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     

Alzheimer型痴呆患者血清胰岛素及血糖水平的检测及其临床意义

用放射免疫（双抗体）法及葡萄糖氧化酶法对Ａｌｚｈｅｉｍｅｒ型老年性痴呆（ＳＤＡＴ）和血管性痴呆患者各１８例及正常对照２３例作了空腹血清胰岛素与血糖水平的检测，计算了胰岛素敏感性指数。结果显示：ＳＤＡＴ组、血管性痴呆组与正常对照组的空腹血糖水平相近（Ｐ＞０．１０）．ＳＤＡＴ组的血清胰岛素水平明显低于血管性痴呆组（Ｐ＜０．０５）及正常对照组（Ｐ＜０．０１），血管性痴呆组与正常对照组比较无显著差异（Ｐ＞０．０１）。正常对照组的相对胰岛素敏感性为１．０时．ＳＤＡＴ组则高达１．６７．予静脉点滴胰岛素，结果轻型ＳＤＡＴ患者记忆力及认知能力短期内均有不同程度的改善。结果提示ＳＤＡＴ与胰岛素代谢紊乱有关。     

老年糖尿病患者血浆纤溶活性与胰岛素抵抗的关系

检测４２例老年Ⅱ型糖尿病患者和２６例正常对照者血浆组织型纤溶酶原激活剂（ｔＰＡ）及其抑制物（ＰＡＩ）、α２纤溶酶抑制物（α２ＰＩ）活性、血清纤维蛋白（原）降解产物（ＦＤＰ）、胰岛素水平及胰岛素敏感性指数（ＩＳＩ）的改变。结果表明,糖尿病患者血浆ＰＡＩ和α２ＰＩ活性及血清胰岛素水平高于对照组,而ｔＰＡ活性和ＩＳＩ则降低（Ｐ值均＜０．０１）。ＰＡＩ和α２ＰＩ活性与血清胰岛素水平呈正相关（ｒ值分别为０．５８２７和０．６５１９,Ｐ＜０．０１）,而与ＩＳＩ呈负相关（ｒ值分别为－０．４８１７和－０．５３７８,Ｐ＜０．０１）。提示老年Ⅱ型糖尿病患者血浆纤溶活性明显异常并存在显著的胰岛素抵抗（ＩＲ）和高胰岛素血症（ＨＩＳ）,纤溶活性失调和ＩＲ和ＨＩＳ有关,提示ＨＩＳ可能促使ＰＡＩ和α２ＰＩ合成及分泌增加,减轻和消除ＩＲ有助于避免ＨＩＳ及其引起的血浆纤溶活性异常。     

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。     

233例非糖尿病人群空腹血浆胰岛素水平预测体重增加的？…

目的 探讨非糖尿病人群胰岛素抵抗及血浆胰岛素水平对体重增加的影响。方法：人群调查中以口服葡萄糖耐量试验（ＯＧＴＴ）筛选的非糖尿病者２３３例（正常糖耐量（ＮＧＴ）１３４例,糖耐量低减（ＩＧＴ）９９例）,随访观察６年,以多因素回归分析初庐互岛素水平、胰岛素抵抗与体重增加的关系。结果 在总组,体重增加与初访体重指数（ＭＢＩ）呈显著负相关（Ｐ＝０．００３）,与胰岛素敏感指数及家腹血糖水平呈显著正相关（Ｐ＝     

肥胖症患者和新诊断的2型糖尿病患者真胰岛素和前胰岛素的改变

目的 了解真胰岛素（ｔｒｕｅ ｉｎｓｕｌｉｎ，ＴＩ）和前胰岛素（ｐｒｏｉｎｓｕｌｉｎ，ＰＩ）在肥胖症和２型糖尿病患者中的改变，了解免疫活性胰岛素（ｉｍｍｕｎｏｒｅａｃｔｉｖｅ ｉｎｓｕｌｉｎ，ＩＲＩ）能否准确反映ＴＩ。方法 ３３例糖耐量正常（ＮＧＴ），２４例糖耐量减低（ＩＧＴ）和５３例新诊断的２型糖尿病患者行口服葡萄糖耐量实验，并根据体重指数（ＢＭＩ）分为肥胖和非肥胖组；采用ＥＬＩＳＡ方法（其单克     

小剂量胰岛素,葡萄糖持续静脉滴注法测定高血压病胰岛素敏感性

目的探讨以小剂量胰岛素、葡萄糖持续静脉滴注法测定高血压病患者的胰岛素敏感性及培哚普利对其的影响。方法３６例高血压患者，依糖耐量试验，将其分为单纯高血压组（ＨＴ）与高血压合并糖尿病或糖耐量异常组（ＨＴ＋ＤＭ或ＩＧＴ），以小剂量胰岛素、葡萄糖持续静滴法测定两组胰岛素敏感性差异。患者经服用长效ＡＣＥＩ培哚普利４～８ｍｇ，一日１次，４周后９例完成再次小剂量胰岛素、葡萄糖持续静滴试验，以研究ＡＣＥＩ对胰岛素敏感性的影响。胰岛素敏感性指数（ＩＳＩ）以每血清胰岛素浓度葡萄糖清除率表示。结果ＨＴ＋ＤＭ或ＩＧＴ组胰岛素敏感性指数明显低于ＨＴ组：ＨＴ组ＩＳＩ为１９．６４±１０．８９，ＨＴ＋ＤＭ或ＩＧＴ组：７．７９±４．８９（Ｐ＜０．０１）。服用培哚普利前后ＩＳＩ具统计学显著性差异：治疗前：１４．７２±８．１９；治疗后：１５．３２±８．１８（Ｐ＜０．０１）。结论单纯高血压病患者胰岛素敏感性与高血压合并ＤＭ或ＩＧＴ者具有差异；服用４周培哚普利对胰岛素敏感性有正性作用，进而可能对高血压病患者的心血管系统的重构有逆转作用。然而，尚需对本课题作长期的大样本临床观察。     

2型糖尿病,糖耐量低减及糖尿病患者亲属胰岛β细胞功能变 …

目的 观察四川地区２型糖尿病（ＤＭ）患者、糖耐量低减（ＩＧＴ）者及糖尿因缘亲属的胰岛β细胞功能的变化，包括血中脂岛素原（ＰＩ）水平的变化及其意义。方法 采用特异性胰岛素（Ｉ）、Ｃ肽（ＣＰ）和人脂岛素原放射免疫式剂盒（均为美国Ｌｉｎｃｏ公司产品），测定了糖耐量正常（ＮＧＴ）对照组者（Ａ组，４９例）、型ＤＭ血缘亲属ＮＧＴ者（Ｂ组，５２例）、ＩＧＴ／空腹血糖升高（ＩＦＧ）者（Ｃ组，３３例）和新诊断的２型     

糖尿病患者维生素D_3水平与糖耐量试验后胰岛素释放的关系

目的　探讨Ⅱ型糖尿病患者血维生素Ｄ３（ＶＤ３）水平对胰岛素分泌及血糖的影响。方法　用非水反相色谱法测定了４５ 例Ⅱ型糖尿病病人血ＶＤ３ 水平及糖耐量后葡萄糖及胰岛素水平。结果　Ⅱ型糖尿病病人血ＶＤ３ 水平显著低于正常人。糖耐量３０ 及６０ｍｉｎ 胰岛素水平与ＶＤ３ 水平呈正相关（ Ｐ ＜ ０－０１, Ｐ＜ ０－０１）。糖耐量后３０、６０ 及１２０ｍｉｎ 葡萄糖水平与ＶＤ３ 水平呈负相关（ Ｐ＜ ０－０５,Ｐ＜０－０５）。结论　Ⅱ型糖尿病病人存在ＶＤ３ 缺乏。ＶＤ３ 缺乏可能与Ⅱ型糖尿病患者餐后胰岛素分泌不足有关。ＶＤ３ 缺乏可能是Ⅱ型糖尿病餐后高血糖的原因之一     

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…     

Relationship between proinsulin and beta cell function in different states of glucose tolerance

To measure proinsulin concentrations in different states of glucose tolerance and examine the relationship between proinsulin and beta cell function. Serum true insulin (TI), proinsulin (PI), immunoreactive insulin (IRI), C peptide (CP) and blood glucose (BG) levels were measured in the fasting state and during an oral glucose tolerance test (OGTT) in 32 individuals with normal glucose tolerance (NGT), 42 individuals with impaired glucose tolerance (IGT), and 54 individuals with newly diagnosed type 2 diabetes mellitus. All participants were also subdivided into nonobese [body mass index (BMI) <25?kg/m²] and obese (BMI ??25?kg/m²) subgroups. The levels of TI, PI, IRI and CP were higher in obese patients compared with the corresponding NGT subgroup, whereas there was no difference in PI/TI. The levels of IRI, PI and PI/TI were higher in nonobese patients with type 2 diabetes mellitus than in the corresponding NGT subgroup. The levels of PI and TI increased in obese patients with NGT and IGT, whereas PI/TI did not change. In contrast, PI increased but TI did not in subjects with newly diagnosed diabetes mellitus, which led to an increase in PI/TI, and a decrease in beta cell function. Therefore, PI and the PI/TI ratio could offer markers for beta cell dysfunction in DM.     

不同糖耐量个体血清瘦素水平与特异胰岛素、胰岛素原及胰岛素敏感性的关系探讨

目的　研究不同糖耐量人群空腹瘦素水平与特异胰岛素、胰岛素原及胰岛素敏感性之间的关系。方法　用放射免疫法测量 5 4例正常糖耐量 (NGT)、33例糖耐量低减 (IGT)、4 7例新发 2型糖尿病 (DM )的空腹瘦素水平、口服葡萄糖耐量试验 (OGTT) 0、1/2、1、2h的特异胰岛素 (SI)和胰岛素原 (PI)。结果　 (1)多元逐步回归分析显示 ,性别、体重指数 (BMI)、胰岛素敏感性指数是影响空腹瘦素水平最重要的因素 (校正的R2 分别为 0 .2 5 1、0 .4 19、0 .4 38,P值分别为 <0 .0 0 1、<0 .0 0 1、<0 .0 5 ) ;空腹血清瘦素水平与OGTT各时间点PI、SI、PI/SI值无相关性。 (2 )在校正性别、BMI等影响因素后 ,空腹血清瘦素水平在不同糖耐量组差异无显著性 ;DM组OGTT各时间点PI/SI值明显高于IGT组和NGT组 (P <0 .0 1) ;胰岛素敏感性 (ISI)为NGT组 >IGT组 >DM组 (P <0 .0 0 1)。结论　在测定特异胰岛素、胰岛素原时 ,血清瘦素水平除了与性别、BMI相关外 ,尚与胰岛素敏感性 (按SI水平计算 )相关 ;不同糖耐量状态对血清瘦素水平无明显影响 ;DM组存在胰岛素不敏感、PI/SI失调     

Relative hyperproinsulinemia as a sign of islet dysfunction in women with impaired glucose tolerance.

Proinsulin release is increased relative to insulin secretion in subjects with type 2 diabetes, indicative of islet dysfunction. However, it has not been conclusively shown whether there is an increased relative proinsulin release in subjects with impaired glucose tolerance (IGT), i.e. whether it precedes the development of diabetes. We therefore determined the proinsulin to insulin ratios in the fasting state and after acute stimulation of insulin secretion in 23 postmenopausal women, aged 61-62 yr (mean +/- SD, 61.7 +/- 0.5 yr). Ten women had normal glucose tolerance (NGT), and 13 had IGT. The groups were matched for insulin sensitivity and did not differ in body mass index. Proinsulin and insulin secretion were measured after arginine stimulation (5 g, i.v.) at three glucose levels (fasting, 14 mmol/L, and >25 mmol/L), and the acute insulin (AIR(arg)) and proinsulin responses (APIR(arg)) were calculated as the mean 2-5 min postload increase. At fasting glucose, levels of insulin, proinsulin, or the proinsulin/insulin ratio (13.6 +/- 5.0% vs. 11.1 +/- 2.7%; P = NS) did not differ between NGT and IGT. Although the AIR(arg) values were decreased in the IGT group at all glucose levels (P < 0.05), the absolute proinsulin levels and the APIRs(arg) were similar between IGT and NGT women. Therefore, the IGT women had higher proinsulin/insulin ratios at 14 mmol/L (10.7 +/- 4.4% vs. 6.4 +/- 1.8%; P = 0.006) and more than 25 mmol/L glucose (11.4 +/- 5.2% vs. 6.7 +/- 2.1%; P = 0.007). The IGT group had increased APIR(arg)/AIR(arg) at fasting (2.2 +/- 1.4% vs. 1.3 +/- 0.6%; P = 0.047) and more than 25 mmol/L glucose (3.5 +/- 1.6% vs. 2.3 +/- 0.7%; P = 0.037). We conclude that women with IGT exhibit increased relative proinsulin secretion, suggesting a defect in the intracellular proinsulin processing before diabetes develops.     

Evidence against a rate-limiting role of proinsulin processing for maximal insulin secretion in subjects with impaired glucose tolerance and beta-cell dysfunction

In subjects with impaired glucose tolerance (IGT) insulin secretion is impaired. Increased proinsulin/insulin (PI/I) ratios suggest that there is also reduced processing of proinsulin to insulin in this condition. The PI/I ratio in the insulin secretory granule is ideally assessed by plasma measurements in response to acute stimulation of insulin secretion. In the present study we tested the hypothesis that maximal stimulation of insulin secretion results in exhaustion of the proinsulin conversion pathway to insulin. We therefore determined the PI/I ratio in 11 normal glucose-tolerant subjects (NGT) and 11 subjects with IGT in response to glucose (squarewave hyperglycemic clamp, 10 mmol/L), glucagon-like peptide-1 (GLP-1; primed-continuous infusion), and arginine given during the continued GLP-1 infusion. In IGT, insulin levels were significantly lower during the first phase (144 +/- 20 vs. 397 +/- 119 pmol/L; P = 0.02), at the end of the GLP infusion (2142 +/- 350 vs. 5430 +/- 1091 pmol/L; P: = 0.002), and in response to arginine (3983 +/- 375 vs. 8663 +/- 1430 pmol/L; P = 0.005). In response to glucose, the minimum PI/I ratio was significantly higher in IGT (3.4 +/- 0.6%) than in NGT (1.4 +/- 0.5%; P = 0.02), suggesting defective proinsulin processing in this condition. In subjects with IGT, the PI/I ratio decreased significantly after GLP-1 priming (1.7 +/- 0.2%; P = 0.02) and after arginine given during GLP-1 (1.4 +/- 0.2%; P = 0.007) and was not significantly different from those values in NGT (1.3 +/- 0.2% and 1.3 +/- 0.2%, respectively; both P = NS). In conclusion, during maximal stimulation of insulin secretion in subjects with IGT, the PI/I ratio in plasma decreased significantly and was not different from that in normal controls. This strongly argues against the hypothesis that defective processing of proinsulin to insulin represents a major component of the beta-cell dysfunction in IGT.     

Polymorphism Ncol in tumor necrosis factor B is associated with fasting glycemia and lipid parameters in healthy non-obese caucasian subjects

BACKGROUND: The study was designed to investigate the associations among polymorphisms TNF-B Ncol and TNF-alpha -308G/A, plasma TNF-alpha levels and metabolic and anthropometric parameters related to insulin sensitivity in a set of 113 Caucasian subjects undergoing oral glucose tolerance test (oGTT). METHODS: Genotypes were detected by PCR; BMI, WHR, glycemia during oGTT, fasting immunoreactive insulin, fasting C-peptide, HbA(1c), total cholesterol, triglycerides, HDL, LDL and plasma TNF-alpha levels were measured in each subject. RESULTS: Type 2 diabetes was diagnosed in 10 subjects, impaired glucose tolerance (IGT) in 41, normal glucose tolerance (NGT) in 62. Significant differences among genotypes of the TNF-B Ncol were observed for FPG (P=0.0063), LDL (P=0.0179) and marginally for total cholesterol (P=0.0763) in NGT group. After the classification of NGT subjects into obese and non-obese according to BMI, associations of TNF-B Ncol with FPG, LDL and cholesterol were proved in non-obese subgroup only. TNF-alpha -308G/A polymorphism was not associated with any of the parameters studied. TNF-alpha levels did not revealed difference among NGT, IGT and DM groups or genotype-dependent differences. CONCLUSIONS: Our results indicate significant association of the TNF-B Ncol polymorphism with FPG, LDL and total cholesterol in normoglycemic non-obese Caucasian subjects. This polymorphism could be involved in genetic modulation of glucose and lipid homeostasis and regulation of insulin sensitivity already in healthy state. Disturbances of this regulation could be component of pathogenesis of type 2 diabetes mellitus.     

Insulin secretion and insulin sensitivity in Japanese subjects with impaired fasting glucose and isolated fasting hyperglycemia

Impaired fasting glucose (IFG) is a subgroup of impaired glucose regulation exhibiting an elevated fasting glucose levels without elevated 2-h glucose levels on oral glucose tolerance test (OGTT). Diabetes mellitus with isolated fasting hyperglycemia (DM/IFH) is a similar subgroup of diabetes having higher fasting glucose levels with 2-h glucose levels within the non-diabetic range. The aim of this study is to profile the characteristics of these subgroups to estimate the factors involved in the development from normal glucose tolerance (NGT) via IFG to DM/IFH. Five hundred and sixty seven Japanese males were classified on the basis of 75 g OGTT into four groups, NGT, IFG, DM/IFH, and isolated impaired glucose tolerance (isolated IGT). Insulin secretion was evaluated by insulinogenic index, insulin sensitivity was evaluated by ISI composite, and insulin secretory patterns were compared additionally. IFG and DM/IFH subjects exhibited both lower insulin secretion and lower insulin sensitivity than NGT subjects. There was an insulin peak in NGT, IFG, and DM/IFH at 60 min, which did not occur in isolated IGT. Impaired early-phase and basal insulin secretion and decreased insulin sensitivity both are estimated as factors in progression from NGT via IFG to DM/IFH in these subjects. IFG and DM/IFH subjects have definite fasting hyperglycemia in contrast to isolated IGT subjects, 2-h glucose levels being maintained within the non-diabetic range partly by the insulin peak at 60 min.     

Proinsulin in girls: relationship to obesity,hyperinsulinemia, and puberty

In adults with impaired glucose tolerance (IGT) and obesity (OB), an elevated proinsulin (PI) is predictive of type 2 diabetes mellitus (DM) and precedes the diagnosis by 5-20 yr. In type 2 DM, the PI is disproportionately elevated, i.e. increased PI/insulin ratio (PI/I). Few studies have evaluated PI in children at risk for type 2 DM. In the face of the current epidemic, we evaluated the relationship of PI and PI/I to IGT, insulin resistance (IR) defined by homeostasis model of assessment (HOMA), degree of OB, and stage of puberty in 70 girls (mean age 10.8 yr; body mass index z-score 3.5; ethnicity 64% Hispanic, 19% white, 16% African-American, and 1% other). Family history of DM was reported in 83%, and acanthosis nigricans was present in 80%. Subjects underwent a 2-h oral glucose tolerance test with glucose, insulin, and PI determinations every 30 min. All had normal hemoglobin A1c and fasting glucose. Five had IGT. With higher HOMA-IR, PI increased (P < 0.05), yet the ratio of fasting PI/I was lower (P < 0.05). Girls with body mass index z-score greater than 4 (n = 29) had higher PI than nonobese girls (n = 19, P < 0.05), but PI/I ratios were not different. PI-0 was increased in late puberty (n = 29), compared with prepuberty (n = 26, P < 0.05), but PI/I ratios showed no statistical difference. We found PI increased with increasing IR and OB in girls. Overall, PI/I was not different, suggesting the elevated PI reflects increased beta-cell output proportional to the elevated insulin in these groups and not a defect in PI processing or secretion. In fact, the lower fasting PI/I of the highest HOMA-IR quartile vs. the lowest HOMA quartile indicates more efficient conversion of PI to I in the presence of increasing IR in these girls.     

Proinsulin in pregnant women with normal glucose tolerance or mild gestational diabetes mellitus.

Pregnancy is characterized by peripheral insulin resistance, which is physiologically compensated by an increase in insulin secretion. Type 2 diabetes and impaired glucose tolerance (IGT) have been associated with an inappropriate increase in insulin precursors, namely proinsulin. The aim of this study was to determine levels of proinsulin (PI), specific insulin (SI) and the proinsulin-to-specific insulin (PI/SI) ratio in consecutive pregnant women (n = 209) with normal glucose tolerance (NGT), as assessed by a 2h oral glucose tolerance test, and with mild gestational diabetes (GDM), in comparison to 32 healthy, non-pregnant women. Furthermore, we related these variables to surrogate markers of insulin resistance and insulin secretion. We found no significant differences in the levels of PI and the PI/ SI ratio between pregnant and non-pregnant women (PI: 5.0 +/- 3.6 vs. 4.8 +/- 3.5 pmol/L, p = NS), and between pregnant women with mild GDM and NGT (PI: 5.4 +/- 2.4 vs. 4.9 +/- 3.9 pmol/L, p = NS). SI was elevated in women with mild GDM (112.2 +/- 47.3 vs. 94.8 +/- 43.0 pmol/L in NGT, p=0.02). PI was related to fasting glucose (r = 0.17, p < 0.02), but not post-load glucose levels, and to fasting insulin [specific insulin: r = 0.67, p = 0.0001; total immunoreactive insulin (IRI): r = 0.69, p = 0.0001], as well as post-load insulin levels (IRI at 120 min: r = 0.18, p < 0.03). The PI/SI ratio showed no association with fasting or post-load glucose or insulin levels. Pregnant women presented with a metabolic pattern suggestive of enhanced insulin resistance, namely increased fasting and post-load insulin levels. In women with mild GDM, fasting and post-load hyperglycemia, as well as an additional increase in insulin resistance was found. Group differences weakened when accounting for differences in body weight. The data of the present study suggest that in normal pregnancy as well as mild GDM metabolic alterations including enhanced insulin resistance and hyperglycemia do not result in an increase in circulating levels of proinsulin, both in absolute terms and relative to levels of specific insulin, as indicated by the proinsulin-to-specific insulin ratio.     

Diabetes and impaired glucose tolerance prevalences in Turkish patients with impaired fasting glucose

Impaired fasting glucose (IFG) like impaired glucose tolerance (IGT) has increased risk of progressing to diabetes mellitus (DM). The aim of the study was to evaluate prevalance of IGT and type 2 DM with oral glucose tolerance test (OGTT) in Turkish patients who had fasting glucose of 110 and 125 mg/dl. Hundred and forty-eight (67.3%) women and 72 (32.7%) men (30-65 years old with mean age of 51.3 +/- 8.7 year) who had fasting glucose range 110-125 mg/dl were evaluated with OGTT. Seventy-two patients had IGT (32.8%), 74 (33.6%) patients had type 2 diabetes and 74 (33.6%) patients had normal glucose tolerance (NGT). Mean fasting glucose and insulin levels were higher in the IGT group than in the NGT group. Mean level of total cholesterol was higher in DM than that in NGT and IGT groups. Mean triglyceride (TG) (P = 0.476), high-density lipoprotein (HDL) (P = 0.594), low-density lipoprotein (LDL) (P = 0.612), Apoproteine A (P = 0.876), Apoproteine B (P = 0.518), uric acid (P = 0.948) and ferritin (P = 0.314) were found higher in diabetic patients. Lipoproteine a (P = 0.083), fibrinogen (P = 0.175) and hsCRP (P = 0.621) levels were higher in IGT. Mean HOMA S% levels of NGT, IGT and DM were found to be 65.0 +/- 13.0%, 60.9 +/- 16.0% and 50.1 +/- 11.1%, respectively. HOMA B% levels were measured to be 80.4 +/- 29.1% in NGT, 85.3 +/- 14.59% in IGT and 60.1 +/- 10.1% in DM. Significant difference was found between IFG and DM (P = 0.043) groups. The prevalences of diabetes and IGT were found to be 33.63 and 32.7% in IFG, respectively.