依那普利对高血压病患者血胰岛素水平的影响

目的：探讨依那普利对高血压病患者胰岛素抵抗的影响。方法；对３８例高血压病患者和１８例健康对照者行口服葡萄糖耐量试验，测定其血糖和血胰岛素水平，计算其释放曲线下面积并于３５例ＥＨ患者接受依那普利降压治疗４周后，进行相同检测。结果：治疗前两组空腹血糖无显著差别，ＥＨ组空腹ＩＳ和服糖后ＧＳ，ＩＳ及其ＡＵＣＧ，ＡＵＣＩ均显著高于对照组，依那普利治疗４周后，糖耐量试验显示糖负荷后１小时，２小时的ＧＳ，ＡＵＣ     

胰岛素治疗高血压动脉硬化性脑梗死的实验研究

目的：观察胰岛素（ Ｉｎｓ）对高血压动脉硬化大鼠脑梗死的疗效。方法：５０ 只肾血管性高血压大鼠（ Ｒ Ｈ Ｒ）复制成大脑中动脉闭塞（ Ｍ Ｃ Ａｏ）模型,随机分４ 组： Ａ 组１２ 只（ Ｉｎｓ ２１ Ｕ／ｋｇ）, Ｂ组１２ 只〔 Ｉｎｓ ２１ Ｕ／ｋｇ＋ ５０％ 葡萄糖（２ ｇ／ｋｇ）〕, Ｃ组 １２ 只〔 Ｉｎｓ ４５ Ｕ／ｋｇ＋ ５０％ 葡萄糖（４ ｇ／ｋｇ）〕和 Ｄ组 １４ 只（生理盐水 ４ ｍ ｌ／ｋｇ）。各组均于 Ｍ Ｃ Ａｏ 后即注射胰岛素, Ｍ Ｃ Ａｏ 后 ４ 小时和２４ 小时检查神经功能,２４ 小时处死大鼠取脑,测大脑体积和梗死灶体积。结果： Ａ 组的血糖较其他组有统计学意义的下降（ Ｐ均＜ ００１）, Ｃ组的神经功能障碍评级、梗死灶体积及其与大脑体积的百分比的减少都有统计学意义（ Ｐ 均＜ ００１）, Ａ、 Ｂ、 Ｄ组间比较则无差异（ Ｐ 均＞００５）。结论：胰岛素对缺血脑组织具有不依赖于其降糖作用的直接保护作用, Ｒ Ｈ Ｒ Ｍ Ｃ Ａｏ 后注射胰岛素在较高剂量时才显示疗效,这可能与高血压致脑血管发生病变有关。     

甘精胰岛素联合阿卡波糖治疗老年2型糖尿病合并脑梗死

【目的】观察甘精胰岛素联合阿卡波糖治疗老年2型糖尿病（T2DM）合并脑梗死的疗效。【方法】80例老年T2DM合并脑梗死患者随机分为观察组和对照组各40例,观察组给予阿卡波糖50mg嚼服,每日3次;同时每天睡前皮下注射甘精胰岛素;对照组给予预混胰岛素优泌林70／30每日早晚餐前30min皮下注射;根据血糖值调整胰岛素用量。观察两组血糖控制、低血糖发生情况。采用神经功能缺损（CNN）评分判定疗效。【结果】治疗后两组空腹血糖（FPG）、餐后2h血糖（2hPG）及糖化血红蛋白（HbA1c）明显下降（P〈0．05）,观察组低血糖发生率明显低于对照组（P〈0．05）;两组治疗后CNN评分均明显改善（P〈0．05）,观察组明显优于对照组（P〈0．05）。【结论】甘精胰岛素联合阿卡渡糖治疗老年T2DM合并脑梗死疗效显著。     

充血性心力衰竭胰岛素抵抗检测方法的探讨

目的：探讨充血性心力衰竭（ＣＨＦ）胰岛素抵抗（ＩＲ）的检测方法。方法：采用放射免疫法测定４１例ＣＨＦ患者和２６例正常人的空腹胰岛素（ＦＩＮＳ）,检测空腹血（ＦＰＧ）水平。比较空腹血糖、胰岛素乘积的倒数（ＩＡＩ）和空腹血糖胰岛素比值（ＦＰＧ／ＦＩＮＳ）的应用价值。结果：ＣＨＦ组ＩＡＩ低于对照组（Ｐ〈０．０１）,并随心功能恶化进一步降低（Ｐ〈０．０５５）;ＣＨＦ组ＦＰＧ／ＦＩＮＳ也低于对照组（Ｐ〈０．００１）,但在心功能之间的差别无显著性意义。结论：ＩＡＩ在心衰的ＩＲ评价中明显优于ＦＰＧ／ＦＩＮＳ。     

老年2型糖尿病患者微量白蛋白尿、血脂、胰岛素水平变化及临床意义

目的 探讨老年２型糖尿病（ＤＭ）患者微量白蛋白尿（ＭＡＵ）、血脂、胰岛素（Ｉｎｓ）水平变化及临床意义。方法 对３０例健康对照老年人、５６例老年２型ＤＭ患者，其中２７例合并ＭＡＵ和２９例未合并ＭＡＵ患者进行血脂、空腹血糖（ＦＢＧ）、Ｉｎｓ水平等测定，并进行比较分析。结果 老年２型ＤＭ患者胆固醇（ＴＣ）、甘油三酯（ＴＣ）、低密度脂蛋白－胆固醇（ＬＤＬ－ｃ）、载脂蛋白Ｂ（ａｐｏＢ）、ＦＢＧ和Ｉｎｓ水平显     

不同剂量卡托普利对高血压胰岛素抵抗干预研究

本文通过４５例高血压病（实验组）口服糖耐量（ＯＧＴＴ）及胰岛素（ＩＳ）释放试验观察，旨在了解高血压病胰岛素抵抗及不同剂量卡托普利对高血压胰岛素抵主胰岛素敏感性指数的干预结果发现，实验组空腹血糖与对照组相仿，糖负荷后，于６０、１２０、１８０ｍｉｎ较对照组明显增高（Ｐ值分别〈０．０５、〈０．０５、〈０．０１）。而ＩＳ各时值明显高于对照组ＣＰ值分别为〈０．０５、〈０．０５、〈０．０５、〈０．０１）胰岛素     

急性脑缺血高血糖与胰岛素抵抗的实验研究

目的：研究大鼠急性脑缺血后血糖变化及其与血浆促肾上腺皮质激素（ＡＣＴＨ）、血浆胰岛素（Ｉｎｓ）含量、肝细胞膜胰岛素受体（ＩｎｓＲ）容量和解离常数（Ｋｄ值）变化间的关系。方法：分别采用放射免疫分析法（ＲＩＡ）、放射受体分析法（ＲＲＡ）测定大鼠大脑中动脉（ＭＣＡ）缺血和再灌注后不同时间点血糖、血浆ＡＣＴＨ和Ｉｎｓ、肝细胞膜ＩｎｓＲ容量和Ｋｄ值。结果：ＭＣＡ缺血后３０分钟至再灌注９６小时血浆ＡＣＴＨ浓度均显著高于术前,血糖变化与ＡＣＴＨ相似,两者间呈显著正相关（ｒ＝０．６７６,Ｐ＜０．０１）;再灌注２４小时后出现持续高胰岛素血症,而肝细胞膜ＩｎｓＲ结合容量却显著降低,Ｋｄ值无显著变化。结论：急性脑缺血再灌注后血糖持续升高与应激密切相关,其中胰岛素抵抗是一个重要原因     

老年急性脑梗死患者治疗前后胰岛素抵抗变化：对照组分析

目的：以胰岛素相对敏感性为胰岛素抵抗的代表指标，分析老年急性脑梗死患者治疗前后，并与急性期非相应治疗及恢复期脑卒中患者和健康对照组比较胰岛素抵抗的变化及其意义。方法：选择2000-07／2003-04解放军总医院第三0九临床部第二干部病房收治老年脑梗死患者49例，年龄&;gt;60岁，无糖尿病和胰岛素应用史，按病程、头颅CT或MRI将其分为两组：①急性脑梗死组33例，病程&;lt;3周，影像学显示有新鲜的病灶。其中25例进行了治疗，包括低分子肝素钠1432Iu，皮下注射，2次／d，共1周；葛根素注射液0．5g及胞二磷胆碱注射液0．75g，静滴，1次／d，共2周。②恢复期脑梗死组16例，病程≥3周。对照组26例为同期老年健康查体者。所有被试者均测定了空腹血糖、空腹血清胰岛素及C肽、胰岛素敏感性指数和胰岛素相对敏感性。以胰岛素相对敏感性为主要观察指标，同时进行其他相关因子的比较分析。结果：3组75例受试者全部进入结果分析。①以对照组胰岛素相对敏感性为100％，急性脑梗死组和恢复期脑梗死组分别为420h，和67％。②25例经治疗的急性脑梗死组患者，以治疗前胰岛素相对敏感性为100%，治疗后为150．7％。结论：①老年急性脑梗死患者对胰岛素的相对敏感性下降，即存在着胰岛素抵抗现象，恢复期患者仍存在胰岛素抵抗现象，但程度明显减轻。②治疗干预后急性脑梗死患者的胰岛素敏感性可有一定程度的恢复，从而提示早期干预胰岛素抵抗可起到脑血管疾病的一级康复预防作用。     

202例糖耐量分析和糖耐量异常诊断标准的探讨

目的：探讨糖耐量异常（ＩＧＴ）诊断标准改变的临床意义。方法：２０２例实验者依据的血糖水平分为３组，第Ⅰ组为正常对照组，１０３名，口服糖耐量试验（ＯＧＴＴ）糖负荷后２小时血糖低于７０ｍｍｏI／Ｌ，第Ⅱ组４８例，ＯＧＴＴ糖负荷后２小时血糖为７．０ｍｍｏＩ／Ｌ至７．８ｍｍｏＩ／Ｌ；第Ⅲ组５１例，为ＯＧＴＴ糖负荷后２小时血糖为７．９ｍｍｏＩ／Ｌ至１１．１ｍｍｏＩ／Ｌ。进行糖耐量试验并检测血脂水平和尿清蛋白     

新生儿应激性高血糖的胰岛素治疗探讨——附107例报告

目的：探讨胰岛素治疗新生儿应激性高血糖时停用胰岛素治疗的最佳血糖终点值,研究胰岛素使用的安全范围,为临床用药提供参考。方法：107例应激性高血糖新生儿随机分为A组（38例）、B组（34例）和C组（35例）3组。A、B组患儿将短效胰岛素3U加入0．9％生理氯化钠15ml／L中,用注射泵按0．1U／（kg·h）泵入,严格控制输液速度,减少葡萄糖输入量,补糖速度为1—2mg／（kg·min）,测血糖1次／小时,使血糖下降速度控制在3—5mmol／（L·h）,当A组血糖降至10．0—11．1mmol／L,B组血糖降至5．6～8．4mmol／L时停用胰岛素,上调输糖速度至2～4mg／（kg·min）,继续测血糖1次／小时,血糖稳定后改每4～6h测血糖,3次测量值正常后停止监测。C组采用限糖方法,输糖速度为1～2mg／（kg·min）。观察各组治疗6h后血糖下降情况、有否血糖反跳现象或低血糖发生情况。结果：A、B两组患儿经胰岛素治疗后血糖均明显下降,A组无发生血糖反跳现象或低血糖;B组6例出现低血糖,A、B两组低血糖发生率比较差异有统计学意义（P〈0．05）;C组仅限糖治疗效果不明显,加用胰岛素治疗后血糖下降。结论：胰岛素治疗新生儿应激性高血糖效果肯定,但需定时监测血糖,当血糖下降至10．0～11．1mmol／L时,及时停用胰岛素,可避免发生低血糖所造成脑损伤。     

The pattern of plasma insulin response to glucose in patients with a previous myocardial infarction--the respective effects of age and disease

Plasma insulin and blood sugar variations were investigated during oral (OGTT) and intravenous (IVGTT) glucose tolerance tests in 10 patients aged 32 to 41 and 10 Patients aged 48 to 60 who had suffered a myocardial infarction at least three months previously. The results obtained in each group of patients were compared with those of ten normal subjects of corresponding age. The respective influences of age and cardio-vascular disease on the pattern of the plasma insulin and blood sugar responses to the glucose load were dissociated on the basis of analysis of variance.—Advancing age was associated with a rise in the mean blood sugar level during OGTT and a lowering of the glucose assimilation coefficient during IVGTT, but it was not accompanied by a significant change in the plasma insulin levels during either of the two tests.—Cardiovascular disease was associated with an augmentation of the mean blood sugar level during OGTT, but also with a prolonged and excessive response in plasma insulin. During IVGTT the glucose assimilation coefficient and the plasma insulin variations were not statistically different in the patients with a previous myocardial infarction and in the normal subjects.—The previous occurrence of a myocardial infarction is thus associated with a hyperinsulinism during OGTT, but not after a rapid stimulation as realized during IVGTT. The nature of the gastrointestinal factors involved in the genesis of this hyperinsulinism remains a matter of conjecture.     

老年人体脂分布类型与脑梗死、胰岛素抵抗相关性的研究

目的　研究老年人体脂分布类型与脑梗死、胰岛素抵抗之间的关系。方法　选取老年脑梗死病人作为研究对象 ,调查体重指数 (BMI)、腰围 /臀围比值 (WHR)、血压、血胆固醇 (TC)、甘油三脂 (TG)、高密度脂蛋白 胆固醇 (HDL C)、血糖 (FBG)、胰岛素 (INS)及胰岛素敏感性指数 (ISI)。结果　外周型超重组脑梗死发生及血压、TG、INS高于非超重组 ,HDL C、ISI低于非超重组 ;而中心型超重组脑梗死发生、血压、INS水平高于外周型超重组 ,HDL C ,ISI低于外周型超重组。结论　老年人体脂分布类型与胰岛素抵抗密切相关 ,是脑梗死的重要危险因素。     

不同类型脑梗死与胰岛素抵抗的关系

目的探讨三种不同类型的脑梗死与胰岛素抵抗（IR）的关系。方法将50例已排除公认危险因素的脑梗死患者分为动脉粥样硬化性脑梗死（ATCI）组、腔隙性脑梗死（LCI）组及心源性脑梗死（CCI）组，分别检测空腹和葡萄糖耐量试验2h后血糖及血清胰岛素浓度，计算胰岛素抵抗指数（IRI）。同时测定甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋白At（ApoA1）、载脂蛋白B（ApoB）的浓度，并分析血脂／载脂蛋白各指标与IRI的相关性。结果ATCI组和LCI组患者IRI与正常对照组比较差异均有显著性（均为P〈0．01）；同时ATCI和LCI患者血清TG、LDL-C及ApoB含量增加，而HDL-C、ApoA．含量显著降低（P〈0．01或P〈0．05），其中TG、LDL-C及ApoB与IRI呈显著正相关（r值分别为0．590、0．918、0．671，均为P〈0．01），HDL-C、ApoA1与IRI呈显著负相关（r值分别为-0．582、-0．378。分别为P〈0．01和P〈0．05）。结论ATCI和LCI患者体内存在着IR，而CCI患者体内不存在IR；IR是ATCI和LCI的危险因素。     

Evaluation of genetic predisposition to insulin resistance by nutrient-induced insulin output ratio (NIOR).

BACKGROUND: New tools to identify genotype-phenotype interactions need to be described and implemented. The aim of this study was to identify correlation between the risk originating from gene variation and diet-dependent development of insulin resistance. METHODS: Insulin output in terms of area under the curve after an oral glucose tolerance test (AUC Ins OGTT) and lipid tolerance tests (AUC Ins OLTT) were measured in 167 overweight/obese patients. Estimation of the 18 common gene polymorphisms for obesity risk and standard phenotyping were performed. RESULTS: Insulin output (AUC Ins OGTT) correlated strongly between both insulin treatments across the whole group. However, within the genotype sub-groups, correlation was lower or did not exist. Using a nutrient-induced insulin output ratio (NIOR), calculated as AUC Ins OLTT/AUC Ins OGTT, values ranged from 0.42 to 5.83 and correlated significantly with body mass index (BMI) and leptin, but not with age, gender, waist-to-hip ratio (WHR) and homeostasis model assessment of insulin resistance (HOMA-IR) or plasma adiponectin. High NIOR was found in a subgroup of carriers of rare allelic variants of genes characteristic for poorer tolerance to lipids in the diet. Low NIOR values were found within a sub-group with rare genetic variants regulating carbohydrate metabolism. Thus, the new insulin index NIOR may distinguish gene variant carriers into groups of glucose- or lipid-sensitive phenotypes. CONCLUSIONS: We suggest that the OLTT/OGTT insulin output ratio (NIOR) may be predictive for identifying individuals who are phenotypically susceptible to insulin resistance in response to high fat or carbohydrate in their habitual diet.     

Risk of progression to type 2 diabetes based on relationship between postload plasma glucose and fasting plasma glucose

OBJECTIVE: We sought to assess the risk of progression to type 2 diabetes in normal glucose tolerance (NGT) subjects based on the relationship between the plasma glucose concentration during oral glucose tolerance tests (OGTTs) and the fasting plasma glucose (FPG) concentration. RESEARCH DESIGN AND METHODS: Subjects with NGT (n = 1,282) from the San Antonio Heart Study received an OGTT with measurement of the plasma glucose concentration at 0, 30, 60, and 120 min at baseline and after 7-8 years of follow-up. Subjects were divided into four groups based on the relationship between the plasma glucose concentration during the OGTT and the FPG concentration on the same day as the OGTT. Insulin resistance was calculated by the homeostasis model assessment of insulin resistance (HOMA-IR) and Matsuda index. Early-phase insulin secretion was calculated as the ratio between the incremental plasma insulin and glucose concentrations during the first 30 min of the OGTT (DeltaI(0-30)/DeltaG(0-30)). Total insulin secretion was calculated as the ratio between the incremental areas under the insulin and glucose curves during the OGTT [DeltaG(AUC)/DeltaI(AUC)]. RESULTS: In 23 subjects (group I), the plasma glucose concentration during the OGTT returned to levels below the FPG concentration at 30 min; in 111 subjects (group II) and in 313 subjects (group III), the plasma glucose concentration during the OGTT returned to levels below the FPG concentration at 60 and 120 min, respectively. In the remaining 835 subjects (group IV), the plasma glucose concentration during the OGTT never fell below the FPG concentration. Insulin resistance, measured by HOMA-IR and the Matsuda index, increased progressively from group I through group IV, while insulin secretion measured by DeltaI(0-30)/DeltaG(0-30) and DeltaG(AUC)/DeltaI(AUC) decreased progressively from group I through group IV. The incidence of type 2 diabetes was 0% in group I and progressively increased to 0.9% in group II, 3.2% in group III, and 6.4% in group IV. CONCLUSIONS: Subjects whose postload plasma glucose concentration returned to baseline (i.e., FPG level) more quickly had greater insulin sensitivity, a higher insulinogenic index, and a lower risk of developing type 2 diabetes after 8 years of follow-up compared with subjects whose postload glucose concentration returned to baseline more slowly.     

Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes.

OBJECTIVE: In normal adults, a small (catalytic) dose of fructose administered with glucose decreases the glycemic response to a glucose load, especially in those with the poorest glucose tolerance. We hypothesized that an acute catalytic dose of fructose would also improve glucose tolerance in individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: Five adults with type 2 diabetes underwent an oral glucose tolerance test (OGTT) on two separate occasions, at least 1 week apart. Each OGTT consisted of 75 g glucose with or without the addition of 7.5 g fructose (OGTT + F or OGTT - F), in random order. Arterialized blood samples were collected from a heated dorsal hand vein twice before ingestion of the carbohydrate and every 15 min for 3 h afterward. RESULTS: The area under the curve (AUC) of the plasma glucose response was reduced by fructose administration in all subjects; the mean AUC during the OGTT + F was 14% less than that during the OGTT - F (P < 0.05). The insulin AUC was decreased 21% with fructose administration (P = 0.2). Plasma glucagon concentrations declined similarly during OGTT - F and OGTT + F. The incremental AUC of the blood lactate response during the OGTT - F was approximately 50% of that observed during the OGTT + F (P < 0.05). Neither nonesterified fatty acid nor triglyceride concentrations differed between the two OGTTs. CONCLUSIONS: Low-dose fructose improves the glycemic response to an oral glucose load in adults with type 2 diabetes, and this effect is not a result of stimulation of insulin secretion.     

脑梗死患者胰岛素抵抗状态与血脂代谢异常

目的研究脑梗死患者的胰岛素抵抗状态与血脂代谢异常. 方法测定 2000-05/09在中国医科大学附属二院住院的 44例脑梗死患者的血脂、血糖、胰岛素及 C-肽,与健康对照组( 20例)比较. 结果脑梗死合并高血压组与不合并高血压组的空腹胰岛素( fasting insulin,FINS)、 C-肽、三酰甘油、高密度脂蛋白( high-density lipoprotein,HDL)、载脂蛋白 B(apolipoprotein B,ApoB) 、胰岛素敏感指数( insulin sensitivity index ,ISI) 与对照组比较有显著性差异( P< 0.01) ,空腹血糖 (FBS)、总胆固醇 (TC)、低密度脂蛋白( low-density lipoprotein,LDL)与对照组比较差异有显著性意义( P< 0.05).脑梗死两组间差异无显著性意义( P >0.05). ISI与 FINS( r=- 0.82～- 0.71,P< 0.001), C-肽 (r=- 0.55～- 0.53,P< 0.01), ApoB(r=- 0.46 ～- 0.45,P< 0.05) 及神经功能缺损评分 (r=- 0.56～- 0.58,P< 0.01)呈显著负相关,与 HDL(r=0.50～ 0.55,P< 0.05)呈显著正相关. 结论脑梗死患者存在胰岛素抵抗,胰岛素抵抗与血脂代谢异常关系密切.     

脑梗死患者体内胰岛素抵抗和红细胞胰岛素受体的关系

背景流行病学研究显示胰岛素水平升高和冠状动脉疾患相关,代谢研究也表明胰岛素抵抗、高胰岛素血症和非胰岛素依赖性糖尿病、高血压、肥胖及脂质紊乱密切相关.目的探讨脑梗死患者体内胰岛素抵抗与红细胞胰岛素受体之间的关系.设计病例-对照观察.单位吉林大学中日联谊医院神经内科.对象选择40例2004-01/10在吉林大学中日联谊医院住院的脑梗死患者.同时选取了30例健康的医护人员作为对照组.方法检测脑梗死患者和对照者的空腹血糖、血清胰岛素及葡萄糖耐量试验后2 h的血糖、血清胰岛素浓度,并将空腹血糖和血清胰岛素浓度的乘积作为胰岛素抵抗指标.采用改良甘氏法检测红细胞胰岛素受体,同时分析胰岛素受体数目与胰岛素抵抗指标的关系.主要观察指标脑梗死组与正常对照组①空腹及葡萄糖耐量试验后2 h血糖和血清胰岛素的比较.②胰岛素抵抗指标比较.③红细胞胰岛素受体分析.结果40例脑梗死患者和30例对照者的数据均进入结果分析,无脱落者.①空腹及葡萄糖耐量试验后2 h血糖和血清胰岛素的比较脑梗死组空腹血清胰岛素、葡萄糖耐量试验后2 h血糖和胰岛素均大于正常对照组[(13.30±5.15),(9.85±4.36)mU/L,(8.27±1.65),(6.32±1.37)mmol/L,(75.21±21.12),(28.26±6.31)mU/L,P＜0.01,P＜0.001].②胰岛素抵抗指标比较脑梗死组大于正常对照组(68.69±22.91,48.36±10.16,P＜0.001).③红细胞胰岛素受体分析脑梗死组每个红细胞膜胰岛素高、低两型亲和力受体数目及最大特异性结合率均小于正常对照组[20.30±4.50,23.80±4.10;2 223.80±509.30,2 610.10±435.10;(10.62±3.55)%,(13.21±2.94)%,P均＜0.01];直线回归与相关分析表明脑梗死患者胰岛素高、低两型亲和力受体数目与胰岛素抵抗指标呈负相关(r=-0.458,-0.439,P均＜0.01).结论脑梗死患者体内存在着胰岛素抵抗;胰岛素受体数目减少在胰岛素抵抗引发的脑梗死中起着重要作用.     

高血压患者动态血压变化与糖代谢异常55例分析

目的 探讨糖代谢异常对高血压患者动态血压变化的影响。方法 对55例既往无糖尿病的高血压患者行24小时动态血压监测和糖耐量试验（OGTT），根据OGTT分为糖耐量正常（NGT）、糖耐量减低（IGT）和新发现2型糖尿病（2-DM）3组。结果 从NGT至IGT至2-DM，非杓型血压发生率逐渐增高（分别为52．17％、64．70％和80．00％，P〈0．01），且2-DM患者夜间高血压的发生率较NGT及IGT显著增加（分别为13．04％、17．64％和33．33％，P〈0．01）；IGT组的24小时舒张压负荷、24小时舒张压和夜间舒张压均显著低于NGT组和2-DM组（P〈0．05），且脉压增大；并且发现，从NGT至IGT至2-DM过程中，胰岛素抵抗指数逐渐增加（分别为1．41、1．66和1．92，P〈0．05），胰岛素敏感指数在IGT阶段较NGT增高（39．90比33．83，P〈0．05），而到2-DM阶段较NGT下降（27．15比33．83，P〈0．05）；Logistic回归分析显示，影响脉压的主要因素为餐后血糖。结论 糖代谢异常的高血压惠者其24h血压的昼夜节律紊乱，其中以IGT患者的舒张压降低和脉压增大为著，而脉压增大与餐后血糖及血浆胰岛素水平相关。     

Association of hypertriglyceridemia and insulin resistance in uremic patients undergoing CAPD.

OBJECTIVE: Hyperlipidemia is frequently encountered in uremic patients and may be worsened by continuous ambulatory peritoneal dialysis (CAPD) treatment. The lipid abnormalities in these patients may be multifactorial. Insulin resistance (or its compensatory hyperinsulinemia) is commonly observed in uremic patients, but its association with hyperlipidemia in these patients has not been studied. PATIENTS AND METHODS: Lipid profiles of 35 nondiabetic nonobese patients undergoing CAPD for more than 1 year (mean 52.3 months) were studied. Current laboratory data and parameters related to peritoneal dialysis (PD) within the previous 3 months were recorded. After overnight fasting and interruption of PD, an oral 75-g glucose tolerance test (OGTT) was examined. RESULTS: After CAPD treatment for more than 12 months, these patients had higher serum triglyceride (TG) (p = 0.001) and total cholesterol (p = 0.0058) levels than their values before commencing CAPD. Twelve of 14 patients with serum TG higher than 200 mg/dL (high-TG) were diagnosed de novo, in contrast with only 1 patient diagnosed of de novo hypercholesterolemia (total cholesterol > 240 mg/dL). There was no difference in age, gender, body mass index (BMI), duration of PD treatment, serum albumin, hematocrit, intact serum parathyroid hormone (iPTH), peritoneal glucose load, solute transport, or weekly Kt/V urea between normal-TG and high-TG patients. After adjusting for age, gender, BMI, weekly Kt/V urea, and iPTH, the high-TG patients had higher levels of area under the curve for glucose (AUC(Glu)), area under the curve for insulin (AUC(Ins)), and AUC(Ins)/AUC(Glu) ratios (F = 10.63, 10.14, and 8.65; p = 0.0029, 0.0035, and 0.0065, respectively), indicating that the high-TG patients were more insulin resistant. There were 24 patients with normal glucose tolerance (NGT), and 11 patients with impaired glucose tolerance (IGT). The IGT group had higher serum TG (F = 10.43, p = 0.003) and total cholesterol (F = 8.05, p = 0.009) than the NGT group, after adjusting for BMI, duration of CAPD treatment, peritoneal glucose load, solute transport, serum albumin, and lipid levels before PD treatment. TheTG levels after CAPD treatment were positively correlated with AUC(Glu), AUC(Ins), and AUC(Ins)/AUC(Glu) ratio (r = 0.48, 0.53, and 0.49; p = 0.0037, 0.001, and 0.0028, respectively). CONCLUSIONS: These results indicate that insulin resistance is an important factor in the development of hypertriglyceridemia in CAPD patients.