高血压遗传史与胰岛素抵抗,高血压的关联

目的探讨高血压遗传史对第二,三代直系亲属血压水平,胰岛素抵抗及致动脉粥样硬化危险因素的影响.方法对象为高血压家族史阳性病例187人,高血压家族史阴性99人及他们的配偶子女286家858人.指标包括血压、血糖、总胆固醇、甘油三脂、高密胆固醇、纤维蛋白原、胰岛素敏感指数.结果调整年龄、性别影响后,高血压家族史阳性的第二代高血压,血压正常者之胰岛素敏感指数相似,但均相当于高血压家族史阴性第二代非高血压的2/3.高血压家族史阳性的第二代高血压,血压正常者组的FSG、TC、TG、FB均高于而HDL-c低于后者.第三代子女间血压、TC、TG、FSG、HDL-c趋势与第二代结果相似,但胰岛素敏感指数仅为家族史阴性组的4/5.结论高血压遗传因素可影响第二代及第三代子女,不管遗传或不遗传高血压,但毫无例外地遗传胰岛素抵抗及相关的代谢,表明胰岛素抵抗是高血压遗传因素的主要内容;胰岛素抵抗是否产生高血压尚必须有其他辅助条件或环境因素.     

血压健4号对气虚痰浊型高血压病患者血管活性物质的影响

目的探讨高血压遗传史对第二,三代直系亲属血压水平,胰岛素抵抗及致动脉粥样硬化危险因素的影响.方法对象为高血压家族史阳性病例187人,高血压家族史阴性99人及他们的配偶子女286家858人.指标包括血压、血糖、总胆固醇、甘油三脂、高密胆固醇、纤维蛋白原、胰岛素敏感指数.结果调整年龄、性别影响后,高血压家族史阳性的第二代高血压,血压正常者之胰岛素敏感指数相似,但均相当于高血压家族史阴性第二代非高血压的2/3.高血压家族史阳性的第二代高血压,血压正常者组的FSG、TC、TG、FB均高于而HDL-c低于后者.第三代子女间血压、TC、TG、FSG、HDL-c趋势与第二代结果相似,但胰岛素敏感指数仅为家族史阴性组的4/5.结论高血压遗传因素可影响第二代及第三代子女,不管遗传或不遗传高血压,但毫无例外地遗传胰岛素抵抗及相关的代谢,表明胰岛素抵抗是高血压遗传因素的主要内容;胰岛素抵抗是否产生高血压尚必须有其他辅助条件或环境因素.     

胰岛素抵抗--遗传和环境因素致高血压的共同途径?

目的　探讨胰岛素抵抗是否是遗传和环境因素致高血压的共同途径。方法　大庆地区具有血缘关系的三代内直系亲属 2 86核心家庭成员 858人 ,年龄 1 8～ 74岁。测血压、空腹血糖 (FPG)、胰岛素 (FINS)、胆固醇、甘油三酯、高密度脂蛋白胆固醇 (HDL C)、纤维蛋白原。计算胰岛素敏感性(ISI) =1 / (FPG×FINS) ,胰岛素抵抗 (IR) =(FPG×FINS) / 2 2 .5。以多因素回归分析探讨遗传和环境因素对血压水平的贡献。结果　原发性高血压组无论其有无阳性高血压家族史 ,胰岛素敏感性都较差。多因素逐步回归分析结果显示 ,胰岛素敏感性是高血压伴高血压家族史者、高血压不伴高血压家族史者及正常血压不伴高血压家族史 (且其配偶血压也正常 )者血压升高最重要的因素 ,能解释平均血压 (MBP)变化的 1 7% ;而空腹血糖、总胆固醇与HDL C 3项只能解释MBP变化的 9%。在分析自变量中加入高血压家族史一项时 ,则阳性高血压家族史成了血压升高最重要的因素 ,仅此一项就可解释MBP变化的 30 % ,而胰岛素敏感性对血压水平的贡献大幅度削弱 ,仅能解释MBP的 7%。对配偶组的分析显示同样趋势。结论　胰岛素抵抗是遗传及环境因素致高血压重要的共同途径 ,遗传因素还通过胰岛素抵抗以外的途径使血压升高     

血清胰岛素与糖尿病合并高血压关系的探讨

本实验对92例非胰岛素依赖型糖尿病(NIDDM)合并高血压病人及92例NIDDM血压正常者同步检测了空腹血清胰岛素(FINS)、C—肽、血糖(FBG)、血脂。结果发现:(1)NIDDM合并高血压组FINS及C—肽水平显著高于对照组;(2)排除干扰因素后,血压与FINS、C—肽显著相关;(3)胰岛素敏感指数(FBG/FINS)与血压、体重指数(BMI)、甘油三酯(TG)显著负相关,与高密度脂蛋白胆固醇(HDL—ch)显著正相关。提示:FINS水平增高是NIDDM合并高血压的独立危险因素之一,胰岛素抵抗与高血压、肥胖、高FINS、高TG、低HDL—ch血症之间存在密切的内在联系。     

高血压与胰岛素抵抗关系的临床研究

目的探讨老年原发性高血压患者与高胰岛素血症、胰岛素抵抗(INSR)、高血脂和肥胖相关因素进行分析。方法对无糖尿病病史的老年原发性高血压患者100例,老年对照组50例的空腹血糖及餐后2 h血糖(FBG)、胰岛素(FINS)、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白(HDL)、体重指数(BMI)、胰岛素敏感指数(ISI)和脂肪分布指数(WHR)进行对照分析对比。结果高血压组的BMI,WHR,FBG,FINS,TG水平高于对照组,ISI低于对照组。经多元分析,ISI与TG,BMI,WHR呈负相关,与HDL呈正相关。结论老年高血压患者多伴有糖代谢和脂蛋白代谢异常,胰岛素抵抗所产生的高胰岛素血症为其基本的代谢异常,这是造成高血压病并发冠心病发生的重要原因之一。     

高血压家族对子代胰岛素抵抗影响的研究

目的 :探讨老年高血压胰岛素抵抗 (IR)对子代的影响。方法 :老年高血压 IR患者及其直系第一代子女与健康老年人及其直系第一代子女各 33例 ,分别检测血压、体重指数 (BMI)、血糖、胰岛素、血脂、血尿酸(UA )、纤维蛋白原 ,并计算胰岛素敏感指数 (IAI)及胰岛素抵抗指数 (IRI)。结果 :高血压 IR老年人及其子女组与健康老年人及其子女组对比 ,空腹胰岛素 (In S)、总胆固醇 (TC)、甘油三酯 (TG)、IAI、IRI有极显著性差异 (P<0 .0 1)。 BMI、空腹血糖 (SG)、UA、餐后 2 h血糖 (SG2 )、餐后 2 h胰岛素 (In S2 )、In S/ SG有显著性差异 (P <0 .0 5 ) ,而 C肽 (CP)、高密度脂蛋白 (HDL- C)、低密度脂蛋白 (L DL- C)、纤维蛋白原 (Fg)两者比较则无显著性差异(P >0 .0 5 )。结论 :老年高血压 IR患者子代存在 IR现象 ,机体对胰岛素的敏感性降低     

两代高血压家族史子代的动态血压负荷值及胰岛素抵抗研究

目的 探讨早期发现高血压家族史血压正常子女在高血压发生前的异常表现,延缓甚至预防其未来高血压及一些代谢性疾病的发生.方法 选择高血压患者子代亲属194例(观察组),其中父母中仅一方患高血压者101例(单亲组),仅父亲患高血压者62例(单亲父亲组),仅母亲患高血压者39例(单亲母亲组),父母双方均患高血压者93例(双亲组);另选血压正常的非高血压子代亲属157例作为对照组.对各组受检者行24h动态血压监测、血脂、空腹血糖及胰岛素抵抗指标检测,并进行比较.结果 双亲组和单亲组的血脂、BMI、24 h舒张压、24 h收缩压、24h平均动脉压比较,P均＞0.05;与对照组比较,双亲组和单亲组的24 h平均及昼夜血压负荷值、胰岛素抵抗指数、胰岛素敏感指数、空腹血糖均有统计学差异(P均＜0.01).结论 有高血压家族史而血压正常的子女,在血压正常时已出现血压负荷值升高,并在早期出现胰岛素抵抗现象.因此,检测血压负荷值与胰岛素抵抗指标可能预测有高血压家族史而血压正常者的血压发展倾向.     

原发性高血压与脂肪肝及血脂相关性调查

目的 探讨原发性高血压与血脂代谢水平及脂肪肝发生率的关系.方法 收集海南医学院附属医院原发性高血压患者351例,以及血压正常者100例,抽血检测甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、血糖、血尿酸、尿素氮和肌酐水平,B超检测脂肪肝比率,同时测量体重及体重指数.结果 高血压患者的TG、TC、AST、血糖、血尿酸、肌酐水平及脂肪肝患病率、体重和体重指数明显高于血压正常者,HDL-C低于血压正常者,差异均有统计学意义,LDL-C、ALT、尿素氮则差异无统计学意义.结论 高血压患者的脂肪肝患病率、体重及体重指数、TG、TC、AST、血糖、血尿酸、尿素氮和肌酐水平明显高于血压正常者,其与高血压呈正相关.     

高血压大家系中胰岛素抵抗与高血压关系的研究

目的探讨胰岛素抵抗是否为所研究高血压大家系的遗传中间表型,研究胰岛素抵抗与高血压关系.方法我们在北京石景山区收集到一个高血压大家系,共4代约220人,以该高血压大家系成员为观察对象,检测其空腹血糖(FPG),血脂,血浆胰岛素(FINS),计算胰岛素抵抗指数(IR)反映胰岛素抵抗的情况.结果该家系直系成员高血压组和血压正常组IR值都显著高于家族旁系血压正常(亦无高血压家族史)组.Logistic回归分析显示在家族直系成员中,年龄为影响血压的主要因素,旁系中年龄,IR为影响血压的主要因素,而以IR对血压的影响最大.结论胰岛素抵抗对该高血压大家系血压水平有一定影响,能否作为其遗传中间表型尚需进一步研究,但在该家系居住的同一地区人群中,胰岛素抵抗是影响血压的重要危险因素,可能同高血压有共同的遗传因素.     

高血压合并脂肪肝与胰岛素抵抗的相关分析

目的：探讨高血压合并脂肪肝与胰岛素抵抗（IR）的相关性。方法：根据超声影像学的诊断结果将住院治疗的高血压患者分为高血压合并脂肪肝组（98例）和高血压未合并脂肪肝组（104例），研究两组的体重指数（BMD、血压（BP）、血糖、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）、肝酶和血浆胰岛索，胰岛素抵抗指数（IRI）水平。结果：高血压合并脂肪肝组较高血压未合并脂肪肝组的血糖、胰岛素水平、甘油三酯和胰岛素抵抗指数均明显增高（P〈0．05）。Logistic回归结果表明空腹血糖（FBG）、肥胖、丙氨酸氨基转氨酶（ALT）、葡萄糖负荷试验后3h胰岛素水平、甘油三醋（TG）是脂肪肝形成的独立危险因素（OR=1．980～3．245，P〈0．05）。结论：高血压和脂肪肝均是胰岛素抵抗的重要表现，高血压合并的脂肪肝其发病机制与胰岛素抵抗有关。     

高血压遗传因素与胰岛素抵抗

目的探讨高血压遗传因素与胰岛素抵抗及其他代谢因素的关系。方法采用家系调查方法，共调查高血压家系２５个，包括直系亲属１５８例，其中高血压５４例，血压正常者１０４例；对照家系１５个，直系亲属６５人。对比分析高血压家系有无高血压及对照家系直系亲属尿酸、血脂、血糖及胰岛素的差异。结果调整年龄、性别后，在高血压家系中无论是否患高血压，甘油三酯（ＴＧ）、ＴＧ的对数转换值（ｌｏｇＴＧ）、高密度脂蛋白胆固醇（ＨＤＬＣ）、血浆总胆固醇（ＴＣ）／ＨＤＬＣ、尿酸、胰岛素（ＩＮ）及其对转换值（ｌｏｇＩＮ）均显著高于对照家系，而高血压家系内有无高血压两组比较，除胰岛素、ｌｏｇＩＮ外，其他因素均无显著差别，进一步调整年龄、性别、体重指数后比较，ＴＧ、ｌｏｇＴＧ在三组间差异不再显著，尿酸、ＴＣ／ＨＤＬＣ、ｌｏｇＩＮ在高血压家系内高血压及血压正常人群间无显著统计学差别，但两者与对照家系相比均显著升高。结论具有高血压遗传因素者无论是否患高血压均有显著的胰岛素抵抗和代谢紊乱，这些代谢异常可能在超重和高血压发生前就已存在。     

Inflammation, insulin resistance and carotid IMT in first degree relatives of north Indian type 2 diabetic subjects

Inflammation is associated with insulin resistance, atherosclerosis and type 2 diabetes but whether it causes insulin resistance and accelerated atherosclerosis or an epiphenomena of insulin resistance is not clear. Thirty-eight young normoglycemic, non-obese, first degree relatives of type 2 diabetic subjects (FH(+)) and 38 control subjects without family history of diabetes (FH(-)) (age and sex matched), were studied to determine difference in inflammatory markers, insulin resistance and carotid intima-media thickness (IMT). Plasma glucose, insulin (fasting and 2h after 75gm oral glucose) lipids and serum levels of C-reactive protein (CRP), tumour necrosis factor (TNF)-alpha and fibrinogen were measured after an overnight fast of 10-12h. First degree relative group (FH(+)) have higher BMI (p<0.05), composite IMT (p<0.05) and CRP level (p<0.05), however, after adjustment for BMI, the two groups did not significantly differ. Fibrinogen was not significantly correlated with composite IMT in FH(+) group after controlling with BMI. In FH(+) group composite IMT was significantly correlated with systolic blood pressure (p<0.05), LDL-cholesterol (p<0.05), postprandial insulin level (p<0.05) and HOMA-IR (p<0.05) after adjustment of BMI. Thus insulin resistance is a major determinant of atherosclerosis in subjects with high risk of type 2 diabetes showing the strong relationship between inflammation, obesity and insulin resistance.     

老年高血压患者胰岛素抵抗与血脂代谢的关系

目的探讨老年高血压患者胰岛素抵抗(IR)与血脂代谢的关系。方法将60例老年高血压患者根据有无合并糖尿病分为单纯高血压组30例(HP)组,高血压合并2型糖尿病组30例(HP+DM组);30名正常健康者作为对照组(NC组),3组患者进行动态血压、血空腹血糖(FBG)、空腹胰岛素(FINS)、血脂分析包括血甘油三酯(TG)、胆固醇(TC)及高密度脂蛋白(HDL)等的检测。结果三组比较FBG、FINS、收缩压(SBP)、TG、TC和IAI有显著性差异,相关分析显示SBP、TG、TC均与IAI成明显负相关。结论高血压与IR密切相关,IR可导致脂质代谢紊乱,血脂异常又参与IR的发生与进展。     

Early 24-hour blood pressure elevation in normotensive subjects with parental hypertension

Subjects with a family history of parental hypertension are reported to have a slightly higher office blood pressure in the prehypertensive stage. Whether this reflects a hyperreactivity to blood pressure measurement or a more permanent blood pressure elevation, however, is not known. In the present study, blood pressure was measured in 15 normotensive subjects whose parents are both hypertensive (FH++), 15 normotensive subjects with one hypertensive parent (FH(+)-), and 15 normotensive subjects whose parents are not hypertensive (FH--); among the three groups, subjects were matched for age, sex, and body mass index. The measurements were made in the office during a variety of laboratory stressors and during a prolonged resting period, and for a 24-hour period (ambulatory blood pressure monitoring). Office blood pressure was higher in the FH++ group than in the FH-- group (p less than 0.05). The pressor responses to laboratory stressors were similar in the two groups, but the FH++ group had higher prolonged resting and 24-hour blood pressure than the FH-- group; the difference was always significant (p less than 0.05) for systolic blood pressure. The FH++ group also had a greater left ventricular mass index (on echocardiographic examination) than the FH-- group (p less than 0.01). The blood pressure values and echocardiographic values of the FH(+)- group tended to be between those of the other two groups. Thus, the higher blood pressure shown by individuals in the prehypertensive stage with a family history of parental hypertension does not reflect a hyperreactivity to stress but an early permanent blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Low adiponectin level in young normotensive men with a family history of essential hypertension.

Circulating level of adiponectin, an adipocyte-derived protein, is reduced in states of insulin resistance such as obesity and type 2 diabetes. We have previously shown that hypoadiponectinemia is related to insulin resistance in essential hypertension. Recent studies have shown that normotensive subjects with a positive family history of essential hypertension (FH+) have decreased insulin sensitivity compared to subjects with a negative family history of essential hypertension (FH-). We here examined the association between adiponectin concentration and insulin sensitivity in FH+ and FH-. Thirty young, non-obese and normotensive men without a family history of diabetes mellitus were enrolled. A total of 15 subjects were FH+, and the remaining 15 subjects were FH-. Insulin sensitivity index (ISI) was evaluated by the euglycemic hyperinsulinemic glucose clamp technique. Concentrations of adiponectin and other metabolic variables were measured. The FH+ group had significantly lower levels of ISI and adiponectin than did the FH- group. In all of the subjects, ISI was positively correlated with adiponectin concentration and high-density lipoprotein (HDL) cholesterol level and was negatively correlated with insulin level. Adiponectin concentration was the only independent determinant of ISI in a multiple regression analysis. Our results showed that adiponectin level was significantly decreased and that this was accompanied by reduced insulin sensitivity in young, nonobese and normotensive men with a family history of essential hypertension. Phenotype of reduced adiponectin level as an earlier penetrance may be especially useful in genetic analyses of insulin resistance and essential hypertension.     

Changes in 24 Hour Blood Pressure and in Cardiac and Vascular Structure in Normotensive Subjects with Parental Hypertension

Subjects with family history of hypertension represent a suitable model to investigate the mechanisms responsible for early cardiovascular structural and functional changes occurring in essential hypertension. In our study we have addressed the factors involved in determining the mild elevation in office blood pressure frequently observed in normotensive subjects with hypertensive parents. In 15 normotensive subjects with both parents hypertensive (FH++) and in 15 normotensive subjects with one parent hypertensive (FH+?) we found no evidence of a hyperreactivity to stress as compared to the responses of 15 normotensive subjects with no parental hypertension (FH–). On the contrary FH++ subjects were characterized by a significant although mild increase in their blood pressure values recorded either at rest and in ambulatory conditions over the 24 hours, including night sleep. FH++ and FH+? subjects also showed a greater left ventricular mass thickness and a greater minimal forearm vascular resistence than FH subjects. Thus, the elevation in blood pressure found in the pre-hypertensive stage in subjects with positive family history for hypertension does not reflect a hyperreactivity to the stress associated with physician's visit but indicates an early and persistent blood pressure elevation. This blood pressure elevation is accompanied by early cardiovascular structural changes which may indicate that these subjects are exposed to a higher risk even before developing overt hypertension.     

A family history of Type 2 diabetes is associated with increased plasma levels of C-reactive protein in non-smoking healthy adult women.

AIMS: The aim of our study was to test whether a family history of Type 2 diabetes (FH) in women is associated with plasma C-reactive protein (CRP). METHODS: CRP plasma levels were measured in 162 women, aged 18-60 years; 95 had a positive family history of Type 2 diabetes in a parent or grandparent (FH+), and 67 gave no family history of this disease (FH-). Other measurements included: central fat accumulation, as evaluated by waist circumference; insulin resistance, as calculated by homeostatic model assessment (HOMAIR); systolic and diastolic blood pressure; and fasting concentrations of glucose, insulin, and lipids. RESULTS: CRP plasma levels were significantly higher in FH+ than in FH- subjects. Moreover, CRP was independently associated with age, body mass index, waist circumference, HOMAIR, and FH. CONCLUSIONS: Our study, performed in a selected population of women free from well-known risk factors for atherothrombosis, demonstrates that subjects with a family history of Type 2 diabetes have higher CRP plasma levels than age- and BMI-matched controls with no family history. Our results show that a family history of Type 2 diabetes is an independent contributor of CRP concentrations, in addition to age, total fatness, central fat accumulation, and insulin resistance.     

The pressor response to acute hyperlipidemia is enhanced in lean normotensive offspring of hypertensive parents

Family history is an important predictor of the cardiovascular risk factor cluster associated with insulin resistance. The dyslipidemia associated with insulin resistance may contribute to elevated blood pressure (BP). This study was undertaken to further explore the link between family history, dyslipidemia, and BP regulation. Twenty-three lean normal volunteers with a negative family history (FH-, n = 11) or positive family history (FH+, n = 12) of hypertension were evaluated under baseline conditions and during a 4-h infusion of intralipid and heparin (acute hyperlipidemia). Fasting blood was drawn for lipids including nonesterified fatty acids (NEFA). After 2 and 4 h of intralipid and heparin, blood was drawn for NEFA. The BP was measured at baseline and every 30 min after starting the intralipid and heparin infusion. Baseline triglycerides and very low density lipoprotein cholesterol concentrations were higher in FH+ than FH- subjects (P < .05). However, NEFA increased similarly in both groups during the infusion of intralipid and heparin. The BP and heart rate increased with acute hyperlipidemia in all subjects combined (P < .05). Despite the similar increase of NEFA, mean BP, pulse pressure, and pressure-rate product increased significantly in FH+ subjects but not in FH- volunteers with acute hyperlipidemia. Although systolic BP increased in both groups, the increase was greater in FH+ than in FH- volunteers during acute hyperlipidemia (14 +/- 2 v 10 +/- 2 mm Hg, P < .05). These results suggest that higher plasma lipids combined with a greater pressor response to hyperlipidemia may contribute to the development of high BP in subjects with a family history of hypertension.     

Hyperinsulinemia,family history of hypertension,and essential hypertension

The aim of this study was the evaluation of the relationships among hyperinsulinemia, a family history of hypertension, and essential hypertension. Insulin and C-peptide responses to an oral glucose load were studied in 175 lean normotensives (N) and untreated hypertensives (H) with (F+) and without (F−) a family history of hypertension: 30 NF-, 30 NF+, 45 HF-, and 70 HF+. The groups were comparable for age, sex, body mass index, and blood pressure. The following parameters were evaluated: plasma glucose (G), serum insulin (I), and C-peptide (Cp) before and 30, 60, 90, and 120 min after the glucose load, fasting glucose/insulin ratio (ISI), fasting insulin/C-peptide ratio (I/Cp), and 24-h ambulatory blood pressure monitoring. Plasma glucose was measured, fasting and during the test, and it and I/Cp were similar in the four groups. Serum insulin and Cp, both fasting and stimulated, were significantly higher and ISI lower in normotensives and hypertensives with hypertensive parents. Grouping the subjects first on the basis of blood pressure and then on the basis of family history, no differences were found between normotensives and hypertensives, whereas I and Cp, fasting and stimulated, were significantly higher and ISI lower in subjects with positive as compared to negative family history. The closest correlations between insulin and ambulatory blood pressure were found in normotensives with hypertensive parents; in hypertensives with hypertensive parents we only found a direct correlation between fasting Cp and nocturnal blood pressure fall; in hypertensives with normotensive parents insulin inversely correlated with nocturnal blood pressure fall. Insulin resistance seems to have a familial basis, independently of the presence of hypertension. Instead of showing a causal relationship between insulin resistance and hypertension, our results indicate that the two are partly independent components of a common familial pattern.