Quality, function and genetic assessments of NO, ACE and HDL in patients with coronary artery disease
Quality, function and genetic assessments of NO, ACE and HDL in patients with coronary artery disease
批准号:
09670773
负责人:
SAKU Keijiro
金额:
$2.3万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1999
中文摘要
1. cholesterification rate of cholesterol (C) in apolipoprotein B-depleted plasma (FER D2 HDL D2) is a functional assay of high density lipoprotein (HDL)。在案例控制研究中[与/无angiographically defined coronary artery disease (CAD)],我们发现高FER D2 HDL D2与CAD相关的风险较高。FER D2 HDL D2和CAD之间的关联未被调整为潜在混淆和HDL-C水平,而FER D2 HDL D2和HDL-C之间的相互作用是有意义的。FER D2 HDL D2 is an independent risk factor for CAD and the combination of FER D2 HDL D2 and HDL-C could be a potent indicator for CAD.2。胰岛素抵抗力之间的关联,由homeostasis模型评估、HDL-C和CAD在案例控制研究中进行了调查。案例是用地理上定义的CAD和控制器与案例匹配,以规范性别和年龄。病例是由高胰岛素和正常特征引起的。 ... More 葡萄糖耐受性。多变量条件逻辑回归分析表明,胰岛素抵抗和HDL-C与CAD独立相关,但在高胰岛素高碱性碱性蛋白质和CAD之间发现了许多更强的关联。低HDL-C和高胰岛素综合性地增加了CAD的风险。两种氮氧化物(NO)和血管紧张素转换酶(ACE)在维持内皮素依赖放松/接触和抑制/激活细胞增殖、吸附和化学酶中发挥重要作用。我们筛选了1002名患者中缺失的Glu 298 Asp变体的eNOS基因和ACE I/D多态性。在糖尿病患者中,eNOS和ACE基因多态性的组合与CAD无关,而非DM患者(n=727)、缺失的Glu 298 Asp变体(TT+TG)和ACE-DD基因型的组合被发现是CAD的重要预测者,以及其他基因型组合不是。缺失Glu 298 Asp eNOS变体与ACE-DD基因型可能是CAD在非DM患者中的标志。ACE基因多态性和胰岛素抵抗(IR)之间的关联是在与Angina pectoris患者进行的研究。使用ACE-ID基因型基因型有明显的低IR的患者,根据口腔葡萄糖耐受性测试(OGTT)进行评估,并通过稳态模型评估(HOMA)进行比较,与ACE-II基因型进行比较。患者被分成两组,分为低HOMA-IR和高HOMA-IR组,而我发现自己经常出现在高HOMA-IR组,而不是低HOMA-IR组。逻辑回归分析显示了患者与II型基因型的胰岛素抵抗率的比值,将这些与ID和DD基因型进行比较,为4.0,并且不对显著的冠状动脉粥样硬化的存在进行调整。患者与ID和DD基因型相关,与胰岛素抵抗的明显较低风险,与那些与第二基因型相比。Less(低)
英文摘要
1. The fractional esterification rate of cholesterol (C) in apolipoprotein B-depleted plasma (FERィイD2HDLィエD2) is a functional assay of high density lipoprotein (HDL). In the case-control study [with/without angiographically defined coronary artery disease (CAD)], we found that high FERィイD2HDLィエD2 was associated with an increased risk of CAD. The association between FERィイD2HDLィエD2 and CAD was not eliminated by adjusting for potential confounders and HDL-C levels, and the interaction between FERィイD2HDLィエD2 and HDL-C was significant. FERィイD2HDLィエD2 is an independent risk factor for CAD and the combination of FERィイD2HDLィエD2 and HDL-C could be a potent indicator for CAD.2. The association among insulin resistance, as assessed by the homeostasis model assessment, HDL-C, and CAD was investigated in a case-control study. Cases were patients with angiographically defined CAD and controls were matched with cases with regard to gender and age. Cases were characterized by hyperinsulinemia and norm … More al glucose tolerance. Multivariate conditional logistic regression analysis indicated that insulin resistance and HDL-C were independently associated with CAD, but a much stronger association was found between hyperinsulinemic hypoalphalipoproteinemia and CAD. Low HDL-C and hyperinsulinemia synergistically increased the risk of CAD.3. Both nitric oxide (NO) and angiotensin converting enzyme (ACE) play important roles in maintaining endothelium-dependent relaxation/contraction, and in inhibiting/activating cell proliferation, adhesion and chemotaxis. We screened the missense Glu298Asp variant of the eNOS gene and ACE I/D polymorphism in 1002 patients with/without CAD. In diabetic patients, none of the combinations of eNOS and ACE gene polymorphism were related to CAD, while in non-DM patients (n=727), the combination of the missense Glu298Asp variant (TT+TG) and the ACE-DD genotype was found to be a significant predictor of CAD, and other genotypic combinations were not. The combination of the missense Glu298Asp eNOS variant with the ACE-DD genotype may be a marker of CAD in non-DM patients.4. The association between ACE gene polymorphism and insulin resistance (IR) was investigated in patients with angina pectoris. Patients with the ACE-ID genotype had significantly lower IR, as assessed by an oral glucose tolerance test (OGTT) and by homeostatic model assessment (HOMA), compared to those with the ACE-II genotype. Patients were divided into two groups with low and high HOMA-IR, and the I allele was seen more frequently in the high HOMA-IR group than in the low HOMA-IR group. Logistic regression analysis showed that the odds ratio for insulin resistance in patients with the II genotype, compared to those with the ID and DD genotypes, was 4.0, with and without adjusting for the presence of significant coronary atheroscierosis. The patients with the ID and DD genotypes were associated with a significantly lower risk of insulin resistance, compared to those with the II genotype. Less
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Saku K., Zhang B., et al.: "Associations among serum lipoprotein(a) [Lp(a)] levels, apolipoprotein(a) phenotypes, and myocardial infarction in patients with extremely low and high serum levels of Lp(a)"Jpn Circ J. 63. 659-665 (1999)
Saku K.、Zhang B. 等人:“血清 Lp(a) 水平极低和极高的患者的血清脂蛋白 (a) [Lp(a)] 水平、载脂蛋白 (a) 表型与心肌梗死之间的关联
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Saku K.,Zhang B.,et al.: "Associations among serum lipoprotein(a)[Lp(a)]levels,apolipoprotein(a)phenotypes,and myocardial infarction in patients with extremely low and high serum levels of Lp(a)."Jpn Circ J. 63. 659-665 (1999)
Saku K.,Zhang B.,et al.:“血清脂蛋白(a)[Lp(a)]水平、载脂蛋白(a)表型与血清 Lp(a)水平极低和极高的患者中的心肌梗死之间的关联
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Bai H.,Saku K.,et.al.: "Polymorphism of the apolipoprotein A-IV gene and its significance in lipid metabolism and coroanry heart disease in a Japanese population." Europ J Clin Invest.26. 1115-1124 (1996)
Bai H.,Saku K.,et.al.:“载脂蛋白 A-IV 基因的多态性及其在日本人群脂质代谢和冠心病中的意义。”
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Kiyonaga A., Imai K., Zhang B., Saku K.: "Exercise Prevent Comm Dis"Springer-Verlag. 10 (1999)
Kiyonaga A.、Imai K.、Zhang B.、Saku K.:“Exercise Prevent Comm Dis”Springer-Verlag。
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Saku K., Zhang B., Ohta T., Arakara K.: "Troglitazone lowers blood pressure and enhance insulin sensitivity in Watanabe heritable hyperlipidemic rabbits"Am J Hypertension. 10. 1027-1033 (1997)
Saku K.、Zhang B.、Ohta T.、Arakara K.:“曲格列酮可降低渡边遗传性高脂血症兔的血压并增强胰岛素敏感性”Am J 高血压。
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共 61 条
New diagnostic and therapeutic strategies for atherosclerosis using newly developed apolipoprotein A-I mimetic peptide
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批准号:24591123
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.24万
-
财政年份:2012
-
负责人:SAKU Keijiro
-
依托单位:
Possibility of drug discovery : Development of new peptide type of reconstituted HDL
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批准号:21590960
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.75万
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财政年份:2009
-
负责人:SAKU Keijiro
-
依托单位:
Advanced medical technology on cardiovascular disease- Elucidation of the molecular mechanism and the application on various pathological conditions for the establishment of HDL therapy
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批准号:18590826
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.56万
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财政年份:2006
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负责人:SAKU Keijiro
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依托单位:
Therapeutic strategy for atherosclerosis targeting for CETP
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批准号:12670712
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.05万
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财政年份:2000
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负责人:SAKU Keijiro
-
依托单位:
Quantity, function and genetics of HDL as an indicator of CHD.
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批准号:07670827
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.34万
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财政年份:1995
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负责人:SAKU Keijiro
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依托单位:
HDL-apoAI gene expression and its kinetics in vivo
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批准号:04671503
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$0.9万
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财政年份:1992
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负责人:SAKU Keijiro
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依托单位:
HDL-apoAI and its isoproteins kinetics in rabbits and gene expressin of apoAI.
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批准号:02671114
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.02万
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财政年份:1990
-
负责人:SAKU Keijiro
-
依托单位:
海外基金