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.     

口服降糖药物对糖尿病患者骨代谢影响的研究进展

糖尿病患者骨质疏松及脆性骨折风险增加,这与疾病本身及其治疗用药有关。不同降糖药物通过不同的生物学途径治疗糖尿病,然而这些药物可能对骨代谢产生影响。二甲双胍对糖尿病患者骨代谢具有积极作用,在临床应用中不会额外增加骨折风险;DPP-4抑制剂、SGLT2抑制剂、GLP1受体激动剂对骨折发生风险的影响与药物种类有关,应考虑单个药物背景下对骨脆性的潜在影响;噻唑烷二酮类使骨质流失并导致骨折风险增加,与其他降糖药物或抗骨质疏松药物联合可减少其对骨骼的负面影响;关于磺酰脲类药物对骨骼影响的大型临床研究目前仍缺乏,尚需更多的数据支持。临床制定糖尿病用药方案时,为了预防糖尿病治疗过程中骨量减少或骨质疏松带来的严重并发症,应考虑各种降糖药物对骨代谢的影响。     

降糖药物对糖尿病患者骨质疏松的影响

糖尿病引起骨质疏松已被多数学者所公认.近来相关研究发现降糖药物在控制血糖的同时对骨代谢亦有影响,噻唑烷二酮类药物可显著增加2型糖尿病女性患者骨折发生率,胰岛素亦可增加骨折风险,胰岛素促泌剂可以降低骨折的风险,二甲双胍的作用为中性,而新型胰高血糖素样肽-l类似物和二肽基肽酶-Ⅳ抑制剂具有保护骨代谢的潜能.     

屈格列酮对以胰岛素治疗的2型糖尿病患者的影响

噻唑烷二酮类（Ｔｈｉａｚｏｌｉｎｅｄｉｏｎｅｓ）是一类能降低有高血糖及高胰岛素血症动物胰岛素抵抗的药物，其中屈格列酮（Ｔｒｏｇｌｉｔａｚｏｎｅ）已应用于肥胖者及２型糖尿病患者，能加速胰岛素刺激的葡萄糖处理，这说明该药能改善胰岛素的抵抗性。本研究主要报...     

糖尿病治疗药物与水钠潴留相关性及临床对策

随着糖尿病患病率的逐年增加，降糖药物的使用越来越广泛，其不良反应也在迅速增加。其中，由于水钠潴留导致心力衰竭的风险增加，因此降糖药物治疗与水钠潴留相关性近年来受到重视。引起水钠潴留的降糖药物主要包括噻唑烷二酮类（TZDs）和胰岛素。在临床工作中如何科学选择和应用这些药物，确保患者的安全，已成为糖尿病治疗中的主要问题之一。     

利拉鲁肽对血糖控制不佳的腹型肥胖2型糖尿病患者的疗效

肥胖尤其是腹型肥胖是2型糖尿病、高血压、脂代谢紊乱和动脉粥样硬化的高度危险因素。80％以上的2型糖尿病患者合并超重和肥胖,是心脑血管死亡的第一要因素。传统的降糖药物如磺脲类、胰岛素和噻唑烷二酮类通过不同的机制在降血糖的同时可导致体重的增加,从而加重胰岛素抵抗,往往导致血糖控制的失败,增加心脑血管事件发生的风险。     

过氧化物酶体增殖物激活受体γ与肥胖

过氧化物酶体增殖物激活受体 (PPAR)γ与胰岛素抵抗、脂肪细胞分化和肥胖有密切关系。PPARγ2是前脂肪细胞分化为成熟脂肪细胞以及脂肪细胞内甘油三酯蓄积的重要调节因子。PPARγ为噻唑烷二酮类 (TZD)药物的靶分子 ,长期应用TZD类药物可能会引起体重增加 ,加重代谢紊乱。近年研究显示PPARγ抑制剂可抑制肥胖和改善胰岛素抵抗。PPARγ激动剂和抑制剂与肥胖及胰岛素抵抗的关系需要进一步研究。     

马来酸罗格列酮（文迪亚）致白细胞下降一例报道

马来酸罗格列酮（文迪亚）属于噻唑烷二酮类TZD降糖药。可增强胰岛素在外周组织如肝脏，肌肉，脂肪的敏感性，减少胰岛素抵抗，为胰岛素增敏剂。药物进入靶细胞之后与核受体结合，     

过氧化物酶体增殖物激活受体γ与肥胖

过氧化物酶体增殖物激活受体(PPAR)γ与胰岛素抵抗、脂肪细胞分化和肥胖有密切关系。PPARγ2是前脂肪细胞分化为成熟脂肪细胞以及脂肪细胞内甘油三酯蓄积的重要调节因子。PPARγ为噻唑烷二酮类(TZD)药物的靶分子，长期应用TZD类药物可能会引起体重增加，加重代谢紊乱。近年研究显示PPARγ抑制剂可抑制肥胖和改善胰岛素抵抗。PPARγ激动剂和抑制剂与肥胖及胰岛素抵抗的关系需要进一步研究。     

日服1次或2次罗格列酮可改善2型糖尿病患者血糖状况

罗格列酮(Ｒｏｓｉｇｌｉｔａｚｏｎｅ)属于噻唑烷二酮类降糖药,通过改善外周组织的胰岛素抵抗而发挥降糖效应。作者探讨剂量和服药次数对罗格列酮疗效的影响。方法 选择经排除明显肾脏病变、冠脉供血不足或充血性心力衰竭、伴有症状的糖尿病神经病变、肝功能不良等疾患,年龄４０~８０岁,     

Thiazolidinediones and inflammation

Thiazolidinediones (TZDs) are selective ligands of peroxisome-proliferator-activated receptor gamma increasingly used in the treatment of type 2 diabetes. Both in vitro and in vivo studies provide evidence that TZDs have anti-inflammatory properties. TZDs inhibit macrophage activation and decrease inflammatory cytokine expression and release in macrophage and monocyte. In vivo, treatment with TZDs decreases circulating mononuclear cells nuclear NF-kB content while increasing, in the same cells, expression of IkB, an NK-kB inhibitor. Furthermore, TZD treatment results in decreased plasma levels of inflammation and cardiovascular risk markers such as CRP, MMP9, PAI-1 and sCD40 in both obese and type 2 diabetic patients. Finally, TZDs induce synoviocyte apoptosis and reduce secretion of TNFalpha, IL-6 and IL-8 in synoviocyte from rheumatoid arthritis patients. TZDs might thus be considered for use in clinical trials targeting prevention of atherosclerosis and cardiovascular diseases and in pilot trials exploring the possibility that TZDs might help in the treatment of rheumatic diseases.     

Differentiating members of the thiazolidinedione class: a focus on efficacy

The thiazolidinediones (TZDs) or 'glitazones' are a new class of drug used for the treatment of type 2 diabetes. Although their precise mechanism of action is not known, TZDs target insulin resistance directly and thus tackle an underlying cause of the disease. Two TZDs are indicated for use in type 2 diabetes in the USA, pioglitazone and rosiglitazone. A third, troglitazone, has been associated with significant hepatotoxicity and has been withdrawn from use. In clinical trials, all three TZDs effectively lower blood glucose levels as monotherapy and in combination therapy with sulfonylureas, metformin and insulin. To date, head-to-head comparative studies with these agents have not been performed. It is difficult, therefore, to make direct comparisons of their efficacy since other variables, including baseline glucose levels and study design, can have a significant impact on treatment outcome. Despite this and in light of unique safety issues characterized with certain TZDs, it is useful to look closely at the efficacy data for these agents. It is not sufficient to assume that 'all glitazones are the same' because the studies have not yet been done to support this statement. This article will review what is known about the relative efficacy of the TZDs.     

Thiazolidinediones protect mouse pancreatic β-cells directly from cytokine-induced cytotoxicity through PPARγ-dependent mechanisms

Since most of the current studies of thiazolidinediones (TZDs) are only focused on improving glycemic control, increasing insulin sensitivity, and regulating inflammatory states in Type 2 Diabetes, it is still controversial whether TZDs have direct, protective effects on pancreatic β-cells in autoimmune diabetes. Here, we show the protective effects of TZDs on mouse pancreatic β-cell line cells (NIT-1) impaired by exposure to inflammatory cytokines (IL-1β and IFN-γ) and explore the potential mechanisms for this. The apoptosis rate and caspase-3 activity were remarkably increased, and insulin secretion response to glucose was impaired severely by exposure to IL-1β/IFN-γ for 48 h compared to control cells, whereas apoptosis rate and caspase-3 activity were significantly decreased in cells with treatment of rosiglitazone (RGZ) or pioglitazone (PIG), and the capacity for insulin secretion response to glucose was recovered. TZDs protect pancreatic β-cells from cytokine-induced cytotoxicity through PPARγ activation. The protective effects of the TZDs on NIT-1 cells disappeared when PPARγ was blocked with PPARγ-siRNA interference or treatment with GW9662, the PPARγ antagonist. Additionally, the enhancement of PPARγ expression by treatment with TZDs inhibited the expression of caspase 3 in IL-1β/IFN-γ-induced NIT-cells. Also, the inhibition of caspase 3 expression by TZDs was blocked by co-treatment with GW9662 or infection with PPARγ-siRNA. Taken together, our data suggest that TZDs might serve to protect pancreatic β-cells directly from cytokine-induced cytotoxicity through a PPARγ-dependent pathway, and caspase-3 may play an important role in the mechanisms involved.     

Thiazolidinediones: a review of their mechanisms of insulin sensitization, therapeutic potential, clinical efficacy, and tolerability

The thiazolidinediones (TZDs) rosiglitazone and pioglitazone are newer additions to the antidiabetic armamentarium and are indicated for the treatment of type 2 diabetes mellitus (T2DM) in the United States. The TZDs are peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists that provide clinically effective glycemic control and unique pharmacologic effects on multiple risk factors for T2DM-related morbidity, including improvement of insulin sensitivity and endothelial dysfunction, reduction of blood pressure, and amelioration of dyslipidemia. Weight gain and fluid retention occur with TZD therapy, especially when they are administered in higher doses and in combination with insulin. Although fluid retention associated with the use of TZDs is generally mild and reversible, these agents should not be used in patients with New York Heart Association Class III or IV heart failure symptoms. The findings of ongoing, long-term, prospective studies will clarify the role of the TZDs in the treatment of T2DM, particularly in terms of the durability of improvements in glycemic control, insulin sensitivity, pancreatic beta- cell function, and cardiovascular health.     

PPAR‐γ Agonism for Cardiovascular and Renal Protection

Diabetes mellitus is an established risk factor for cardiovascular disease and the leading cause of end‐stage renal disease in the Western World. Thiazolidinediones (TZDs) represent a class of antidiabetic agents that exert their glucose‐lowering effects by reducing insulin resistance, through stimulation of a type of nuclear receptor, called peroxisome proliferator‐activated receptor‐γ. Apart from improving glycemic control, TZDs were shown to exert beneficial effects on several components of the metabolic syndrome and cardiovascular risk markers. Furthermore, background and human studies have shown that TZDs reduce urinary albumin and protein excretion and interfere with most of the pathogenentic pathways involved in the development and progression of diabetic nephropathy. On the other hand, currently used TZDs have side effects, most important of which is fluid retention leading to wait gain and heart failure deterioration. With regards to cardiovascular outcomes, the anticipated benefit of TZDs was demonstrated for pioglitazone, whereas a series of previous meta‐analyses linking rosiglitazone treatment with increased risk of myocardial infarction and cardiovascular death raised uncertainty around the cardiovascular safety of rosiglitazone. This article will discuss the effects of TZDs on established and emerging cardiovascular risk factors, the data on possible beneficial renal effects of these compounds, and the existing evidence from large‐scale clinical trials and meta‐analyses on their effects on cardiovascular outcomes, aiming to provide an overview of the cardio‐ and renoprotective properties of these drugs.     

噻唑烷二酮类药物在动脉粥样硬化中的抗炎作用

噻唑烷二酮类药物是一类新的治疗2型糖尿病和胰岛素抵抗的药物。越来越多的证据表明噻唑烷二酮类药物在防治动脉粥样硬化方面有良好的疗效。噻唑烷二酮类药物通过对动脉粥样硬化炎症反应细胞、炎症因子、心血管事件的影响,在动脉粥样硬化中发挥其积极的抗炎作用。     

A atrial flutter consisted of two different conduction pathways

Thiazolidinediones (TZDs) represent insulin-sensitizing agents that have several pleiotropic properties, possibly related to their favorable effects on cardiovascular remodeling. We briefly describe 2 diabetic patients who experienced a remarkable improvement in their paroxysmal atrial fibrillation (AF) after treatment with rosiglitazone. Current evidence suggests that atrial remodeling represents a prominent mechanism of AF development and perpetuation while inflammation and oxidative stress are possibly implicated in this process. It could therefore be speculated that the pleiotropic effects of TZDs favorably affect atrial remodeling reducing the arrhythmia burden. Further studies are needed in order to elucidate the merit of this pharmacological approach in AF.     

噻唑烷二酮类药物对骨代谢的影响

噻唑烷二酮类（TZDs）药物是核转录因子过氧化物酶体增殖物激活受体γ（PPARγ）的激动剂,是临床上常用的胰岛素增敏剂,用来治疗2型糖尿病等存在胰岛素抵抗的疾病。近年发现TZDs增加女性骨折的危险性。体外及动物实验证实TZDs促进间充质干细胞向脂肪细胞系分化,而抑制其向成骨细胞系分化,减少骨形成,还可能具有促进破骨细胞分化、增加骨吸收的作用,从而导致骨量减少。TZDs还可能通过改变某些激素和细胞因子的水平间接地影响骨代谢。     

噻唑烷二酮类药物的抗肿瘤作用

噻唑烷二酮（TZDs）是用于治疗以胰岛素抵抗为特征的2型糖尿病的药物。它主要通过作用于核受体家族中的过氧化物酶增殖体的激活受体γ（PPARγ）来发挥抗糖尿病的作用。近年来,越来越多的实验证据发现其具有一定的抗肿瘤作用,涉及的机制主要有诱导细胞周期的终止,促进细胞的凋亡或分化,抑制肿瘤的转移及血管新生等。