原发性高血压赖诺普利治疗前后血清胰岛素样生长因子-Ⅰ的变化

目的观察原发性高血压(EH)患者服用赖诺普利治疗前后血清胰岛素样生长因子-Ⅰ(IGF-Ⅰ)的变化,探讨IGF-Ⅰ在EH的发生发展过程中所起的可能作用.方法47例EH患者均行超声心动图检查,用放免法测定赖诺普利治疗前、治疗后半年及23例正常对照者血清IGF-Ⅰ水平.结果EH患者血清IGF-Ⅰ水平明显高于对照组分别为(22.23±10.06)ng/ml对(15.91±7.59)ng/ml,P＜0.01.Ⅰ～Ⅲ级间比较也有显著性差异(F=3.53,P＜0.05),Ⅲ级(28.61±13.10)ng/ml高于Ⅱ级(22.64±9.94)ng/ml,Ⅱ级高于Ⅰ级(18.09±6.11)ng/ml.EH伴左心室肥厚(LVH)者高于无LVH者(25.95±11.20)ng/ml对(18.68±7.43)ng/ml,P＜0.05.IGF-Ⅰ与左心室重量指数中度相关(r=0.54).赖诺普利治疗6个月后,血清IGF-Ⅰ水平由(22.23±10.06)ng/ml降至(16.82±7.93)ng/ml,P＜0.05.结论EH LVH患者IGF-Ⅰ水平升高,赖诺普利治疗后IGF-Ⅰ水平下降,IGF-Ⅰ可能参与EH LVH的形成.     

原发性高血压患者福辛普利治疗前后血清胰岛素样生长因子-1水平的变化

目的：探讨原发性高血压（EH）患者福辛普利治疗前后血清胰岛素样生长因子-1（IGF-1）水平的变化及其与EH心肌肥厚形成的关系。方法：用放射免疫分析法测定46例EH患者（EH组）福辛普利治疗前后、治疗3个月及18例正常血压者（对照组）的血清IGF-1水平。结果：EH患者的血清IGF-1为（13．28±3．59）nmol/L,明显高于对照组（9．50±l．65）nmol/L（P＜0．001）。Ⅱ期EH患者的平均血清IGF-1水平（14．73±3．21）nmol／L明显高于Ⅰ期患者（11．58±3．48）nmol/L（P＜0．005）;伴左室肥厚（LVH）者IGF-1为（15．83±3．36）nmol／L,高于无LVH者［（1．69±2．29）nmol/L）（P＜0．01）;与对照组比较均P＜0.00I。EH患者血清IGF-1水平与左室重量指数（LVMI）呈显著正相关（r＝0．811,P＜o．001）。福辛普利治疗3个月后,血清IGF-1水平降到（10．93±2．44）nmol／L（P＜0.00I）,与对照组比较P＜0．05;LVH者仍高于无LVH者［（12．67±1．79）比（10．62±1．98）nmol／L,P＜0．OI〕。结论：EH患者血清IGF-1水平升高,尤其是伴LVH的患者,经福辛普利治疗后其水平下降,说明IGF-1可能参与EH心肌肥厚的形成。     

原发性高血压患者福辛普利治疗前后血清胰岛素样生长因子-1水平的变化

目的探讨原发性高血压患者抗高血压治疗前后血清胰岛素样生长因子-1(IGF-1)水平的变化。     

贝那普利对肝纤维化大鼠胰岛素样生长因子-I受体的影响

目的研究血管紧张素转换酶抑制剂贝那普利对大鼠肝纤维化模型的疗效,以及对其肝组织胰岛素样生长因子-1受体（IGF—IR）的影响。方法取Wistar雄性大鼠42只随机分为3组,正常对照组12只,模型组15只,贝那普利治疗组15只。制备四氯化碳诱导的大鼠肝纤维化模型,同时应用贝那普利灌胃,共8周。对肝组织进行苏木精伊红染色及马松三色染色,观察各组肝纤维化的程度,并测定血清丙氨酸氨基转移酶（ALT）水平,采用SABC免疫组织化学方法检测大鼠肝组织中IGF—IR的表达水平。结果贝那普利治疗组的肝纤维化程度明显较同期模型组轻（P〈0．05）;与对照组相比,模型组体重降低（P〈0．05）及血清ALT升高（P〈0．05）,IGF-IR在肝组织中表达明显增多（P〈0．05）,贝那普利治疗组IGF—IR表达减少（P〈0．05）。结论贝那普利可改善肝纤维化程度,可能与肝组织IGF—IR的表达减少有关。     

原发性高血压患者血清胰岛素样生长因子Ⅰ的变化

目的 :探讨胰岛素样生长因子 ( IGF- )与原发性高血压 ( EH)的关系 ,评价 IGF- 对EH左心室肥厚 ( L VH)患者的病理生理意义。方法 :采用特异性放射免疫分析法测定了 30例未治疗的 EH患者和 2 0例正常人的血清 IGF- 水平。结果 :EH患者血清 IGF- 水平明显高于正常人〔( 13.90± 3.5 0 ) nmol/ L∶ ( 9.40± 1.60 ) nmol/ L,P<0 .0 0 1〕,而且随病情的加重而升高 ;EH伴有L VH者 IGF- 高于无 L VH者〔( 15 .34± 3.48) nmol/ L∶ ( 12 .2 5± 2 .82 ) nmol/ L ,P <0 .0 2〕;EH伴有肾功能损害者亦高于无相应病变者〔( 15 .79± 3.79) nmol/ L∶ ( 12 .64± 2 .73) nmol/ L,P <0 .0 2〕。结论 :EH患者的循环 IGF- 水平升高 ,其升高程度与 EH病情的严重程度有关 ,IGF- 可能参与 EH心肌肥厚的调节。     

苯磺酸氨氯地平联合赖诺普利治疗原发性高血压的临床研究

目的探讨苯磺酸氨氯地平联合赖诺普利治疗原发性高血压的疗效和安全性。方法将64例原发性高血压患者分为苯磺酸氨氯地平、赖诺普利联合组(A组)32例和单用氨氯地平组(B组)32例,用药24周后观察疗效。结果两组患者治疗后血压均较治疗前有明显改善,治疗前后比较差异具有统计学意义。苯磺酸氨氯地平、赖诺普利联合组治疗收缩压总有效率为90.6%,舒张压84.4%,单用氨氯地平组收缩压71.9%,舒张压65.6%,两者比较差异有统计学意义(P0.05)。苯磺酸氨氯地平、赖诺普利联合组不良反应发生率为12.5%,单用氨氯地平组9.3%,两组间比较差异无统计学意义(P0.05),左室重量指数(LVMI)较治疗前明显改善(P0.05),A组较B组更明显(P0.01)。结论苯磺酸氨氯地平联合赖诺普利具有明显的降压作用,对LVH逆转有协同作用,且不良反应少。     

胰岛素样生长因子1与原发性高血压

目的探讨原发性高血压病的发病机制。方法对28例原发性高血压患者和16名正常人测定了血清胰岛素样生长因子1(IGF1)，并与高血压分级进行了相关分析。结果原发性高血压患者IGF1水平显著低于正常人(分别为26.22μg／L±20.23μg／L和48.02μg／L±33.43μg／L，P＜0.05)，且IGF1水平与临床分级呈负相关(r=-0.437，P＜0.05)。结论IGF1可能参与了原发性高血压的病理生理过程。     

贝那普利对肝纤维化大鼠胰岛素样生长因子-Ⅰ受体的影响

目的研究血管紧张素转换酶抑制剂贝那普利对大鼠肝纤维化模型的疗效,以及对其肝组织胰岛素样生长因子-Ⅰ受体(IGF-ⅠR)的影响.方法取Wistar雄性大鼠42只随机分为3组,正常对照组12只,模型组15只,贝那普利治疗组15只.制备四氯化碳诱导的大鼠肝纤维化模型,同时应用贝那普利灌胃,共8周.对肝组织进行苏木精-伊红染色...     

原发性高血压血清胰岛素样生长因子-1的临床研究

目的：观察原发性高血压患者胰岛素样生长因子－１（ＩＧＦ－１）血清水平与原发性高血压及原发性高血压合并左心室肥厚（ＬＶＨ）的关系。　　方法：对３８ 例原发性高血压患者进行超声心动图检查,确定有无ＬＶＨ及左心室舒张功能减低,同时用放射免疫法测定其血清中ＩＧＦ－１的浓度,根据有无合并ＬＶＨ,将３８ 例原发性高血压患者分为单纯原发性高血压组（ｎ＝ ２０）,原发性高血压合并ＬＶＨ组（ｎ＝ １８）。另选２４ 例正常人为正常对照组,比较３ 组之间血清ＩＧＦ－１ 水平。　　结果：原发性高血压合并ＬＶＨ组血清ＩＧＦ－１水平高于正常对照组（２４７．９±４６．４ ｖｓ．２０８．４±６１．７,Ｐ＜ ０．０５）,左心室重量指数（ＬＶＭＩ）与血清ＩＧＦ－１中度相关（ｒ＝ ０．４１,Ｐ＜ ０．０５）。　　结论：ＩＧＦ－１可能参与了原发性高血压ＬＶＨ的发生发展过程。     

原发性高血压患者血清胰岛素样生长因子Ⅱ和生长激素的变化

目的:探讨原发性高血压患者血清胰岛素样生长因子Ⅱ(IGFⅡ)和生长激素(GH)含量的变化及其临床意义。方法:用放射免疫法测定92例原发性高血压(EH)患者和45例非高血压患者的血清IGFⅡ和GH的水平,并进行对照统计分析。结果:EH组血清IGFⅡ水平显著高于对照组(P<0.01),而GH水平显著低于对照组,2参数间呈显著负相关(P<0.05),IGFⅡ与平均动脉压成显著正相关(P<0.05),GH与平均动脉压、体重指数均无相关性意义。男女组间2参数比较亦无统计学差异。在高血压Ⅰ、Ⅱ、Ⅲ期组间,血清GH水平依次递减(F检验,P<0.01),且Ⅲ期组显著低于Ⅰ期组(P<0.05),伴心脑肾并发症组血清GH水平也显著低于无并发症组(P<0.05);血清IGFⅡ水平3期间则均无显著差异。结论:EH患者血清IGFⅡ水平显著升高,而GH水平显著降低,两参数间呈负相关。     

原发性高血压患者血清胰岛素样生长因子1浓度的变化

目的:探讨原发性高血压(EH)患者血清胰岛素样生长因子-1(IGF-1)水平的变化,评价IGF-1对EH及其并发症左室肥厚(LVH)的病理生理意义。方法:用特异性放射免疫法测定50例EH患者(EH组)和25例正常人(正常对照组)的血清IGF-1水平。结果;EH患者血清IGF-1水平明显高于正常对照组(P<0.01),EH并发LVH患者乎均血清IGF-1水平明显高于无LVH者(P<0.01)。结论:EH患者尤其是伴发LVH者血清IGF-1水平升高,提示IGF-1可能参与EH及其并发症LVH的形成。     

胰岛素治疗对血清中胰岛素样生长因子I水平的影响

探讨胰岛素治疗对2型糖尿病患者血清中胰岛素样生长因子I(IGF-I)水平的影响以及两者之间的关系.结果 发现2型糖尿病患者外源性胰岛素治疗可增加血清中的IGF-I水平[(126.70±51.91对90.04±43.68)μg/L,P<0.01],并且IGF-I水平与胰岛素水平呈正相关(r=0.298,P<0.05).

Abstract：

To explore the effect of insulin therapy on serum level of insulin-like growth factor-I(IGF-I)in patients with type 2 diabetes mellitus.The results showed that serum IGF-I level increased[(126.70±51.91 vs 90.04±43.68)μg/L,P<0.01]and was positively correlated with insulin level in patients with type 2 diabetes mellitus after exogenous insulin therapy(r=0.298,P<0.05).     

高血压病患者福辛普利治疗前后血浆肾上腺髓质素水平的变化

目的 探讨高血压病患者抗高血压治疗前后血浆肾上腺髓质素（ＡＭ）水平的变化。方法 用特异性的放射免疫分析法测定３３例高血压病患者福辛普利治疗前、治疗３个月后及３０例正常对照组的血浆ＡＭ水平。结果 高血压病患者的基础血浆ＡＭ水平明显高于对照组［（５５．７８±１５．０８）ｎｇ／Ｌ比（３９．９０± ６．９３）ｎｇ／Ｌ,Ｐ＜０．０１］。ＩＩ期患者的平均血浆ＡＭ水平显著高于Ｉ期患者［（６１．８７±１３．４８）ｎｇ／Ｌ比（４８．６４±１４．６２）ｎｇ／Ｌ,Ｐ＜０．０１］;伴有左心室肥厚（ＬＶＨ）者高于无ＬＶＨ者［（６６．４９±１４．１１）ｎｇ／Ｌ比（５３．２９±９．６２）ｎｇ／Ｌ,Ｐ＜０．０２］;有肾功能损害者也高于无相应病变者［（６７．３２±１５．９２）ｎｇ／Ｌ比（５３．０９±１１．４７）ｎｇ／Ｌ,Ｐ＜０．０２］。福辛普利治疗３个月后,高血压病患者的血浆ＡＭ水平降至（４５．９１±１０．２５）ｎｇ／Ｌ（Ｐ＜０．０１）,但ＬＶＨ或肾功能损害者仍高于无相应病变者（均Ｐ＜０．０５）。结论 本研究结果显示高血压病患者的血浆ＡＭ水平升高,尤其是伴ＬＶＨ和肾功能损害的患者,福辛普利治疗后其水平显著下降,说明ＡＭ可能对血压的调节和肾功能的保     

缬沙坦与赖诺普利治疗原发性高血压的疗效和安全性的比较研究

目的研究缬沙坦降压疗效及安全性并与赖诺普利相比较。方法经2w冲洗期后,60例Ⅰ、Ⅱ级原发性高血压患者随机分为缬沙坦组(A组),赖诺普利组(B组),分别给予缬沙坦80mg/d,赖诺普利10mg/d共4w,全部病例治疗前后行偶测血压(CBP)和血脂、血糖、尿素氮、肌酐、转氨酶、心率测定。两组中各选10例治疗前后行24h动态血压测定(ABPM)。结果 两组降压总有效率CBP分别为80.64％和65.52％(P>0.05),ABPM分别为70％和60％,两组比较无显著差异(P>0.05);谷/峰比值(SBP分别为72.6％、68.4％,DBP分别为69.0％、60.4％)两组比较无显著差异(P>0.05)。两组血脂、血糖、尿素氮、肌酐、转氨酶以及心率均无明显变化。A组中发生不良反应1例,B组中发生不良反应3例。结论缬沙坦80mg/d能有效地控制血压,不良反应轻,安全耐受性好。     

Serum insulin-like growth factor-I is negatively associated with serum adiponectin in type 2 diabetes mellitus

Background

Although insulin-like growth factor-I (IGF-I) and dehydroepiandrosterone-sulfate (DHEA-S) are involved in age-related diseases such as cardiovascular disease and diabetes mellitus, the association of these hormones with serum adiponectin level is still unclear.

Objective and methods

To investigate the association between serum IGF-I and DHEA-S versus adiponectin, we conducted a cross-sectional study of 348 Japanese men with type 2 diabetes mellitus and examined their relationships. Serum total adiponectin level was measured by an ELISA kit.

Results

Simple correlation analysis showed that patients' age and duration of diabetes were negatively correlated with IGF-I and DHEA-S (p < 0.01) and positively with adiponectin (p < 0.01), while body mass index (BMI) was positively correlated with IGF-I and DHEA-S (p < 0.001) and negatively with adiponectin (p < 0.001). IGF-I was negatively correlated with adiponectin (r = − 0.25, p < 0.001) and DHEA-S was negatively correlated with adiponectin and HbA1c (r = − 0.17, p = 0.003 and r = − 0.12, p = 0.027, respectively). In multiple regression analysis adjusted for age, duration of diabetes, BMI, and serum creatinine, HbA1c was negatively associated with IGF-I and DHEA-S (β = − 0.12, p = 0.036 and β = − 0.22, p < 0.001, respectively). Adiponectin was negatively associated with IGF-I (β = − 0.15, p = 0.013), but not DHEA-S. Moreover, this association was still significant after additional adjustment for HbA1c (β = − 0.18, p = 0.005).

Conclusions

Present cross-sectional study for the first time showed a negative association of serum IGF-I with serum adiponectin in Japanese men with type 2 diabetes independent of age, duration of diabetes, BMI, renal function, and HbA1c.     

Direct effect of insulin and insulin-like growth factor-I on the secretory activity of rat pancreatic beta cells

Summary Purified pancreatic Beta cells were labelled with ³H-tyrosine before studying their secretory activity in perifusion. At 1.4 mmol/l glucose, the cells released similar fractions (0.01% per min) of their contents in preformed and in newly formed insulin. At 20 mmol/l glucose plus 10^–8 mol/l glucagon, these fractional release rates increased by 16 and 40-fold respectively. The preferential release of newly synthesized as compared to stored insulin is attributable to a heterogeneity in individual cell responses. The secretory responsiveness to glucose plus glucagon was completely suppressed by 10^–7 mol/l clonidine. Insulin induced a 20% reduction at 10^–6 mol/l, but remained without effect at 10^–7 mol/l. Insulin-like growth factor-I provoked a 30% decrease at 5.10^–9 mol/l. It is concluded that the type-I insulin-like growth factor receptors on pancreatic Beta cells mediate a suppressive action on the insulin release process. Their high affinity for insulin-like growth factor-I allows physiologic levels of this peptide to participate in the regulation of insulin release. Their low affinity for insulin provides the basis for a minor feedback action by this hormone at concentrations exceeding the normal circulating levels.Part of this study has been presented at the 25th Annual Meeting of the European Association for the Study of Diabetes, Lisbon, Portugal, 1989     

胰岛素治疗对血清中胰岛素样生长因子I水平的影响

To explore the effect of insulin therapy on serum level of insulin-like growth factor-I(IGF-I)in patients with type 2 diabetes mellitus.The results showed that serum IGF-I level increased[(126.70±51.91 vs 90.04±43.68)μg/L,P<0.01]and was positively correlated with insulin level in patients with type 2 diabetes mellitus after exogenous insulin therapy(r=0.298,P<0.05).     

Blood levels of insulin-like growth factors I and II in neonates of non-insulin-dependent diabetic rats

Circulating levels of insulin like growth factor I (IGF-I) and insulin like growth factor II (IGF-II) were evaluated in plasma samples during the first 72 h of life in neonates of diabetic and control mother rats. Diabetes had been induced in the diabetic dams by streptozotocin at 2 days of age. The rats developed non-insulin dependent diabetes (at 6 weeks of age) and became pregnant at 11 weeks of age. Maternal blood glucose levels were higher in the diabetic mothers (P<0.05) during the last two-thirds of gestation. Complications occurred at the end of 7.1% of the diabetic pregnancies but none of the controls. Analysis of neonates plasma glucose, IGF-I, and IGF-II concentrations in the first 12, 24, 48, and 72 h after birth revealed higher glucose levels in neonates of diabetic mothers at 72 h compared with controls (118±7 vs 85±5 mg/dl,P<0.05) but there was no difference in IGF-I or IGF-II levels between the groups at any time point. Thus, acquired impaired glucose homeostasis may be seen in neonates of mildly diabetic mothers at early stages of their life but their circulating insulin-like growth factors levels are normal. These data do not support the proposition that fetal IGF-I and —II affect the outcome of pregnancies complicated by mild diabetes in the rodent.