运动对老年高血压患者血压和糖,脂代谢的影响

目的探讨运动对老年高血压患者血压和糖、脂代谢的影响。方法将４３例老年高血压患者随机分为运动组和对照组，两组均接受尼群地平降压治疗，同时运动组进行为期３个月的体育运动。测量两组入组时和３个月后血压、血脂、空腹血糖、胰岛素及负荷后１ｈ和２ｈ血糖及血胰岛素。结果经过３个月规则运动，运动组空腹及糖负荷后１ｈ、２ｈ胰岛素水平、血胆固醇、甘油三酯及低密度脂蛋白较对照组降低（Ｐ值均＜０．０５），高密度脂蛋白较对照组增高（Ｐ＜０．０５）；试验后两组血压均较入组时降低，而运动组服药量较对照组减少（Ｐ＜０．０５）。结论规则的体育运动能降低老年高血压患者空腹及糖负荷后血胰岛素水平，并有利于血脂代谢紊乱的纠正和血压的控制     

冠心病、高血压病、高血压病伴冠心病患者的胰岛素抵抗及卡托普利对其的影响

目的：比较冠心病、高血压病、高血压病伴冠心病患者胰岛素抵抗及卡托普利（ｃａｐｔｏｐｒｉｌ）对其胰岛素抵抗的影响。方法：２０例正常对照组及２０例冠心病组、２０例高血压病组、１８例高血压病伴冠心病组患者均行口服葡萄糖耐量试验，测血糖、血胰岛素，之后除正常对照组外，其余３组服卡托普利１２．５ｍｇ／ｄ，共４周，于第４周重复葡萄糖耐量试验，通过血糖、血胰岛素来计算空腹血胰岛素与血糖比值（Ｉ／Ｇ），糖耐量、胰岛素释放曲线下面积多组均数间的两两比较用方差分析和ｑ检验，同组治疗前后配对资料用ｔ检验。结果：冠心病组、高血压病组、高血压病伴冠心病组患者血糖、血胰岛素、Ｉ／Ｇ均高于正常对照组；高血压病组Ｉ／Ｇ大于冠心病组（Ｐ＜０．０５）；高血压病伴冠心病组糖负荷后２小时血胰岛素下降慢，其值高于其它两组（Ｐ＜０．０５）；卡托普利治疗后３组患者血糖、血胰岛素、Ｉ／Ｇ、糖耐量、胰岛素释放曲线下面积均较治疗前下降。结论：冠心病组、高血压病组、高血压病伴冠心病组患者均存在胰岛素抵抗，高血压病伴冠心病组患者高胰岛素血症更明显，持续时间更长。卡托普利能改善以上３组患者的胰岛素抵抗。     

老年高血压患者血压昼夜节律与胰岛素抵抗

目的为了探讨高血压病患者２４ｈ血压昼夜节律变化与糖、胰岛素（ＩＳ）代谢的关系。方法４６例老年高血压病患者，按昼夜血压节律不同，分为杓型组（ＤＧ）与非杓型组（ＮＤＧ），行葡萄糖耐量试验和ＩＳ释放试验。结果ＤＧ与ＮＤＧ２组各时相血糖、血糖面积及空腹ＩＳ水平无显著性差异（Ｐ＞００５）；而ＮＤＧ在糖负荷后的６０ｍｉｎ、１２０ｍｉｎＩＳ水平和ＩＳ释放指数（ＩＲＩ）以及ＩＳ面积（ＩＡＵＣ）明显高于ＤＧ（Ｐ＜００１、００５、００１、０００１、００１）；ＤＧ的ＩＳ敏感指数（ＩＳＳＩ）明显大于ＮＤＧ（Ｐ＜００１）；夜间平均血压下降率与ＩＡＵＣ、１２０ｍｉｎＩＲＩ及６０ｍｉｎＩＳ水平呈显著负相关（γ＝－０５９８、－０５１１和－０４８６，Ｐ＜００１、００１和００５），与１２０ｍｉｎＩＳＳＩ呈显著正相关（γ＝０４６２，Ｐ＜００１）。结论老年高血压节律异常者有更显著的胰岛素抵抗及高胰岛素血症。     

盐敏感性高血压病患者的胰岛素抗性与应激血压反应特点

目的观察盐敏感者胰岛素抗性与应激血压反应的关系。方法对３３例高血压病患者和２７例血压正常对照者用静脉盐水负荷和速尿缩容相结合的方法确定盐敏感性（ＳＳ）基础上，进行糖耐量、胰岛素释放试验；精神激发，冷加压和运动等试验。结果ＳＳ与盐不敏感者（ＳＲ）比较，空腹及糖负荷后各时点血糖及胰岛素含量均明显增高，胰岛素敏感指数降低（Ｐ均＜０．０５）；空腹血胰岛素在百分位Ｐ７５以上者或胰岛素敏感指数在百分位Ｐ２５以下者，精神激发及冷加压后平均动脉压上升幅度（ΔＭＡＰ）明显增加，且与空腹血胰岛素水平呈正相关（ｒ值分别为０．３８１及０．４２３，Ｐ＜０．０５），与胰岛素敏感指数呈负相关（ｒ值为－０．３９３和－０．２６７，Ｐ＜０．０５）。结论盐敏感者有胰岛素抗性增加的表现，且与应激血压明显增强相关联     

高血压病患者血清脂蛋白、载脂蛋白异常与胰岛素抵抗的关系

目的：探讨高血压病患者血脂／载脂蛋白异常与胰岛素抵抗的关系。方法：以空腹胰岛素／空腹葡萄糖比值和口服葡萄糖负荷后胰岛素曲线下面积／葡萄糖曲线下面积比值作为胰岛素抵抗指标，与空腹血脂／载脂蛋白进行直线相关分析。结果：与正常对照组（ｎ＝２１）比较，高血压病组（ｎ＝３２）血清甘油三酯（ＴＧ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）、载脂蛋白（Ａｐｏ）Ｂ、空腹胰岛素、空腹胰岛素／空腹葡萄糖比值以及胰岛素曲线下面积、葡萄糖曲线下面积和胰岛素曲线下面积／葡萄糖曲线下面积比值均显著增加（Ｐ＜０．０５～０．００１），高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）、ＨＤＬ２－Ｃ、ＡｐｏＡＩ及ＡｐｏＡＩ／ＡｐｏＢ比值均显著降低（Ｐ＜０．０５～０．００１）。高血压病组空腹胰岛素／空腹葡萄糖比值和胰岛素曲线下面积／葡萄糖曲线下面积比值均分别与甘油三酯、低密度脂蛋白胆固醇和ＡｐｏＢ呈正相关（Ｐ＜０．０５～０．０１），与ＨＤＬ２－Ｃ、ＡｐｏＡＩ和ＡｐｏＡＩ／ＡｐｏＢ比值呈负相关（Ｐ＜０．０５～０．００１）。正常对照组上述指标间则无相关（Ｐ＞０．０５）。结论：高血压病患者血脂／载脂蛋白异常与胰岛素抵抗密切相关。     

原发性高血压胰岛素及其拮抗激素改变与冠心病的关系

观察原发性高血压患者基础血糖负荷后血清胰岛素及其部分拮抗激素的变化。结果显示：各组空腹胰岛素水平接近。糖负荷后各时点胰岛素和生长激素均显著高于对照组（Ｐ＜０．０５）；胰岛素敏感指数患者组显著低于对照组（Ｐ＜Ｏ．０１），并与生长激素水平呈显著负相关（γ＝－０．８０９，Ｐ＜０．０１）．患者组泌乳素明显低于对照组（Ｐ＜０．０５），尤以高血压合并冠心病组差别最为显著（ｐ＜０．０１）。血清胆固醇无组间差别。甘油三酯水平患者组显著高于对照组（Ｐ＜０．０５），而高密度脂蛋白胆固醇明显低于对照组（Ｐ＜０．０５）。结果提示：本组患者存在着胰岛素抵抗和高胰岛素血症。其原因可能与下丘脑兴奋性增强致胰岛素拮抗激素分泌紊乱有关。由此造成的脂质代谢紊乱可能是单纯降压治疗不能降低冠心病患病率的原因之一。     

高血压病患者的胰岛素抵抗及与动态血压的关系

我们用葡萄糖耐量试验对３３例Ⅱ期、Ⅲ期高血压病患者和２５例正常对照者的研究发现：口服葡萄糖后３０ｍｉｎ、６０ｍｉｎ、１２０ｍｉｎ和１８０ｍｉｎ时前者的血糖浓度显著高于后者（Ｐ＜０．０２，Ｐ＜０．０１，Ｐ＜０．００５，Ｐ＜０．００５）。空腹、服糖后１２０ｍｉｎ、１８０ｍｉｎ时前者的血清胰岛素浓度显著高于后者（Ｐ＜０．０５，Ｐ＜０．０１，Ｐ＜０．０２），这是典型的胰岛素抵抗。高血压病患者空腹血胰岛素浓度及胰岛素曲线下面积与动态的收缩压、舒张压、平均动脉压呈线性正相关。     

老年高血压和冠心病患者的高胰岛素血症

目的探讨老年原发性高血压和冠心病患者的血胰岛素水平及胰岛素敏感性指数的变化。方法对无糖尿病病史的老年原发性高血压患者３０例、老年冠心病患者３２例、老年对照组３０例测定空腹及餐后２小时血糖、胰岛素、Ｃ肽值,计算胰岛素敏感性指数,进行对照分析。结果空腹胰岛素,高血压组为（１３．１±５．４）ｍＵ／Ｌ,冠心病组为（１１．１±０．３）ｍＵ／Ｌ,对照组为（１０．３±１．９）ｍＵ／Ｌ;餐后２小时胰岛素,３组分别为（６２．３±１６．８）、（４４．３±６．４）及（１０．８±３．１）ｍＵ／Ｌ。均为高血压组高于冠心病组,二者又高于对照组（分别为Ｐ＜０．０５及Ｐ＜０．０１）。胰岛素敏感性指数为对照组大于冠心病组,二者又大于高血压组（分别为Ｐ＜０．０１及Ｐ＜０．０５）。结论老年高血压患者及冠心病患者均伴有高胰岛素血症和胰岛素抵抗,胰岛素敏感性指数降低是血管病变的危险因素之一。     

依那普利对高血压病患者胰岛素抵抗影响的临床观察

测定５１例高血压病患者与２２例正常人空腹血糖（ＳＧ）、血胰岛素水平（ＩＳ）、Ｃ肽（ＣＰ），显示ＩＳ、ＩＳ／ＳＧ、胰岛素敏感指数（ＩＡＩ）、两组间有显著性差异（Ｐ＜０．０１），而ＣＰ／ＩＳ比值无统计学差异。高血压病患者用依那普利５～１０ｍｇ／ｄ，疗程４～１５个月（平均１１．２９±３．７１个月），后复查上述指标并与用药前进行对比分析。结果除血压明显下降外（Ｐ＜０．００１），空腹ＩＳ、ＩＳ／ＳＧ、ＩＡＩ亦均显著下降（Ｐ＜０．０１），而ＣＰ／ＩＳ比值治疗前后差异无显著性（Ｐ＞０．０５）。提示，原发性高血压病患者存在胰岛素抵抗现象，依那普利治疗除可有效降低血压外，尚有改善胰岛素抵抗的作用。     

高血压病与冠心病胰岛素抵抗的比较

检测３５例高血压病（ＥＨ）、３１例冠心病（ＣＨＤ）、２６例对照组糖耐量中胰岛素（ＩＳ）、Ｃ肽（ＣＰ）水平及克分子比值等，结果ＥＨ、ＣＨＤ均存在胰岛素抵抗（ＩＲ）和高胰岛素血症（ＨＩＳ）。但各有特点，ＣＨＤ表现服糖后１小时血糖明显升高，胰岛分泌明显增高，糖耐量异常明显多于ＥＨ（Ｐ＜０．０５）；ＥＨ表现空腹胰岛分泌明显增多，空腹ＩＳ明显高于ＣＨＤ（Ｐ＜０．０５）。ＥＨ服糖后ＩＳ清除明显减少，ＣＨＤ无此现象，特别是１小时ＩＳ清除明显低于ＣＨＤ（Ｐ＜０．０５），提示ＩＳ清除减少可能为ＥＨ所特有。     

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     

Preserved circadian rhythm of serum insulin concentration at low plasma glucose during fasting in lean and overweight humans

Circadian rhythms in glucose metabolism are well documented. Most studies, however, evaluated such variations under conditions of continuous glucose supply, either via food intake or glucose infusion. Here we assessed in 30 subjects circadian variations in concentrations of plasma glucose, serum insulin, and C-peptide during a 72-hour fasting period to evaluate rhythms independent from glucose supply. Furthermore we assessed differences in these parameters between normal-weight (n = 20) and overweight (n = 10) subjects. Blood was sampled every 4 hours. During fasting, plasma glucose, serum insulin, and C-peptide levels gradually decreased (all P < .001). While there was no circadian variation in plasma glucose levels after the first day of fasting, serum levels of insulin were constantly higher in the morning (8.00 h) than at night (0.00 h) (P < .001), although the extent of this morning-associated rise in insulin levels decreased with the time spent fasting (P = .001). Also, morning C-peptide concentrations were higher compared to the preceding night (P < .001). The C-peptide/insulin ratio (CIR) decreased during prolonged fasting (P = .030), suggesting a decrease in hepatic insulin clearance. Moreover, CIR was significantly lower in the morning than at the night of day 1 and day 2 of fasting (P = .010 and P = .004, respectively). Compared to normal-weight subjects, overweight subjects had higher plasma glucose, as well as serum insulin and C-peptide levels (all P < .03). Data indicate preserved circadian rhythms in insulin concentrations in the presence of substantially decreased glucose levels in normal-weight and overweight subjects. This finding suggests a central nervous system contribution to the regulation of insulin secretion independent of plasma glucose levels.     

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（BG）、血清胰岛素S）、C-肽（CP）和血脂测定结果与12例正常血压者进行比较分析。高血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（P＜0．01）。胰岛素释放指数亦以高血压组为高（P＜0．05）。高血压组HDL／LDL、ApoA／ApoB均明显低于正常血压组（P＜0．01）；前者血清IS水平与ApoA／ApoB比值呈显著负相关（r=-0．409，P＜0．01），血清胰岛素释放指数（IS／BG）与ApoA／ApoB比值也呈明显负相关（r=－0.298．P＜0．05）。     

A close association between insulin resistance and dehydroepiandrosterone sulfate in subjects with essential hypertension

To examine the serum levels of dehydroepiandrosterone sulfate (DHEAS) and its relation with insulin resistance and the other risk factors in essential hypertension, serum DHEAS and insulin sensitivity were assessed in 35 male hypertensive and 17 male healthy control subjects aged 50-59 years. Fasting plasma insulin and the area under curve of plasma insulin were determined during a 75 g oral glucose tolerance test. Insulin sensitivity was measured by the steady state plasma glucose method. Fasting plasma insulin and the area under curve of plasma insulin were significantly higher in the hypertensive group than in control group. Steady state plasma glucose was significantly higher in hypertensive subjects indicating insulin resistance compared with control subjects. On the other hand, fasting serum DHEAS levels were significantly lower in the hypertensive group than in the control group. Fasting serum DHEAS levels were inversely correlated with steady state plasma glucose significantly (p=0.0008), indicating a close association between DHEAS levels and insulin resistance. Fasting serum DHEAS was inversely correlated with systolic blood pressure and fasting plasma insulin. In multiple regression analysis of hypertensive subjects, steady state plasma glucose was the strongest determinant of the fasting serum level of DHEAS, followed by systolic blood pressure and fasting plasma insulin. These 3 factors accounted for 51.6% of the variation in DHEAS. In nonobese and nondiabetic essential hypertension, serum DHEAS was lower and insulin resistance was the most significant independent determinant of reduced serum DHEAS, followed by systolic blood pressure and fasting plasma insulin.     

Insulin action during acute starvation: evidence for selective insulin resistance in normal man

The effects of insulin on glucose utilization, lipolysis, and potassium and phosphate metabolism were studied during short-term fasting in six lean subjects using a sequential euglycemic glucose clamp technique (two additional subjects were used in 70 mU/m2/min clamp studies). The subjects were infused with insulin for four hours at four rates ranging from 6 to 442 mU/m2/min before and after a 48-hour fast. Insulin was infused for one hour at each rate in all experiments. Fasting markedly reduced glucose utilization at all insulin infusion rates. On the other hand, the decline in levels of free fatty acids that occurred at insulin concentrations of 30 microU/ml was virtually identical before and after fasting. After insulin was infused for four hours, serum phosphate had decreased in all subjects (P less than 0.001) and strongly correlated with glucose disposal rates (r = 0.76, P less than 0.005). The plasma potassium level also declined in all subjects but did not relate to fasting or glucose disposal. These studies demonstrate that starvation produces selective insulin resistance. The biologic effect of insulin on glucose utilization and plasma phosphate shifts is clearly diminished. Free fatty acid and potassium metabolism are unaffected by starvation.     

培哚普利对高血压病患者血胰岛素水平的影响

对４０例高血压病（ＥＨ）患者和２０例健康对照者行口服葡萄糖耐量试验，测定其血糖（ＧＳ）和血胰岛素（ＩＳ）水平，计算其释放曲线下面积（ＡＵＣＧ、ＡＵＣＩ），发现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。提示高血压患者存在糖耐量降低、高胰岛素血症和胰岛素抵抗。３１例ＥＨ患者接受培哚普利降压治疗４周后，糖耐量试验显示糖负荷后１ｈ、２ｈ的ＧＳ和ＡＵＣＧ及空腹与糖负荷后各点的ＩＳ和ＡＵＣＩ均较治疗前显著降低。提示培哚普利能够降低ＥＨ患者血ＩＳ水平，具有改善其胰岛素抵抗的作用。     

2型糖尿病患者口服葡萄糖后胆囊收缩素及生长激素释放肽分泌规律分析

目的研究2型糖尿病(T2DM)患者口服葡萄糖后不同时间点血清胆囊收缩素(CCK)及生长激素释放肽(ghrelin)的分泌规律。方法选择T2DM患者82例为T2DM组,纳入同期的健康体检者34例为对照组,收集两组受试者的一般临床资料,检测其空腹和口服葡萄糖后不同时间点血糖、胰岛素、C肽、CCK及ghrelin水平并进行比较。采用Pearson相关分析探讨血清CCK及ghrelin与受试者血糖、胰岛素等因素的相关性。结果T2DM组患者服糖后0、30、60、120和180 min的血糖水平均较对照组高,胰岛素和C肽水平在服糖后30、60和120 min均较对照组低,CCK水平在服糖后60和120 min均较对照组低,ghrelin水平在空腹、服糖后30、60和120 min均较对照组低(P<0.05)。Pearson相关分析结果显示,T2DM患者血清ghrelin水平与BMI水平呈负相关(r=-0.282,P=0.047)。结论T2DM患者口服葡萄糖后CCK及ghrelin分泌较正常人群减少,CCK分泌高峰明显延迟,空腹血清ghrelin与BMI呈负相关。     

Acarbose attenuates Basal and postprandial insulin concentrations but fails to lower blood pressure in the spontaneously hypertensive rat

Background: Patients with essential hypertension and the spontaneously hypertensive rat (SHR) are insulin-resistant and hyperinsulinemic. These findings suggest the possibility that insulin resistance and hyperinsulinemia may play a pivotal role in blood pressure regulation. Acarbose, an oral antihyperglycemic drug, decreases hyperinsulinemia and hyperglycemia. The purpose of this study was to assess the influence of acarbose on basal and postprandial insulin and glucose levels and whether changes in beta-cell function result in a change in blood pressure measurements. Methods: SHRs were fed custom diets ad libitum, six with and six without acarbose (40mg/100g of chow). Fasting and postprandial glucose and insulin levels were analyzed following glucose administration (1.75 g/kg body weight). Blood pressure was determined by the tail cuff method. Results: Fasting glucose values were similar, but fasting insulin levels declined 23% in the acarbose treated group (P < .05). Postprandial glucose and insulin levels decreased 18% and 20%, respectively (P < .01), in the acarbose group vs the control animals. Despite the decrease in fasting and postprandial insulin concentrations, systolic, mean, and calculated diastolic blood pressures were insignificantly different in the acarbose group after six weeks of treatment compared to control animals. Conclusion: Acarbose decreases fasting insulin levels and postprandial glucose and insulin levels without effectively lowering blood pressure in the SHR. The ability of acarbose to attenuate the hyperinsulinemic state in the SHR without effectively lowering blood pressure suggests that factors other than serum insulin concentration are important in the modulation of blood pressure.     

Association between insulin resistance, glucose intolerance, and hypertension in pregnancy

There is an association between insulin resistance, glucose intolerance, and essential hypertension, but the relation between insulin resistance, glucose intolerance, and hypertension diagnosed during pregnancy is not well understood. Transient hypertension of pregnancy, the new-onset nonproteinuric hypertension of late pregnancy, is associated with a high risk of later essential hypertension and glucose intolerance; thus, these conditions may have a similar pathophysiology. To assess the association between insulin resistance, glucose intolerance, essential hypertension, and subsequent development of proteinuric and nonproteinuric hypertension in pregnancy in women without underlying essential hypertension, we performed a prospective study comparing glucose (fasting, 1 and 2 hours postglucose load), insulin, glycosylated hemoglobin (HbA1c), high-density lipoprotein cholesterol (HDL-C), and triglycerides levels on routine screening for gestational diabetes mellitus. Women who developed hypertension in pregnancy (n = 37) had higher glycemic levels (fasting, 1 and 2 hours postglucose load) on a 100-gram oral glucose loading test, although only the fasting values showed a statistical significance (p < 0.05), and a significantly higher frequency of abnormal glucose loading tests, two hours after glucose load (>or=140 mg/dL) (p < 0.05) than women who remained normotensive (n = 180). Glucose intolerance was common in women who developed both subtypes of hypertension, particularly preeclampsia. Women who developed hypertension had greater prepregnancy body mass index (p < 0.0001), higher frequency and intensity of acanthosis nigricans (p < 0.0001), and higher baseline systolic and diastolic blood pressures (p 相似文献   

Higher cholesterol and insulin levels in pregnancy are associated with increased risk for pregnancy-induced hypertension

Hyperinsulinemia and dyslipidemia are known to be associated with essential hypertension but their role in pregnancy-induced hypertension remains unclear. We performed a case-control study comparing cholesterol, insulin, and glucose levels in the early third trimester of pregnancy among 31 women who developed pregnancy-induced hypertension (PIH) (either preeclampsia [n = 6] or nonproteinuric gestational hypertension [n = 25]), with 31 women remaining normotensive through pregnancy. As compared with women remaining normotensive, women subsequently developing PIH had higher fasting cholesterol levels (279 v 247 mg/dL; P = .02) and higher fasting insulin levels (13.3 v 7.9 microU/mL; P = .03), although fasting glucose levels and levels of glucose and insulin after glucose load did not differ significantly between groups. In comparing hypertensive subgroups, fasting insulin levels were significantly higher among women who subsequently developed preeclampsia, but not among those subsequently developing nonproteinuric gestational hypertension. Although women developing PIH had higher pregravid body mass index (25.1 v 22.6 kg/m2, P = .06), fasting cholesterol and insulin levels were associated with risk for PIH even after adjustment for body mass index and age (relative risks for one unit increase, respectively: 1.02 (P = .03) and 1.12 (P = .03). Higher fasting cholesterol and insulin levels in mid- to late pregnancy are associated with increased risk for PIH. These observations support a role for insulin resistance in the development of this complication of pregnancy.