胰岛素抵抗是糖耐量正常人群糖耐量恶化的重要危险因素

目的 探讨胰岛素抵抗和胰岛素分泌对糖在耐量正常人群糖耐量恶化的影响。方法 以口服葡萄糖耐量试验（ＯＧＴＴ）做人群普查一，确定糖耐量正常者（ＮＧＴ）（空腹血糖（ＦＰＧ）〈５．８ｍｍｏｌ／Ｌ及２小时血糖（ＰＧ２ｈ〈６．７ｍｍｏｌ／Ｌ＿１２５例，测定血浆胰岛素。６年后随访再以ＯＧＴＴ确定盲人 群糖耐量状态，以稳态模型（Ｈｏｍａ Ｍｏｄｅｌ）公式评估胰岛素抱搞（ＩＲ）、胰岛素分泌功能（ＩＳ），并分析其对糖     

胰岛素抵抗体内检测方法的探讨

目的 探讨几种常用胰岛素抵抗（ＩＲ）体内检测方法的优缺点,并试图进行改良。方法 分别用三种最小模型技术（ＭＭＴ）、三种基础状态法,四种口服葡萄糖耐量试验（ＯＧＴＴ）法对１６例葡萄糖耐量正常（ＮＧＴ）者和１３例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）病人计算胰钫敏感性指数（ＩＳＩ）,并以经典ＭＭＴ得出的ＩＳＩ为标准,其余方法得出ＩＳＩ与之进行比较和相关分析。结果 除空腹血糖、空腹胰岛素比值（ＦＳＧ／ＦＩｎ     

血糖,血浆胰岛素水平与血压升高的关系发生于糖尿病之前？

对年龄２５岁～７４岁２０１例糖耐量正常（ＮＯＧＴＴ）、３０７例ＩＧＴ、３６６例新发现ＮＩＤＤＭ，进行Ｐｅｒｓｏｎ单相关分析。年龄、性别、ＢＭＩ、空腹及服糖后血糖、胰岛素（ＩＮＳ）水平分别与血压正相关，调整年龄、性别、ＢＭＩ、血浆胆固醇、抽烟等因素后，ＮＯＧＴＴ及ＩＧＴ血糖与血压相关，ＮＩＤＤＭ者血糖与血压不相关，提示血糖水平对血压的影响发生于糖尿病之前。ＮＯＧＴＴ、ＩＧＴ、和ＮＩＤＤＭ总组，ＮＯＧＴＴ及ＩＧＴ组血浆ＩＮＳ水平与血压不相关，只有年龄小于５０岁，非肥胖的ＮＯＧＴＴ者血浆ＩＮＳ水平与血压相关，提示血浆胰岛素水平对血压的影响发生于年轻非肥胖的糖耐量正常者。     

不同糖耐量水平人群血清真胰岛素和胰岛素原水平的临床意义

目的 探讨不同糖耐量者血清真胰岛素（ＴＩ）及胰岛素原（ＰＩ）水平的变化及临床意义。方法 用特异的单克隆抗体夹心放大酶联免疫分析法（ＢＡ－ＥＬＩＳＡ）检测１３５例正常糖耐量（ＮＧＴ）、８６例糖耐量低减（ＩＧＴ）及１０１例Ⅱ型糖尿病（ＤＭ）者口服葡萄糖耐量试验（ＯＧＴＴ）各点血清ＴＩ及ＰＩ水平。结果 ３组血清空腹ＴＩ差异无显著性（Ｐ〉０．０５）,免疫反应胰岛素（ＩＲＩ）Ⅱ型ＤＭ组明显升高（Ｐ〈０．０１     

2型糖尿病脓系胰岛素分泌功能的研究

目的 探讨胰岛素抵抗（ＩＲ）和胰岛细胞功能障碍在２型糖尿病（ＤＭ）发病中的作用，方法２ＤＭ家系中，对部分成员进行口服葡萄糖耐量试验（ＯＧＴＴ）〈按ＷＨＯ标准将家系成员ＤＭ一级亲属正常组（１０６例，糖耐量低减组（ＩＧＴ）组（３９例），新诊断ＤＭ组（６３例）和原诊断ＤＭ组（８３例，病程１年以上）〉计算各组成员的胰岛素敏感性指数（ＩＳＩ）以及有遍初期分泌功能的指数，民无ＤＭ家族史的健康人（５３例）相比较     

非胰岛素依赖型糖尿病和糖耐量低减患者的胰岛素敏感性及其相关因素研究

为评价糖耐量异常者的胰岛素敏感性改变及其有关因素，对５７２例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）、６４７例糖耐量低减（ＩＧＴ）和５４３名正常对照者进行了研究。结果显示，空腹血浆胰岛素（ＦＩｎｓ）水平和高胰岛素血症的百分率，在ＮＩＤＤＭ组＞ＩＧＴ组＞正常对照组（Ｐ＜０．０１）。胰岛素敏感性指数（ＩＳＩ）［－ｌｎ（ＦＩｎｓ×空腹血糖）］从大到小的排列顺序为：正常对照组、ＩＧＴ组，新诊断糖尿病组和原诊断糖尿病组（Ｐ＜０．０１）。各组肥胖者的ＩＳＩ小于非肥胖者（Ｐ＜０．０１）。单因素相关性分析显示，各组ＩＳＩ与体重指数（ＢＭＩ）呈负相关，与高密度脂蛋白胆固醇呈正相关。糖尿病组和ＩＧＴ组的ＩＳＩ与血压也呈负相关。多元逐步回归分析显示，ＩＳＩ与ＢＭＩ呈负相关，部分与血压、血脂也有相关性。提示糖耐量异常者伴有高胰岛素血症和胰岛素抵抗，ＩＳＩ与血管病变的危险因素有相关性。     

胰岛素抵抗、胰岛β细胞分泌功能对妊娠糖尿病发生的影响

妊娠糖尿病 (ＧＤＭ)往往是妊娠中晚期伴随胰岛素抵抗(ＩＲ)的发展而发生的 ,故经典的观点认为ＧＤＭ主要与ＩＲ有关。ＩＲ是指胰岛素靶组织 (如骨胳肌、脂肪组织、肝脏等 )对胰岛素敏感性降低 ,对葡萄糖的利用降低及抑制肝葡萄糖输出的作用减弱。妊娠期的ＩＲ与胎盘分泌具有拮抗胰岛素作用的激素有关。不过 ,单一的ＩＲ尚不能引起ＧＤＭ。因为妊娠中晚期ＩＲ均增加 ,但仅约 5 %发展为ＧＤＭ。提示ＧＤＭ妇女除了有ＩＲ ,胰岛素分泌可能也存在缺陷〔1〕。本研究通过观察不同糖耐量状态〔ＧＤＭ、糖耐量低减(ＩＧＴ)、糖耐量正常 (ＮＧＴ)〕…     

2型糖尿病患者空腹和口服葡萄糖负荷后血清真胰岛素、胰岛素原水平初探

本研究应用特异、灵敏的ＥＬＩＳＡ法分别测定肥胖和非肥胖糖耐量正常者 (ＮＧＴ)、ＩＧＴ者和 2型糖尿病 (ＤＭ)患者基础状态和糖负荷状态下的真胰岛素 (ＴｒｕｅＩｎｓｕｌｉｎ ,ＴＩ)、胰岛素原的释放水平 ,并与传统ＲＩＡ法所测的免疫反应性胰岛素(Ｉｍｍｕｎｏｒｅａｃｔｉｖｅｉｎｓｕｌｉｎ ,ＩＲＩ)比较 ,以更确切地探讨其 β细胞分泌功能和胰岛素抵抗状态。一、对象和方法1.对象 :按 1985年ＷＨＯ提出的诊断标准新诊断的 2型ＤＭ 34例 ,ＩＧＴ 2 0例 ,ＮＧＴ 2 8例。各组均排除心血管疾病和其它内分泌代谢疾病 ,肝肾功能正常。ＮＧ…     

胰岛素分泌及胰岛素敏感性与葡萄糖耐量的关系

最近,除糖耐量减低(ＩＧＴ)以外,研究者提出了一个新的糖耐量阶段———空腹血糖损害(ＩＦＧ),即空腹血糖(ＦＢＧ)在6.1～6.9ｍｍｏｌＬ。目前尚不清楚ＩＦＧ与ＩＧＴ个体是否具有相同的代谢紊乱。本文旨在探讨ＩＦＧ与ＩＧＴ在胰岛素分泌及胰岛素敏感性方面是否存在差异。对象与方法　研究对象为来自芬兰Ｂｏｔｎｉａ研究项目的5396例处于不同糖耐量阶段的个体。根据ＦＢＧ及餐后2ｈ血糖水平分为正常糖耐量(ＮＧＴ)、ＩＦＧ、ＩＧＴ、ＩＦＧ合并ＩＧＴ(ＩＦＧＩＧＴ)、轻度糖尿病及糖尿病(ＤＭ)。测定其身高、体重、腰围、臀围,计算体重指…     

真胰岛素测定在分析β细胞功能及胰岛素敏感性的意义初探

目的探讨真胰岛素（Ｔｒｕｅｉｎｓｕｌｉｎ，ＴＩ）测定在分析胰岛β细胞功能及胰岛素敏感性中的意义。方法采用双位点夹心放大酶联免疫分析法（ＢＡＥＬＩＳＡ）及其它方法对４３例糖耐量正常者（ＮＧＴ）、２０例糖耐量低减者（ＩＧＴ）及４７例２型糖尿病（ＤＭ）患者进行血清ＴＩ等的测定，初步分析其胰岛β细胞功能及胰岛素敏感性。结果肥胖的２型ＤＭ组血清空腹ＴＩ水平不高（Ｐ＞０．０５），而免疫反应性胰岛素（ＩＲＩ）则明显升高（Ｐ＜０．０１），ＯＧＴＴ３０分钟ＴＩ水平明显低于ＮＧＴ组（Ｐ＜０．０１）。用ＴＩ计算胰岛素释放指数，ＮＧＴ＞ＩＧＴ＞２型ＤＭ；敏感指数，ＮＧＴ与ＩＧＴ均明显高于２型ＤＭ（Ｐ＜０．０１）；而用ＩＲＩ计算胰岛素释放指数和敏感指数仅在ＮＧＴ与２型ＤＭ组间有显著差异（Ｐ＜０．０１）。结论２型ＤＭ患者的高胰岛素血症可能是高胰岛素原血症；ＴＩ测定较ＩＲＩ更能确切地评价β细胞功能及胰岛素敏感性     

Rosiglitazone improves insulin sensitivity and glucose tolerance in subjects with impaired glucose tolerance

OBJECTIVE: This study was designed to evaluate the effects of rosiglitazone (ROS) on insulin sensitivity, beta-cell function, and glycaemic response to glucose challenge and meal in subjects with impaired glucose tolerance (IGT). METHODS: Thirty patients with IGT (ages between 30 and 75 years and BMI (body mass index) < or = 27 kg/m2) were randomly assigned to receive either placebo (n = 15) or ROS (4 mg/day) (n = 15). All participants underwent a 75-g oral glucose tolerance test (OGTT), meal test, and frequently sampled intravenous glucose tolerance test (FSIGT) before and after the 12-week treatment. RESULTS: After 12 weeks of ROS treatment, there were significant increases in total cholesterol (TC) (4.25 +/- 0.22 vs 4.80 +/- 0.17 mmol/l, P < 0.001), high-density lipoprotein cholesterol (HDL-C) (1.25 +/- 0.07 vs 1.43 +/- 0.06 mmol/l, P < 0.05), and low-density lipoprotein cholesterol (LDL-C) (2.70 +/- 0.15 vs 3.37 +/- 0.17 mmol/l, P < 0.05) without changes in triglyceride concentration, TC/HDL-C and LDL-C/HDL-C ratio. Although the acute insulin response (AIR) to intravenous glucose and disposition index (measured as the ability of pancreatic beta-cell compensation in the presence of insulin resistance) remained unchanged, the insulin sensitivity (SI) and glucose effectiveness (SG) were remarkably elevated (0.38 +/- 0.06 vs 0.54 +/- 0.09 x 10(-5) min(-1)/pmol, P < 0.05; 0.017 +/- 0.002 vs 0.021 +/- 0.001 min(-1), P < 0.05, respectively) in the ROS group. The glucose, insulin, and c-peptide areas under curve (AUC) in response to OGTT and the glucose and insulin AUC during meal were significantly ameliorated in the ROS group. Five out of 15 (33%) and two out of 15 (13%) subjects treated with ROS and placebo, respectively, reversed to normal response during OGTT (P < 0.05). CONCLUSION: Rosiglitazone treatment significantly improved insulin resistance and reduced postchallenge glucose and insulin concentrations in patients with impaired glucose tolerance without remarkable effects on beta-cell secretory function.     

Relationship between glucose tolerance,insulin secretion,and insulin action in non-obese individuals with varying degrees of glucose tolerance

Summary Plasma glucose and insulin concentration following a 75 g oral glucose challenge and glucose uptake during a hyperinsulinaemic glucose clamp study were determined in 50 non-obese individuals. The study population was divided into five groups on the basis of their glucose tolerance: normal, impaired glucose tolerance, Type 2 (non-insulin-dependent) diabetes mellitus with fasting plasma glucose of less than 8 mmol/l, between 8–15 mmol/l, and more than 15 mmol/l. The plasma insulin response was significantly greater (p<0.001) than normal in those with either impaired glucose tolerance or Type 2 diabetes and a fasting plasma glucose concentration less than 8 mmol/l. In contrast, the plasma insulin response was similar to normal in the other two groups of patients with Type 2 diabetes, i.e. fasting plasma glucose concentration 8–15 mmol/l or greater than 15 mmol/l. Glucose uptake rates were significantly lower (p<0.001) than normal in subjects with impaired glucose tolerance and all three groups of patients with Type 2 diabetes. Although glucose uptake rates during the glucose clamp studies were relatively similar in all four groups of glucose intolerant subjects, the values were significantly lower in those patients with Type 2 diabetes who had a fasting plasma glucose concentration greater than 8 mmol/l (p<0.01), These data indicate that a significant degree of insulin resistance exists in patients with impaired glucose tolerance or Type 2 diabetes, relatively independent of fasting plasma glucose concentration. Indeed, glucose uptake during glucose clamp studies fell 8-fold over a range in fasting plasma glucose concentration of from 4.5 to 6.5 mmol/l. In contrast, the plasma insulin response increased over the same range of fasting plasma glucose concentrations. The fact that this defect in insulin action can be seen in patients who are hyperinsulinaemic, not hypoinsulinaemic, and only modestly hyperglycaemic, is consistent with the hypothesis that resistance to insulin-stimulate glucose uptake is a basic characteristic of patients with impaired glucose tolerance or Type 2 diabetes.     

Oral glucose tolerance test and insulin sensitivity in low insulin responders

Oral and iv glucose tolerance, insulin response to iv and oral glucose load as well as insulin sensitivity were evaluated in 58 'low insulin responders'. They were selected from a group of 226 healthy subjects with normal fasting blood glucose and normal iv glucose tolerance test on the basis of a low insulin response during a standardized glucose infusion test (GIT). The insulin response to GIT was analysed by parameter identification in a mathematical model (parameter KI). Insulin sensitivity was also measured by computer analysis of GIT (parameter KG) and, in a limited group of subjects, by a somatostatin infusion test. Thirty-three low insulin responders had normal OGTT, whereas 5 demonstrated borderline-1, 16 borderline-2, and 4 decreased OGTT. The first group of subjects demonstrated normal or enhanced insulin sensitivity. Borderline and decreased OGTT, in most instances, was accompanied by decreased insulin sensitivity, implying that a subgroup of low insulin responders exhibited signs of both impaired insulin response to glucose and insulin resistance. Since these defects characterize manifest type-2 diabetes, these subjects possibly may run a high risk to develop this type of diabetes. On the other hand, low insulin response in combination with increased insulin sensitivity may reflect adaptation of the secretory capacity of B-cells to the need of insulin.     

Effect of sham-feeding on glucose tolerance and insulin secretion

Glucose, 25 g, was infused iv with or without sham-feeding in seven normal males. Sham-feeding improved glucose tolerance, incremental area of blood glucose being 63% (P less than 0.05) of that during iv glucose without sham-feeding. The actual insulin secretion evaluated from the total area under the C-peptide and insulin curves did not differ during iv glucose with or without sham-feeding. These results suggest that the cephalic-vagal reflex improves glucose tolerance during iv glucose, independent of changes in beta-cell function.     

Relationship between insulin sensitivity, insulin secretion and glucose tolerance in cirrhosis

Hepatic insulin extraction is difficult to measure in humans; as a result, the interrelationship between defective insulin secretion and insulin insensitivity in the pathogenesis of glucose intolerance in cirrhosis remains unclear. To reassess this we used recombinant human C-peptide to measure C-peptide clearance in cirrhotic patients and controls and thus derive C-peptide and insulin secretion rates after a 75-gm oral glucose load and during a 10 mmol/L hyperglycemic clamp. Cirrhotic patients were confirmed as insulin-insensitive during a euglycemic clamp (glucose requirement: 4.1 +/- 0.1 mg/kg/min vs. 8.1 +/- 0.5 mg/kg/min; p less than 0.001), which also demonstrated a low insulin metabolic clearance rate (p less than 0.001). Although intolerant after oral glucose, the cirrhotic patients had glucose requirements identical to those of controls during the hyperglycemic clamp (cirrhotic patients: 6.1 +/- 1.0 mg/kg/min; controls: 6.3 +/- 0.7 mg/kg/min), suggesting normal intravenous glucose tolerance. C-peptide MCR was identical in cirrhotic patients (2.93 +/- 0.16 ml/min/kg) and controls (2.96 +/- 0.24 ml/min/kg). Insulin secretion was higher in cirrhotic patients, both fasting (2.13 +/- 0.26 U/hr vs. 1.09 +/- 0.10 U/hr; p less than 0.001) and from min 30 to 90 of the hyperglycemic clamp (5.22 +/- 0.70 U/hr vs. 2.85 +/- 0.22 U/hr; p less than 0.001). However, with oral glucose the rise in serum C-peptide concentration was relatively delayed, and the insulin secretion index (secretion/area under 3-hr glucose curve) was not elevated. Hepatic insulin extraction was reduced both in fasting and during the hyperglycemic clamp (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)