomyopathy: the search for a unifying hypothesis

Although diabetes is recognized as a potent and prevalent risk factor for ischemic heart disease, less is known as to whether diabetes causes an altered cardiac phenotype independent of coronary atherosclerosis. Left ventricular systolic and diastolic dysfunction, left ventricular hypertrophy, and alterations in the coronary microcirculation have all been observed, although not consistently, in diabetic cardiomyopathy and are not fully explained by the cellular effects of hyperglycemia alone. The recent recognition that diabetes involves more than abnormal glucose homeostasis provides important new opportunities to examine and understand the impact of complex metabolic disturbances on cardiac structure and function.     

History of gestational diabetes, insulin resistance and coronary risk

The purpose of this study was to examine characteristics associated with the insulin metabolic syndrome, including insulin resistance, abnormal glucose tolerance, dyslipidemia, obesity, and elevated blood pressure, among women who have experienced gestational diabetes. 39 nondiabetic, young (20-42 years), postpartum (3-18 months) white women were recruited from obstetrical clinics. Twenty-one women had a history of gestational diabetes; 18 had uncomplicated pregnancies. Multivariate analyses revealed a significant difference between groups in insulin resistance (M, measured by euglycemic clamp) and insulin levels (from an oral glucose tolerance test), with insulin resistance showing a statistically stronger difference than insulin levels. Groups also differed significantly when compared on a set of variables associated with insulin metabolic syndrome: glucose tolerance, triglycerides, blood pressure, and body-mass index. Using insulin resistance as a covariate eliminated these group differences, suggesting that insulin resistance is the key factor underlying insulin metabolic syndrome. The higher risk of later developing type 2 diabetes and hypertension in women who have a history of gestational diabetes is explicable by their poorer profile on variables associated with insulin metabolic syndrome, and appears to be attributable to insulin resistance. Thus, insulin resistance appears to distinguish young women at risk for cardiovascular disease.     

糖尿病心肌病变的研究进展

糖尿病心肌病变是糖尿病心脏并发症的重要组成部分,主要表现为心室舒张功能受损和心功能不全。研究提示,糖尿病时,心肌细胞能量代谢紊乱,功能改变,凋亡增加,促使心肌纤维化的一些细胞因子和炎症因子异常表达。这些发现揭示,糖尿病从多个方面损害心肌细胞,引起心室重构,这为进一步阐明糖尿病心肌病变发病机制提供了有力证据。     

Mitochondrial diabetes, DIDMOAD and other inherited diabetes syndromes

Inherited diabetes syndromes are individually rare but collectively make up a significant proportion of patients attending diabetes clinics, some of whom have multiple handicaps. This chapter focuses on syndromes in which major advances have been made in our understanding of the underlying molecular genetics. These conditions demonstrate novel genetic mechanisms such as maternal inheritance and genetic imprinting. They are also fascinating as they aid our understanding of insulin metabolism, both normal and abnormal. As the causative genes are identified, future issues will be the availability of genetic testing, their contribution to the genetic heterogeneity of the more common types of diabetes, and functional studies of the relevant proteins. It is probable that other subtypes of diabetes will be identified as the relevant metabolic pathways are characterized. This is an exciting time to be a diabetes physician as diabetology returns to being a diagnostic rather than a mainly management-based speciality.     

Glucose and cardiovascular risk

The American Diabetes Association and the World Health Organisation have recently redefined the spectrum of abnormal glucose tolerance. The criteria for diabetes mellitus were sharpened and impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) were classified as intermediate stages between normal glucose homeostasis and diabetes, based on fasting and challenged glucose levels, respectively. Criteria were established for 'the metabolic syndrome', as a cluster of cardiovascular risk factors that frequently coincides with the abnormal glucose tolerance state. The extent to which the glucose level itself should be regarded as a cardiovascular risk factor is the subject of ongoing debate. Recent research suggests that cardiovascular risk is related to the plasma glucose level even in the normal range of glucose concentrations. The impact of glucose in relation to cardiovascular events is discussed in this review.     

Metabolic syndrome phenotype in very obese women

Severe obesity is increasingly common in the United States. Very obese persons are at increased risk for the metabolic consequences of obesity. A common multidimensional risk condition associated with obesity is the metabolic syndrome. It is accompanied by increased risk for cardiovascular disease and type 2 diabetes. Clinical manifestations of the metabolic syndrome can vary among obese individuals depending on ethnicity and gender. This study was carried out to determine the pattern of metabolic risk factors in very obese women who were considered candidates for bariatric surgery. Twenty-eight women of this type were compared to 28 nonobese women. Among the former, 11 had categorical hyperglycemia (type 2 diabetes), and 26 had metabolic syndrome by current criteria. Both those with and without diabetes had higher triglycerides and lower high-density lipoprotein (HDL) cholesterol levels than nonobese, but their levels were not categorically abnormal. These changes may have been related to observed lower postheparin lipoprotein lipase activities and higher hepatic lipase activities. In spite of lipid changes, apolipoprotein B levels were only marginally higher in very obese women. In contrast to small changes in lipoprotein metabolism, the obese women were severely insulin resistant, as indicated by hyperglycemia and elevated insulin levels. In addition, they had very high C-reactive protein levels. Thus, the metabolic syndrome, which appears to be typical of very obese women, is characterized by insulin resistance, glucose intolerance and a proinflammatory state. Atherogenic dyslipidemia as a metabolic risk factor in contrast is relatively mild. This pattern is more likely to lead to type 2 diabetes prior to development of clinically evident cardiovascular disease.     

Inflammatory pathways and insulin action

Obesity and type 2 diabetes are associated with a state of abnormal inflammatory response. While this correlation has also been recognized in the clinical setting, its molecular basis and physiological significance are not yet fully understood. Studies in recent years have provided important insights into this curious phenomenon. The state of chronic inflammation typical of obesity and type 2 diabetes occurs at metabolically relevant sites, such as the liver, muscle, and most interestingly, adipose tissues. The biological relevance of the activation of inflammatory pathways became evident upon the demonstration that interference with these pathways improve or alleviate insulin resistance. The abnormal production of tumor necrosis factor alpha (TNF-alpha) in obesity is a paradigm for the metabolic significance of this inflammatory response. When TNF-alpha activity is blocked in obesity, either biochemically or genetically, the result is improved insulin sensitivity. Studies have since focused on the identification of additional inflammatory mediators critical in metabolic control and on understanding the molecular mechanisms by which inflammatory pathways are coupled to metabolic control. Recent years have seen a critical progress in this respect by the identification of several downstream mediators and signaling pathways, which provide the crosstalk between inflammatory and metabolic signaling. These include the discovery of c-Jun N-terminal kinase (JNK) and I kappa beta kinase (I kappa K) as critical regulators of insulin action activated by TNF-alpha and other inflammatory and stress signals, and the identification of potential targets. Here, the role of the JNK pathway in insulin receptor signaling, the impact of blocking this pathway in obesity and the mechanisms underlying JNK-induced insulin resistance will be discussed.