Ⅱ型糖尿病并发脑梗塞与高胰岛素血症的关系探讨

检测２１例正常人（Ｉ组）、３２例非糖尿病伴脑梗塞患者（Ⅱ组）、３８例Ⅱ型糖尿病无脑梗塞患者（Ⅲ组）和３８例Ⅱ型糖尿病伴脑梗塞患者（Ⅳ组）血清葡萄糖、胰岛素、Ｃ肽水平，并计算胰岛素敏感性指数（血糖／胰岛素，ＩＳＩ）、胰岛素／Ｃ肽比值及胰岛素、Ｃ肽释放试验曲线下面积。结果：Ⅳ组患者血清空腹胰岛素水平、胰岛素／Ｃ肽比值及胰岛素曲线下面积高于Ⅰ、Ⅱ、Ⅲ组患者，空腹Ｃ肽值和Ｃ肽曲线下面积高于Ｉ组患者，而ＩＳ     

糖尿病并高血压患者高胰岛素血症初步探讨

对16例NIDDM合并高血压而无心、肾功能损害者与16例NIDDM血压正常者进行配对研究。同步检测空腹及馒头试验后血糖、胰岛素、C-肽等指标。NIDDM合并高血压组血清胰岛素水平、胰岛素/C-肽值明显高于NIDDM血压正常组,而胰岛素敏感指数则明显降低。结果表明,NIDDM合并高血压与高胰岛素血症有关,后者主要是由于肝脏对胰岛素清除率降低所致。     

高血压脂代谢异常与高胰岛素血症的关系

对３５例原发性高血压患者的血糖、血清胰岛素、Ｃ－肽和血脂测定结果与１２例正常血压者进行比较分析。因压组与正常血压组血糖均在正常范围。血清ＩＳ以高血压组明显增高。胰岛素释放指数亦以高血压组为高。高血压组ＨＤＬ．ＬＤＬ，ＡｐｏＡ／ＡｐｏＢ均明显低于正常血压组；前者血清ＩＳ水平与ＡｐｏＡ／ＡｐｏＢ比值呈显著负相关，血清胰岛素放指数与ＡｐｏＡ／ＡｐｏＢ比值也呈明显负相关。     

老年高血压病患者胰岛素抵抗及药物干预的观察

观察了１６例老年高血压病（ＥＨ）患者及１０例健康老年人口服葡萄糖耐量试验（ＯＧＴＴ）的血糖、胰岛素和Ｃ－肽浓度变化。结果显示，ＥＨ组空腹及ＯＧＴＴ后胰岛素、Ｃ－肽及胰岛素／血糖比值明显高于对照组，Ｃ－肽／胰岛素比值明显降低，糖耐量明显下降。老年ＥＨ组经伊拉地平治疗６周后，空腹及ＯＧＴＴ后胰岛素，Ｃ－肽和胰岛素／血糖比值较治疗前上明显下降，Ｃ－肽／胰岛素比值升高，糖耐量改善，但仍未完全恢复正常。提示老年ＥＨ患者存在胰岛素抵抗（ＩＲ），伊拉地平能在一定程度上改善ＥＨ患者的ＩＲ。     

Ⅱ型糖尿病伴高血压患者胰岛素,胰高血糖素水平

配对观察６８例Ⅱ型糖尿病伴高血压和无高血压和无高血压患者ＯＧＴＴ中的血糖，胰岛素、Ｃ肽、胰高血糖素等指标。结果显示伴高血压组患者、胰岛素、胰高血糖素在各时相、Ｃ肽在空腹１２０ｍｉｎ，１８０ｍｉｎ均明显高于无高血压组，而血糖／胰糖素各时相则低于无高血压组。     

高胰岛素血症的高血压患者肾素─血管紧张素─醛固酮系统的变化

本文对３５例原发性高血压患者糖耐量试验前后的血压、血糖、胰岛素、Ｃ肽及肾素－血管紧张素－醛固酮系统（ＲＡＡＳ）进行测定及监测，并与正常人对照。结果显示：高血压病组存在高胰岛素血症及胰岛素抵抗现象，ＲＡＡＳ反应性增高。表明高胰岛素血症的高血压患者其ＲＡＡＳ的变化，在高血压的发病中起着一定作用，由糖负荷诱导的急性血压升高及ＲＡＡＳ的变化，在有胰岛素抵抗的高血压患者要比正常人更为明显。高胰岛素血症患者的ＲＡＡＳ持久性反应增高可能是促进高血压病进展的原因之一。     

老年高血压病患者胰岛素抑抗及药物干预的观察

观察了１６例老年高血压病（ＥＨ）患者及１０例健康老年人口服葡萄糖耐量试验（ＯＧＴＴ）的血糖、胰岛素和Ｃ－肽浓度变化。结果显示，ＥＨ组空腹及ＯＧＴＴ后胰岛素／血糖比值明显高于对照组，Ｃ－肽／胰岛素比值明显降低，静糖耐量明显下降。老年ＥＨ组经伊拉地平治疗６周后，空腹及ＯＧＴＴ后胰岛素，Ｃ－肽和胰岛素／血糖比值较治疗前上明显下降，Ｃ－肽／胰岛素比值升高，糖耐量改善，但仍未完全恢复正常。提示老年ＥＨ患者存     

肥胖患者运动血压与血糖、血浆胰岛素水平的关系

目的探讨肥胖患者运动血压与血糖、血浆胰岛素水平的关系.方法选取完成次极量踏车运动试验的49例肥胖患者(Obesity)及45例体重正常的对照组(Control),比较其静态血压(RBP)、运动血压(PBP)及空腹和口服75克葡萄糖2小时后血糖、血浆胰岛素水平.并分析肥胖组中合并运动性高血压(PBP1)与运动血压正常者(PBP2)的血糖、胰岛素水平.结果静态下两组血压无显著差异,负荷试验后达到运动性高血压标准者,肥胖组21/49例(42.8%),对照组8/45例(17.8%),P<0.01;运动后肥胖组的收缩压与舒张压均较对照组升高,特别是收缩压升高更明显;两组空腹血糖无显著差异,肥胖组的空腹胰岛素、餐后2小时血糖及胰岛素均明显高于对照组;肥胖组中伴运动性高血压者的餐后2小时血糖、胰岛素水平均高于不伴运动性高血压的肥胖患者.结论肥胖患者血压、血糖升高可能与胰岛素水平升高有关.     

老年高血压病患者血清真胰岛素、C肽水平及替米沙坦的干预作用

目的通过对老年高血压非糖尿病患者血清真胰岛素、C肽、血糖的观察,探讨高胰岛素血症、胰岛素抵抗(IR)与老年高血压的关系,以及替米沙坦干预的影响。方法测定20例非肥胖型老年高血压病患者(NHT组),15例肥胖型老年高血压病患者(OHT组)及20例健康老年人(对照组)的空腹血糖、真胰岛素、C肽、血脂、血尿酸和IR指数、胰岛β细胞功能指数。高血压病患者予以替米沙坦(80 mg,1次/d口服)治疗,4 w后复查,观察治疗前后血压和上述指标的变化。结果本研究的3组患者年龄、性别、空腹血糖状况相匹配。OHT组和NHT组血清真胰岛素、C肽水平及IR指数(HOMA-IR)和胰岛β细胞功能指数(HOMA-islet)均高于健康对照组。高血压病患者经替米沙坦治疗后血压、真胰岛素、C肽水平及HOMA-IR和HOMA-islet指数较治疗前均明显下降,差异具有显著性(P<0.05)。结论老年高血压非糖尿病患者,特别是伴有肥胖者,存在IR、高胰岛素血症及代偿性胰岛β细胞功能增高。替米沙坦除了具有强效降低血压的作用外,还具有改善IR和胰岛β细胞功能的作用。     

肥胖患者运动血压与血糖、血浆胰岛素水平的关系

目的　探讨肥胖患者运动血压与血糖、血浆胰岛素水平的关系。方法　选取完成次极量踏车运动试验的 49例肥胖患者 (Obesity)及 45例体重正常的对照组 (Control) ,比较其静态血压 (RBP)、运动血压 (PBP)及空腹和口服 75克葡萄糖 2小时后血糖、血浆胰岛素水平。并分析肥胖组中合并运动性高血压 (PBP1)与运动血压正常者 (PBP2 )的血糖、胰岛素水平。结果　静态下两组血压无显著差异 ,负荷试验后达到运动性高血压标准者 ,肥胖组 2 1/ 49例 (42 8% ) ,对照组 8/ 45例 (17 8% ) ,P <0 0 1;运动后肥胖组的收缩压与舒张压均较对照组升高 ,特别是收缩压升高更明显 ;两组空腹血糖无显著差异 ,肥胖组的空腹胰岛素、餐后 2小时血糖及胰岛素均明显高于对照组 ;肥胖组中伴运动性高血压者的餐后 2小时血糖、胰岛素水平均高于不伴运动性高血压的肥胖患者。结论　肥胖患者血压、血糖升高可能与胰岛素水平升高有关     

Serum Insulin Level Versus Blood Pressure: A Cross-sectional,Case-controlled Study in Non-obese,Middleaged Japanese Subjects with Normal Glucose Tolerance

To assess the relationship between blood pressure (BP) and serum insulin level in nonobese (body mass index (BMI) ≤ 27 kg m^?2), middle-aged (40–64 years of age) Japanese subjects with normal glucose tolerance, a three-phase study protocol was designed. First, the responses of plasma glucose and serum insulin to an oral glucose load were compared between 40 patients with untreated essential hypertension and 40 age-, sex- and BMI-matched normotensive control subjects. Second, the glucose and insulin responses to an i.v. glucose load were evaluated in 7 non-obese hypertensive, 7 non-obese normotensive and 7 obese hypertensive subjects. Third, BP and serum lipid profile were compared between 21 hyperinsulinaemic (serum insulin level (while fasting, after glucose loading, or both) > 2 SDs higher than the mean) and 21 age-, sex- and BMI-matched normoinsulinaemic subjects (serum insulin level within 1 SD of the mean). The glucose and insulin responses to the oral glucose load were comparable between the hypertensive and normotensive groups. Similarly, the glucose and insulin responses to the i.v. glucose load were comparable between the non-obese hypertensive and normotensive groups, whereas the mean AUC_insulin in the obese hypertensive group was significantly greater (p < 0.01) than that in either of the non-obese groups. The respective mean values for systolic and diastolic BPs did not differ between the hyperinsulinaemic and normoinsulinaemic groups. The mean serum triglyceride and HDL cholesterol concentrations were significantly higher (p < 0.01) and lower (p < 0.05), respectively, in the hyperinsuslinaemic than in the normoinsulinaemic group. The results suggest no association between serum insulin level and BP in non-obese, middle-aged, Japanese subjects with normal glucose tolerance.     

长期口服苯那普利对绝经前高血压妇女胰岛素抵抗的影响

目的 :观察绝经前高血压患者口服苯那普利 6个月对胰岛素抵抗 ( IR)的影响。方法 :治疗前后观察血压、体重、体重指数 ;酶法测定口服糖耐量和血脂蛋白 ;放射免疫法测定血胰岛素( INS)和 C肽 ( CP)释放 ,并计算胰岛素敏感性指数 ( ISI)及曲线下面积 ( AUC)。结果 :治疗后与治疗前相比 ,IR组和胰岛素敏感性正常 ( NIS)组血压均明显降低 ( P <0 .0 1 ) ,IR组 ISI显著增高( P <0 .0 5) ,FINS、INS1h、INS2 h、INS3 h及 INS- AUC和 CP2 h、CP3 h及 CP- AUC则明显降低 ( P <0 .0 5～ 0 .0 1 ) ;NIS组治疗前后上述指标无明显改变。两组治疗前后的血糖和脂蛋白无显著改变。结论 :在绝经前高血压 ,口服苯那普利有效降压的同时 ,明显改善存在的 IR。     

高血压病合并脂肪肝发病的危险因素分析

目的探讨高血压病合并脂肪肝发病的危险因素。方法选择进行了肝脏B超检查的住院高血压病患者,根据超声影像的诊断结果分为高血压合并脂肪肝组(98例)和高血压未合并脂肪肝组(102例),分析体重指数(BMI)、收缩压(SBP)、舒张压(DBP)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、γ-谷氨酰转肽酶(GGT)、胰岛素抵抗指数(HO-MA-IR)、糖耐量试验各时段的血糖水平、胰岛素释放试验的胰岛素水平与脂肪肝之间的关系。结果(1)Logistic回归分析的结果表明空腹血糖升高、肥胖、糖负荷后3小时胰岛素水平升高、高甘油三酯血症是高血压患者脂肪肝形成的独立危险因素;(2)高血压合并脂肪肝组的HOMA-IR、TG、空腹和糖负荷后2、3小时的血糖和胰岛素水平高于对照组(均P<0.05)。校正两组BMI后,上述差异仍然存在。结论(1)高血压病患者脂肪肝发病的独立危险因素是空腹血糖升高、肥胖、糖负荷后3小时胰岛素水平升高、高甘油三酯血症,随着这些危险因素的聚集,脂肪肝的检出率增加。(2)脂肪肝是高血压病患者胰岛素抵抗的“重要标志”,脂肪肝是代谢综合征的一种表现。     

Hyperinsulinemia and dyslipidemia in non-obese, normotensive offspring of hypertensive parents in northern India.

Insulin resistance contributes to initiation and acceleration of hypertension and atherosclerosis. This study attempted to detect occurrence of pre-hypertensive metabolic abnormalities, including hyperinsulinemia, in the offspring of hypertensive patients. Thirty-eight healthy offspring of hypertensive parents (group I, mean age 23.6+/-3.7 years) and 18 control offspring of normotensive parents (group II, mean age 24.2+/-2.8 years) were clinically examined, subjected to oral glucose tolerance test (OGTT), and the samples were analysed for blood glucose, insulin and lipid profile. Subjects in group I with fasting serum insulin <90 nmol/L constituted group Ia (n = 23, 62%) and those with >90 nmol/L constituted group Ib (n = 15, 38%). Both groups consisted of non-obese and normotensive subjects matched for body mass index and waist-hip ratio. There were no statistically significant differences in blood glucose levels between groups Ia, Ib and II during OGTT. Serum insulin levels during OGTT in group I were significantly higher than in group II (p<0.05), except at 30 min. Fasting insulin and 2 h post-OGTT insulin in group Ib were significantly higher than the other groups. Serum triglyceride levels, though within normal range, were higher in group I than group II (p<0.01). Similarly, high-density lipoprotein cholesterol levels in groups Ia and Ib were lower than those observed in group II (p<0.01). In conclusion, non-obese, normotensive offspring of hypertensive parents were observed to be hyperinsulinemic and dyslipidemic at an early age. These metabolic abnormalities may be associated with hypertension, glucose intolerance and accelerated atherosclerosis in adulthood.     

Serum ferritin, LDL oxidation and risk factors for atherogenesis in healthy offspring of hypertensive patients

Iron is an important factor in the process of oxidation stress and atherogenesis which is as a rule potentiated in subjects with the insulin resistance syndrome. Hypertension is one of the main components of this syndrome. Ferritin due to its relationship with impaired insulin sensitivity becomes a candidate for a new indicator of insulin resistance. The subject of the present study was to assess whether we shall find in young healthy offspring of hypertensive parents changes in the ferritin level, oxidizability of LDL and whether these are related to parameters of glucose tolerance, insulin secretion and sensitivity. Twelve young (27 +/- 3.6 years) non-obese, normotesive offspring of hypertensive parents were compared with a group of 14 controls. Glucose tolerance, insulin secretion and sensitivity were examined by means of a hyperglycaemic clamp and oGTT. As to the ferritin level, the offspring of hypertensive parents did not differ significantly from controls, differences were not fond in the oxidizability of LDL-C. The glucose tolerance was comparable in the two groups. Offspring of hypertensive parents had however a significantly higher insulin and C peptide level when using the clamp and during the glucose tolerance test (p < 0.05), and a reduced insulin sensitivity (p < 0.05). The negative correlation between the index of insulin sensitivity and ferritin suggests that ferritin could be associated with the syndrome of insulin resistance.     

Insulinemia and blood pressure responses to oral glucose load in primary hypertensive patients.

Fourteen hypertensive patients and 14 normotensive control subjects were submitted to the oral glucose test and their plasma potassium, glucose and insulin levels were measured. Cardiovascular responses were evaluated by blood pressure and pulse rate measurements. Five of 14 hypertensive patients were hyperinsulinemic and had higher blood glucose levels, suggesting insulin resistance. Systolic blood pressure, heart rate and double product increased significantly in normotensive subjects and slightly in hyperinsulinemic patients, but not in normoinsulinemic hypertensive patients. These results seem to indicate the presence of insulin resistance in a particular group of primary hypertensive patients and a smaller cardiovascular response after glucose overload.     

Normalization of Insulin Resistance in Non-Obese Essential Hypertension by Cilazapril Treatment

To determine whether ACE inhibitor other than captopril improves insulin sensitivity in patients with essential hypertension, we measured insulin sensitivity to glucose utilization using SSPG method in 10 lean hypertensive subjects before and after chronic cilazapril treatment (1.5±0.2 mg/day, 15.6±2.1 weeks). The results were compared with those obtained in 10 healthy control subjects. SSPG obtained by insulin sensitivity test was significantly higher in hypertensive subjects, indicating a lower insulin sensitivity than in controls. After cilazapril treatment, SSPG reduced significantly to the level which was statistically not different from control subjects. Hyperinsulinemia diminished after treatment, while no significant change of blood glucose was observed during oral glucose tolerance test in hypertensive subjects. Plasma HDL cholesterol increased by cilazapril treatment. Cilazapril treatment has beneficial effect in the reversal of insulin resistance in patients with essential hypertension.     

Tumor necrosis factor [alpha ] -238 and -308 polymorphisms do not associate with insulin resistance in hypertensive subjects

It is well established that, as a group, patients with essential hypertension are characterized by insulin resistance. Previous studies have shown that a biallelic polymorphism in the tumor necrosis factor (TNF)alpha promoter position -308 and -238 might be involved in the insulin resistance state in diabetic and/or nondiabetic subjects. We determined these polymorphisms in 235 nondiabetic hypertensive subjects and 246 unrelated normotensive controls. Fasting plasma glucose, insulin, lipoprotein, leptin, and TNFalpha concentrations were measured, in addition to plasma glucose and insulin responses to a 75-g oral glucose tolerance test (OGTT). Insulin sensitivity was also determined by an insulin suppression test in 69 hypertensive and 76 normotensive individuals. The results showed no association of these genotypic distributions between hypertensive and normotensive individuals both at -308 (GG, GA, and AA were 80.9%, 17.9%, and 1.3% in hypertensives, 84.2%, 15.4%, and 0.4% in normotensives, chi(2) = 1.68, P =.432) and at -238 (GG, GA, and AA were 98.3%, 1.7%, and 0% in hypertensives, 96.7%, 3.3%, and 0% in normotensives, chi(2) = 1.19, P =.276) sites. These results did not change even after adjustment for values of age and body mass index (BMI). Anthropometric measurements, fasting plasma glucose, insulin, lipoprotein concentrations, glucose, and insulin responses to OGTT, TNFalpha, and leptin concentrations were similar between the genotype at the -308 site both in hypertensive and normotensive groups. Insulin sensitivity, either measured by an insulin suppression test or homeostasis model assessment (HOMA) index, did not differ between the genotype at the -308 site in subjects with hypertension or normotension. Fasting plasma TNFalpha (10.2 alpha 0.5 pg/mL v 10.1 +/- 0.5 pg/mL, P =.928) concentrations did not differ between hypertensive and normotensive subjects even after adjustment for body fat and BMI values. We conclude that TNFalpha promoter gene polymorphisms at position -238 and -308 do not play a major role in the pathogenesis of insulin resistance in Chinese subjects with or without hypertension.     

左旋氨氯地平对原发性高血压患者胰岛素敏感性的影响

目的撅讨左旋氨氯地平对原发性高血压患者胰岛素敏感性的影响。方法将51例原发性高血压并糖耐量异常患者随机分为观察组和对照组,对照组常规使用卡托普利治疗,观察组在对照组基础上加用左旋氨氯地平2．5mg,每天1次,治疗12周比较两组血压、空腹以及餐后血糖、空腹以及餐后血胰岛素、胰岛素敏感指数（ISI）、抵抗指数（HOMA-IR）和血脂的变化。结果治疗12周观察组空腹以及餐后血糖、空腹以及餐后血胰岛素、HOMA-IR显著降低,ISI显著升高,与对照组比较差异有显著性（P〈0．05）。同时观察组收缩压和舒张压水平显著降低,与治疗前和对照组比较差异均有届著性（P〈0．05）。但血脂无显著改变。结论长效钙通道阻滞剂左旋氨氯地平对高血压患者胰岛素的敏感性具有增强作用,可改善原发性高血压患者胰岛素抵抗。