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肝脏在大鼠低密度脂蛋白分解代谢中的作用。

Role of the liver in low-density-lipoprotein catabolism in the rat.

作者信息

Bhattacharya S, Balasubramaniam S, Simons L A

出版信息

Biochem J. 1984 May 15;220(1):333-6. doi: 10.1042/bj2200333.

Abstract

Plasma low-density-lipoprotein (LDL) kinetics and hepatic LDL uptake were studied in the rat after an intravenous pulse injection of [14C]sucrose-labelled LDL. Some 96% of injected radioactivity was associated with apoprotein B of LDL (d 1.020-1.050). The disappearance of labelled LDL from plasma was accompanied by a linear increase in the hepatic uptake of LDL, up to 12 h after injection. Oestradiol treatment lowered plasma cholesterol concentration by 58% and the intravascular pool of LDL by 78%. This was associated with a 4-fold increase in the fractional catabolic rate of LDL and a 2-fold increase in the hepatic uptake of LDL. Oestradiol treatment did not significantly change the synthesis rate of LDL; it decreased the skin and lung uptake of LDL, but increased adrenal uptake. These results suggest that the liver plays an important role in the regulation of plasma LDL concentration.

摘要

在大鼠静脉脉冲注射[14C]蔗糖标记的低密度脂蛋白(LDL)后,研究了血浆LDL动力学和肝脏对LDL的摄取。注射的放射性约96%与LDL的载脂蛋白B(密度1.020 - 1.050)相关。血浆中标记LDL的消失伴随着肝脏对LDL摄取的线性增加,直至注射后12小时。雌二醇治疗使血浆胆固醇浓度降低了58%,LDL的血管内池降低了78%。这与LDL的分解代谢率增加4倍以及肝脏对LDL的摄取增加2倍有关。雌二醇治疗并未显著改变LDL的合成速率;它降低了皮肤和肺对LDL的摄取,但增加了肾上腺对LDL的摄取。这些结果表明,肝脏在血浆LDL浓度的调节中起重要作用。

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