老年高血压和代谢综合征血清脂联素水平变化及其意义

目的:探讨老年高血压和代谢综合症患者血清脂联素水平变化及其意义。方法:60例老年高血压患者、62例老年代谢综合症患者和30例正常老年对照者,检测血压、体重、身高、腰围、空腹血糖、胰岛素、游离脂肪酸、血清脂联素、高敏C反应蛋白、尿素氮、肌酐,计算体重指数,测尿微量蛋白。结果:(1)高血压组和代谢综合症组脂联素水平明显低于正常对照组(P<0.05),体重指数、腹围、尿微量蛋白、游离脂肪酸、血糖、胰岛素、肌酐水平均高于对照组(P<0.05);(2)直线相关分析表明,血清脂联素水平与血压、尿微量蛋白、体重指数、腰围均成负相关(r=-0.230~-0.304,P<0.05~<0.01)。结论:代谢综合症和单纯高血压老年患者脂联素水平降低,且脂联素水平与血压、BMI、腰围及尿微量蛋白呈负相关。     

高血压患者血清脂联素与游离脂肪酸、糖及脂代谢

目的研究不同糖耐量原发性高血压患者(EH )血清脂联素水平、游离脂肪酸(FFA)谱特征及与其他糖脂代谢参数间关系.方法用放射免疫分析法测定122 例EH 患者与43 例正常对照组血清脂联素水平,同时用气相色谱/质谱(GC/MS)联用法测定其血清FFA 成分水平.结果EH 患者血清脂联素水平[(7.2±4.7)mg/L]低于正常对照组[(9.2±4.3)mg/L, P<0.05],伴有糖耐量受损(IGT)、伴有糖尿病(DM)亚组病人血清脂联素均显著下降(P<0.05～0.01).EH患者血清总脂肪酸[TFA(1291.6±503.7 vs 1064.6±470.3)μmol/L]和多不饱和脂肪酸[PUFA(712.5±284.3 vs 517.3±216.3)μmol/L, P<0.05～0.01] 水平显著高于正常对照组.IGT和DM组的TFA和PUFA也显著高于正常对照组和单纯高血压糖耐量正常亚组(P<0.01).脂联素与BMI、腹围(WC)、腹/臀围比(WHR)、TG 呈负相关(r=-0.217, -0.227, -0.172, -0.193,P<0.01～0.05),与HDL-C 呈正相关(r=0.361,P<0.01).结论脂联素水平与游离脂肪酸代谢紊乱,可能在原发性高血压、特别是在伴有糖代谢异常的高血压发病中起重要作用.血清脂联素水平下降可能是原发性高血压伴有糖代谢异常的特征性生化指标之一.     

代谢综合征不同组分患者血清脂联素与游离脂肪酸谱代谢参数的比较

目的研究代谢综合征（MS）患者血清脂联素水平、游离脂肪酸（FFA）谱特征及与其他糖脂代谢参数间的关系。方法用放射免疫分析法测定157例含MS不同组分的患者与43例正常对照（NC）组血清脂联素水平，同时用气相色谱/质谱（GC/MS）联用法测定其血清FFA成分。结果MS组分≥3项组患者血清脂联素水平低于MS组分两项组与NC组（P〈0.05～0.01）。同时，MS组分≥3项组患者平均血压（MBP）、BMI、WC、TG、不饱和脂肪酸（UFA）（C18：2;C20：4;C22：6;C20：3）、多不饱和脂肪酸（PUFA）、n6PUFA等高于MS组分两项组与NC组（P〈0.05～0.01），HDL-C低于MS组分两项组与NC组（P〈0.01）。在研究对象中，脂联素与BMI、WC、TG呈负相关（r=-0.204，-0.203，-0.238，P〈0.01），与HDL-C呈正相关（r=0.238，P〈0.01）。总FFA（TFFA）、PUFA均与BMI、MBP、FPG、TG呈正相关（r=0.163和0.211，0.201和0.288，0.184和0.276，0.274和0.155，P〈0.05～0.01）。结论脂联素与FFA均与MS多种组分相关。脂联素与FFA代谢紊乱、n6系PUFA升高可能在MS发病中起重要作用。     

高血压患者血清脂联素与游离脂肪酸、糖及脂代谢

目的研究不同糖耐量原发性高血压患者(EH)血清脂联素水平、游离脂肪酸(FFA)谱特征及与其他糖脂代谢参数间关系。方法用放射免疫分析法测定122例EH患者与43例正常对照组血清脂联素水平,同时用气相色谱/质谱(GC/MS)联用法测定其血清FFA成分水平。结果EH患者血清脂联素水平[(7.2±4.7)mg/L]低于正常对照组[(9.2±4.3)mg/L,P<0.05],伴有糖耐量受损(IGT)、伴有糖尿病(DM)亚组病人血清脂联素均显著下降(P<0.05~0.01)。EH患者血清总脂肪酸[TFA(1291.6±503.7vs1064.6±470.3)μmol/L]和多不饱和脂肪酸[PUFA(712.5±284.3vs517.3±216.3)μmol/L,P<0.05~0.01]水平显著高于正常对照组。IGT和DM组的TFA和PUFA也显著高于正常对照组和单纯高血压糖耐量正常亚组(P<0.01)。脂联素与BMI、腹围(WC)、腹/臀围比(WHR)、TG呈负相关(r=-0.217,-0.227,-0.172,-0.193,P<0.01~0.05),与HDL-C呈正相关(r=0.361,P<0.01)。结论脂联素水平与游离脂肪酸代谢紊乱,可能在原发性高血压、特别是在伴有糖代谢异常的高血压发病中起重要作用。血清脂联素水平下降可能是原发性高血压伴有糖代谢异常的特征性生化指标之一。     

慢性心力衰竭患者血浆脂联素水平及其与代谢综合征的相关性

目的探讨慢性心力衰竭患者血清脂联素水平及与代谢综合征各项指标、心功能的关系。方法选取心力衰竭患者120例,男76例,女44例,平均年龄(66.7±11.3)岁;测定血脂、血糖、糖化血红蛋白、胰岛素等指标;酶联免疫法(ELISA)检测血清脂联素水平;超声心动图评价心功能。结果相关分析结果显示,心力衰竭患者血清脂联素水平与体重指数、腰围、甘油三酯、ApoB、血红蛋白、白蛋白和血糖呈负相关,与二尖瓣E/E’呈正相关。合并代谢综合征的患者脂联素水平较单纯心力衰竭患者下降;合并代谢综合征的患者胆固醇、甘油三酯、ApoB、BUN、肌酐、CRP、血糖、胰岛素和胰岛素抵抗指数高于单纯心力衰竭患者;HDL、ApoA1低于单纯心力衰竭患者,差异有统计学意义。腰围、血红蛋白含量和E/E’与合并代谢综合征心力衰竭患者的脂联素水平呈负相关(r=-0.425,P=0.032;r=-0.562,P=0.001;r=-0.402,P=0.045)。结论合并代谢综合征的心力衰竭患者血清脂联素水平下降,其下降与炎症、心脏舒张功能异常有关。     

血清脂肪因子与代谢综合征的关系

121例代谢综合征(MS)患者和120名对照者入选本研究以探讨血清脂肪因子与MS的关系.对照组、非腹型肥胖MS组及腹型肥胖MS组的血清抵抗素和脂肪细胞型脂肪酸结合蛋白(A-FABP)依次增高,而脂联素水平依次降低(均P<0.05).MS组抵抗素与体重指数(BMI)、腰围、收缩压、空腹血糖和A-FABP呈正相关(P<0.05或P<0.01);脂联素与高密度脂蛋白胆固醇呈正相关,而与BMI、腰围、空腹胰岛素、甘油三酯、稳态模型评估的胰岛素抵抗指数(HOMA-IR)呈负相关.     

高血压患者血清脂联素水平和动脉顺应性的关系

目的 探讨高血压人群中血清脂联素浓度和动脉顺应性之间的关系.方法 入选非糖尿病的高血压受试者83例,分为药物治疗组和未治疗组.常规检测受试者的坐位血压及部分血清生化指标,包括血糖、血脂、肝功能、肾功能和胰岛素水平;放射免疫法检测血清脂联素浓度;计算稳态模式胰岛素抵抗指数(HOMA-IR);用HDI CVprofilor DO-2020检测大动脉弹性指数(C1)和小动脉弹性指数(C2).结果 比较药物治疗组和未治疗组,发现前者的脂联素浓度(中位数:11.9 μg/mL)、C1(中位数:13.7 mL/mm Hg×10)、C2(中位数:4.3 mL/mm Hg×100)均明显高于后者(5.7 μg/mL,10.7 mL/mm Hg×10,3.7 mL/mm Hg×100,P均＜0.01).对未治疗组进行相关分析发现LogC1与脂联素浓度明显正相关(r=0.54,P＜0.01),与平均血压(MBP)负相关(r=-0.40,P＜0.05);LogC2和脂联素浓度明显正相关(r=0.49,P＜0.01),与HOMA-IR和MBP明显负相关(LogC2-HOMA-IR r=-0.40,P＜0.05;LogC2-MBP,r=-0.32,P＜0.01);另外还发现C1与心率(HR)负相关(LogC1-HR r=-0.41,P＜0.01).多元线性逐步回归分析发现血清脂联素浓度和HR水平以及性别是LogC1的独立影响因素(R2=0.39,P＜0.01);血清脂联素水平和性别是LogC2的独立影响因素(R2=0.44,P＜0.01).结论 高血压人群中C1,C2的减退与血清脂联素浓度的降低密切相关.接受抗高血压药物治疗的患者,血清脂联素浓度和动脉顺应性水平升高.     

血清脂联素水平与老年人代谢综合征的相关性

目的 通过横断面研究,评估血清脂联素水平与老年人代谢综合征的相关性.方法 检测61例代谢综合征患者和140例非代谢综合征老年人血清脂联素、C反应蛋白、血糖、胆固醇、三酰甘油、高密度脂蛋白、低密度脂蛋白等,通过Logistic回归分析评价血清脂联素水平与老年人代谢综合征的关系,并采用等级相关统计方法比较血清脂联素水平. 结果 代谢综合征患者血清脂联素为(7.2±3.6)g/L,低于非代谢综合征组(10.0±3.9)g/L,代谢综合征1级、2级、3级的患者分别为27例(44.3%)、21例(34.4%)和13例(21.3%),脂联素水平分别为(8.5±2.7)g/L、(7.0±2.5)g/L和(4.9±2.4)g/L,随着代谢综合征组分的增多,脂联素的含量呈下降趋势,两两比较呈等级相关(均为P＜0.01).Logistic回归分析显示,在校正了年龄、体质指数和性别比后,高水平脂联素使代谢综合征患病风险降低.脂联素四分法表示中,高脂联素水平组患代谢综合征的风险较其他较低组降低96.0%(OR=0.04,95%可信区间0.023～0.056,P＜0.01).结论 老年人中,高水平脂联素使代谢综合征患病风险降低.     

原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对其影响

目的:探讨原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对血清脂联素的影响.方法:本研究入选原发性高血压患者60例及健康人30例(正常对照组),以正常对照组人群胰岛素敏感性指数(ISI)的均数±标准差作为有无胰岛素抵抗的分界线,将原发性高血压患者分成两组,即胰岛素抵抗组23例及无胰岛素抵抗组37例.检测血清脂联素、空腹血糖、血清胰岛素、总胆固醇、高密度脂蛋白胆固醇、甘油三酯、胰岛素敏感性指数、收缩压、舒张压、平均压、身高、体重及体重指数等指标.另外,从60例原发性高血压患者中选出能够完成整个实验,积极配合随访的40例患者,并分成两部分,每部分20例,分别用血管紧张素转换酶抑制剂培哚普利及血管紧张素Ⅱ受体拮抗剂缬沙坦治疗两周,治疗前、后检测上述指标.结果:①胰岛素抵抗组的血清胰岛素和甘油三酯与正常对照组及无胰岛素抵抗组相比,胰岛素抵抗组明显升高(P＜0.01),胰岛素抵抗组的脂联素和胰岛素敏感性指数与正常对照组及无胰岛素抵抗组相比,胰岛素抵抗组明显降低(P＜0.01).②高血压患者用培哚普利及缬沙坦治疗两周后,平均压显著下降(P＜0.05),血清脂联素浓度和胰岛素敏感性指数明显升高(P＜0.05).③原发性高血压患者血清脂联素与收缩压和舒张压呈直线相关(r分别为0.35和0.28,P＜0.01和P＜0.05);血清脂联素与胰岛素敏感性指数和高密度脂蛋白胆固醇呈直线相关(r分别为0.45和0.53,P均＜0.01);血清脂联素与血清胰岛素、体重指数及甘油三酯负相关(r分别为-0.41,-0.61和-0.35,P＜0.01,P＜0.01和P＜0.05);血清脂联素与平均压无明显相关性.结论:原发性高血压患者低脂联素血症与脂代谢紊乱和胰岛素抵抗密切相关.肾素-血管紧张素系统,可提高原发性高血压患者胰岛素敏感性,从而使血清脂联素浓度升高.     

冠心病合并代谢综合征患者脂联素水平与炎症因子及冠状动脉病变的关系

目的:探讨冠心病合并代谢综合征(metabolic syndrome,MS)患者脂联素水平与炎症因子及冠状动脉病变的关系.方法:将102例患者分为2组,冠心病合并代谢综合征57例(代谢综合征组);冠心病不合并代谢综合征45例(非代谢综合征组).检测血清脂联素、肿瘤坏死因子-白细胞介素－6、超敏C反应蛋白,并以冠状动脉病变积分评价其病变程度.结果:代谢综合征组和非代谢综合征组年龄、性别、总胆固醇、低密度脂蛋白－胆固醇、空腹胰岛素水平差异无统计学意义(P>0.05);代谢综合征组脂联素水平显著低于非代谢综合征组(P<0.05),肿瘤坏死因子-a、白细胞介素6、超敏C反应蛋白浓度显著高于非代谢综合征组(P<0.05～0.01),冠状动脉三支病变发生率和病变总积分显著高于非代谢综合征组(P<0.05).脂联素与肿瘤坏死因子－白细胞介素6、超敏C反应蛋白及冠状动脉病变程度呈负相关(P<0.05).结论:冠心病患者合并代谢综合征较为普遍,且脂联素水平降低,炎症因子水平升高,冠状动脉病变程度严重.     

阻塞性睡眠呼吸暂停低通气综合征患者血清脂联素水平的研究

目的 探讨血清脂联素在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者体内的变化。方法 选择伴有肥胖的OSAHS患者71例(肥胖OSAHS组)、不伴肥胖的OSAHS患者21例(非肥胖OSAHS组)、单纯性肥胖者26例(单纯性肥胖组)和健康成人22例(正常对照组)。其中肥胖OSAHS组和单纯性肥胖组的体重指数(BMI)均大于25,两组间BMI差异无显著性。肥胖OSAHS组又进一步分为轻度(26例)、中度(22例)和重度(23例)。均接受多导睡眠仪监测和放射免疫法测定血清脂联素水平。结果 正常对照组血清脂联素水平[(8.9±0.6)mg/L]显著高于单纯性肥胖组[(7.1±1.3)mg/L](P<0.05)、非肥胖OSAHS组[(5.4±0.6)mg/L,P<0.01]和肥胖OSAHS组[(5.0±1.0)mg/L,P<01]。与单纯性肥胖组的血清脂联素水平相比,无论肥胖OSAHS组或非肥胖OSAHS组均显著降低,差异有显著性(P<0.05)。肥胖OSAHS组与非肥胖OSAHS组的血清脂联素水平相比,差异无显著性(P>0.05)。肥胖OSAHS组与单纯性肥胖组的分析显示:血清脂联素水平与呼吸暂停低通气指数(AHI)(r=-0.78,P<0.01)、BMI(r=-0.21,P<0.05)、腰围(r=-O.36,P<0.01)和颈围呈负相关(r=-0.42,P<0.01),与最低脉搏血氧饱和度呈正相关(r=0.48,P<0.01)。结论 OSAHS患者中血清脂联素水平较正常对照和单纯肥胖者更低,除了腰围和颈围的因素     

Hypoadiponectinemia is closely linked to endothelial dysfunction in man

Vascular endothelial dysfunction has been demonstrated in overweight or obese patients, but the molecular basis for this link has not been clarified. We asked what the relationship was between adiponectin, an adipose-specific molecule, and endothelial function. Forearm blood flow (FBF) was measured during reactive hyperemia by using strain-gauge plethysmography in 76 Japanese subjects without a history of cardiovascular or cerebrovascular disease, diabetes mellitus, hepatic, or renal disease. The peak FBF and total reactive hyperemic flow [flow debt repayment (FDR)] during reactive hyperemia were correlated with waist circumference (r = -0.418 and -0.414, respectively) and body mass index (r = -0.597 and -0.626, respectively). After correcting for age, gender, and body mass index, the peak FBF was correlated with systolic blood pressure (r = -0.294; P = 0.010), free fatty acid (FFA) (r = -0.331; P = 0.004), and adiponectin in log 10 (r = 0.492; P < 0.001), and FDR was correlated with adiponectin in log 10 (r = 0.462; P = 0.001). In stepwise multiple regression analyses, predictive variables for peak FBF were adiponectin in log 10 (r = 0.468) and FFA (r = -0.292; r(2) = 0.487; P < 0.0001); and predictive variables for FDR were adiponectin in log 10 (r = 0.474) and FFA (r = -0.275; r(2) = 0.346, P < 0.0001). Endothelial function was impaired in proportion to the severity of obesity, and the level of severity was closely related to plasma adiponectin levels. Adiponectin may play a protective role against the atherosclerotic vascular change, and loss of effects enhances endothelial dysfunction, as in obese people.     

Weight reduction increases plasma levels of an adipose-derived anti-inflammatory protein, adiponectin

Adiponectin, an adipose tissue-specific plasma protein, was recently revealed to have anti-inflammatory effects on the cellular components of vascular wall. Its plasma levels were significantly lower in men than in women and lower in human subjects with obesity, type 2 diabetes mellitus, or coronary artery disease. Therefore, it may provide a biological link between obesity and obesity-related disorders such as atherosclerosis, against which it may confer protection. In this study, we observed the changes of plasma adiponectin levels with body weight reduction among 22 obese patients who received gastric partition surgery. A 46% increase of mean plasma adiponectin level was accompanied by a 21% reduction in mean body mass index. The change in plasma adiponectin levels was significantly correlated with the changes in body mass index (r = -0.5, P = 0.01), waist (r = -0.4, P = 0.04) and hip (r = -0.6, P = 0.0007) circumferences, and steady state plasma glucose levels (r = -0.5, P = 0.04). In multivariate linear regression models, the increase in adiponectin as a dependent variable was significantly related to the decrease in hip circumference (beta = -0.16, P = 0.028), after adjusting body mass index and waist circumference. The change in steady state plasma glucose levels as a dependent variable was related to the increase of adiponectin with a marginal significance (beta = -0.92, P = 0.053), after adjusting body mass index and waist and hip circumferences. In conclusion, body weight reduction increased the plasma levels of a protective adipocytokine, adiponectin. In addition, the increase in plasma adiponectin despite the reduction of the only tissue of its own synthesis suggests that the expression of adiponectin is under feedback inhibition in obesity.     

Fasting serum free fatty acid composition, waist/hip ratio and insulin activity in essential hypertensive patients

Abnormal fatty acid metabolism may play an important role in the pathogenesis of essential hypertension (EH). We compared fasting serum free fatty acid (FFA) composition between EH patients and nonhypertensive (NH) subjects, and examined the relationships between fasting serum FFA composition and waist/hip ratio, insulin activity, blood pressure, serum zinc, age, and sex in both groups. We conducted a cross-sectional study of 232 community-dwelling subjects aged between 35 and 60 years: 109 EH patients and 123 NH subjects. Serum FFA was determined by HPLC analysis. The data were analyzed by multivariate linear stepwise regression, stratified analysis, and correlation analysis. In men, EH patients had lower C22:6/C20:5 ratios (n-3 Delta6-desaturase activity index, 7.96+/-8.81 vs. 14.5+/-13.1, p<0.01), polyunsaturated fatty acid (PUFA), n-3 PUFA and polyunsaturated/saturated (P/S) ratios compared with male subjects without hypertension. There were no differences in women. Fasting serum FFA composition was significantly related to many variables, including waist/hip ratio, insulin sensitivity index, and serum zinc (all p<0.05 or <0.01) for all the subjects, and included both age- and sex-related differences (both p<0.05). Compared with NH, EH patients had lower levels of serum zinc (14.9+/-5.00 micromol L(-1) vs. 16.8+/-6.38 micromol L(-1), p<0.05). We concluded that EH patients had marked alteration in fasting serum FFA composition, which was affected by upper body obesity, insulin resistance, zinc deficiency, and high dietary fat, and that the differences were age- and sex-related.     

老年人代谢综合征的相关代谢指标和脂联素水平的临床观察

目的 观察老年代谢综合征（MS）患者相关代谢指标和脂联素的变化.方法 对我院就诊的老年患者进行问卷调查、体格检查及血液生化指标测定,了解代谢综合征组与非代谢综合征组的相关代谢指标和脂联素值.结果 代谢综合征患者年龄、体重、体质量指数、腰围、舒张压、收缩压、空腹血糖、餐后2h血糖、甘油三酯、高密度脂蛋白胆固醇、脂联素水平比无代谢综合征者明显升高,差异有统计学意义;脂联素水平随MS代谢紊乱数目的增多而明显升高（P＜0.01）.结论 患有代谢综合征的老年患者相关代谢指标明显升高,脂联素也明显升高,提示脂联素与MS的发生可能相关,应加强对老年患者代谢综合征相关代谢指标及脂联素的监测.     

腹部内脏脂肪沉积的老年非代谢综合征患者脂联素瘦素比值的变化

目的 观察体质指数正常、腹部内脏脂肪沉积的非代谢综合征老年男性患者血清脂联素、瘦素水平及脂联素瘦素比值的变化.方法 将入选的老年非代谢综合征男性患者109例分为2组,内脏无脂肪沉积组67例,内脏脂肪沉积组42例.采用CT方法测定内脏脂肪面积,当腹部内脏脂肪面积≥100cm2,为内脏脂肪沉积;采用LINCO公司提供的放射免疫试剂盒测定空腹血脂联素、瘦素水平;代谢综合征的诊断采用2004年中国糖尿病学会制定的标准.结果 (1)脂肪沉积组与无脂肪沉积组比较,体质指数、内脏脂肪面积均显著升高,体质指数分别为(22.94±1.35)kg/m2对(21.38±2.55)kg/m2(P＜O.001),内脏脂肪面积(135.6±31.7)cm2对(68.6±22.6)cm2(P＜O.001);脂联素瘦素比值降低.分别为2.17±1.77对4.54±7.00(P=0.031);而脂联素、瘦素水平在两者间差异无统计学意义;(2)脂联素瘦素比值与体质指数(r=-0.552,P＜0.001)、腰围(r=-0.390,P＜0.001)、腹部内脏脂肪面积(r=-0.311,P＜0.001)呈负相关.结论 体质指数正常有内脏脂肪沉积与无内脏脂肪沉积的老年男性比较.脂联素瘦素比值明显下降.并与腹部脂肪面积显著负相关.提示血清脂联素瘦素比值可能可用于筛选体质指数正常有腹部内脏脂肪肪沉积的患者.     

Serum aldosterone changes during hyperinsulinemia are correlated to body mass index and insulin sensitivity in patients with essential hypertension

OBJECTIVE: To measure the effects of hyperinsulinemia on serum electrolyte status and associated hormones, and on serum free fatty acid (FFA) concentrations, in patients with essential hypertension. DESIGN AND METHODS: The serum electrolyte status (Na, K, Ca, ionized Ca, Mg, P, pH) and associated hormones [plasma renin activity (PRA), serum parathyroid hormone (PTH) and aldosterone concentrations], and FFA were measured during an euglycemic hyperinsulinemic clamp test in 49 patients with untreated essential hypertension. RESULTS: Serum potassium, phosphate, PTH, and FFA concentrations decreased during hyperinsulinemia, while serum ionized calcium concentration, pH, and PRA increased significantly (P < 0.05). The changes in serum potassium and magnesium were both inversely related to the insulin-mediated glucose uptake (r= -0.62, P< 0.0001; r= -0.31, P< 0.05, respectively). Both body mass index (BMI) and insulin-mediated glucose disposal were significantly correlated to the changes in serum aldosterone concentration during hyperinsulinemia (r = 0.41, P < 0.01; r = -0.40, P < 0.01, respectively). The change in serum aldosterone during the clamp test was not significantly related to the change in PRA, but tended to correlate to the change in potassium concentration (r= 0.25, P= 0.10). A less pronounced reduction in FFA during induced hyperinsulinemia was associated with low insulin sensitivity (r= -0.35, P< 0.05). CONCLUSION: Hypertensive patients with normal BMI and a more pronounced glucose uptake showed a larger serum potassium decline and lowered aldosterone concentrations during induced euglycemic hyperinsulinemia. Insulin-resistant patients showed a less pronounced reduction in FFA during hyperinsulinemia. The observations in the present study may indicate that alterations in aldosterone and FFA metabolism might be linked to the insulin resistance metabolic syndrome.     

Inhibitory effect of insulin on vasopressin-induced intracellular calcium response is blunted in hyperinsulinemic hypertensive patients: role of membrane fatty acid composition

Impaired insulin-mediated vasodilation has been implicated in hypertension that is associated with the metabolic syndrome. The aim of this study was to determine whether an abnormality in membrane fatty acid composition was related to a weakening of insulin's inhibitory effect on agonist-stimulated intracellular free calcium elevation. Mild to moderate hypertensive patients (n = 27) and normotensive controls (n = 11) were studied. Hypertensive patients were divided into normoinsulinemic patients (n = 14) and hyperinsulinemic patients (n = 13) according to the area under the curve of plasma insulin concentrations during a 75-g oral glucose tolerance test. Nonstimulated and arginine-vasopressin (AVP) (1 μmol/l)-stimulated intraplatelet free calcium concentrations (p[Ca²⁺]_i) were measured with or without insulin (100 μU/ml) preincubation. Platelet membrane fatty acid composition, intraerythrocyte sodium content, and the ouabain-sensitive sodium efflux rate constant (K _os) of erythrocytes were also determined. Insulin preincubation reduced AVP-stimulated p[Ca²⁺]_i elevation in both normotensive controls and hypertensive patients. The inhibitory effect of insulin on AVP-stimulated elevation of p[Ca²⁺]_i (%Inhibition) was significantly (P < 0.05) blunted in hyperinsulinemic hypertensive patients (9.7% ± 2.4%) as compared to normoinsulinemic hypertensive patients (17.4% ± 2.7%) and normotensive controls (16.9% ± 1.7%). In hypertensive patients, the %Inhibition was correlated negatively with saturated fatty acids (SFA) (r = −0.51, P < 0.05) and systolic blood pressure (r = −0.44, P < 0.05), and correlated positively with membrane polyunsaturated fatty acids (PUFA) (r = 0.53, P < 0.01) and K _os (r = 0.53, P < 0.005). Multiple regression analysis showed that SFA, PUFA, and K _os were the significant variables for %Inhibition. These findings indicate that an increase in SFA and a decrease in PUFA may cause insulin insensitivity in cellular calcium and sodium handling in hypertension with hyperinsulinemia.     

代谢综合征合并糖尿病患者血清磷脂脂肪酸谱与超敏C反应蛋白相关性研究

研究代谢综合征合并糖尿病患者咀清磷脂脂肪酸谱组分与超敏C反应蛋白的关系.代谢综合征合并2型糖尿病患者饱和脂肪酸升高(45.98±1.55对42.05±2.04,P＜0.01),多不饱和脂肪酸下降(42.38±1.93对46.60±2.06,P＜0.01),血清超敏C反应蛋白明显升高[(6.36±1.28对0.79±0.45)mg/L,P＜0.01)].