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[脂蛋白代谢的激素调节:在冠心病发病机制中的作用]

[Hormonal regulation of lipoprotein metabolism: the role in pathogenesis of coronary heart disease].

作者信息

Sokolov E I, Metel'skaia V A, Perova N V, Shchukina G N

出版信息

Kardiologiia. 2006;46(7):4-9.

Abstract

The character and role of hormonal dysregulation of lipoprotein metabolism during postprandial hyperlipemia were studied in patients with coronary heart disease (CHD) and hyperthyroidism as compared with healthy subjects. Pronounced hypertriglyceridemia alongside with the decreased high density lipoprotein cholesterol (HDL C) after standard fat load were associated with increased level of insulin and decreased level of cortisol. Moreover, in CHD patients fasting hyperinsulinemia becoming even stronger postprandially resulted in prevalence of antilipolytic action of insulin over lipid-mobilizing effect of cortisol; and an extended postprandial hypertriglyceridemia took place. Patients with hyperthyroidism and low cholesterol level both in atherogenic LDL and antiatherogenic HDL, demonstrated decreased level of apo AI (as in CHD patients) and apo B (three times lower than in CHD patients). Very low ratio of apo B/AI in patients with hyperthyroidism both in fasting and postprandial state was a clear indication of their lipoprotein profile antiatherogeneity. Thus, in patients with hyperthyroidism despite of low HDL C and apo AI levels, antiatherogenic properties of lipoprotein profile are probably determined by very low apo B/AI ratio induced by thyroid hormones, and might be explained by the influence of thyroid hormones on the expression of genes coding these apoproteins.

摘要

为了与健康受试者进行比较,研究了冠心病(CHD)和甲状腺功能亢进患者餐后高脂血症期间脂蛋白代谢激素失调的特征和作用。标准脂肪负荷后,明显的高甘油三酯血症以及高密度脂蛋白胆固醇(HDL-C)水平降低与胰岛素水平升高和皮质醇水平降低有关。此外,在冠心病患者中,空腹高胰岛素血症在餐后变得更强,导致胰岛素的抗脂解作用超过皮质醇的脂质动员作用;并出现了餐后高甘油三酯血症的延长。甲状腺功能亢进且致动脉粥样硬化的低密度脂蛋白(LDL)和抗动脉粥样硬化的高密度脂蛋白(HDL)中的胆固醇水平均较低的患者,其载脂蛋白AI(与冠心病患者一样)和载脂蛋白B水平降低(比冠心病患者低三倍)。甲状腺功能亢进患者在空腹和餐后状态下极低的载脂蛋白B/AI比值清楚地表明了其脂蛋白谱的抗动脉粥样硬化性。因此,在甲状腺功能亢进患者中,尽管HDL-C和载脂蛋白AI水平较低,但脂蛋白谱的抗动脉粥样硬化特性可能由甲状腺激素诱导的极低载脂蛋白B/AI比值决定,这可能是由于甲状腺激素对编码这些载脂蛋白的基因表达的影响所致。

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