Drevon C A, Attie A D, Pangburn S H, Steinberg D
J Lipid Res. 1981 Jan;22(1):37-46.
Rat fibroblasts degraded human low density lipoprotein (LDL) very slowly, one-tenth to one-fortieth the rates observed in human fibroblasts. In rat cells, human LDL caused only very small increases in cell cholesterol content and acylCoA:cholesterol acyltransferase (ACAT) activity and caused only small decreases in beta-hydroxy-beta-methylglutaryl CoA (HMG CoA) reductase activity; in human cells, however, human LDL induced very large changes in all three of these parameters, as expected. The binding of human LDL to rat fibroblasts was not reduced by previous incubation with human LDL or with 25-hydroxycholesterol. Thus, in rat fibroblasts there appear to be few, if any, regulated high-affinity receptors that recognize human LDL. Rat LDL fractions (d 1.02-1.05 g/ml), in contrast, were degraded more rapidly than human LDL by rat fibroblasts, caused a significant increase in cell cholesterol content, an increase in ACAT activity, and a significant decrease in HMG CoA reductase activity. Moreover, the degradation of this rat LDL fraction by rat fibroblasts as a function of concentration was biphasic, i.e., there appeared to be a high-affinity component of degradation. Thus, it appears that rat fibroblasts do have a receptor for homologous lipoproteins. However, because both apoprotein B and apoprotein E are present in these rat lipoprotein fractions, the observed effects may relate to recognition of either or both of these apoproteins. The metabolism and metabolic effects of the conventionally defined high density lipoprotein (HDL) fraction of the rat by rat or human fibroblasts resembled those of human LDL in human fibroblasts. It is suggested that rat HDL may, because of its apo E content and higher concentration in rat plasma relative to that of LDL, play an important role in cholesterol homeostasis in vivo.
大鼠成纤维细胞降解人低密度脂蛋白（LDL）的速度非常缓慢，仅为在人成纤维细胞中观察到的速度的十分之一到四十分之一。在大鼠细胞中，人LDL仅使细胞胆固醇含量和酰基辅酶A：胆固醇酰基转移酶（ACAT）活性有非常小的增加，并且仅使β-羟基-β-甲基戊二酰辅酶A（HMG CoA）还原酶活性有小幅下降；然而，在人细胞中，人LDL如预期的那样在所有这三个参数上引起了非常大的变化。人LDL与大鼠成纤维细胞的结合不会因预先与人LDL或25-羟基胆固醇孵育而减少。因此，在大鼠成纤维细胞中，似乎很少（如果有的话）存在识别人类LDL的受调控的高亲和力受体。相比之下，大鼠LDL组分（密度1.02 - 1.05 g/ml）被大鼠成纤维细胞降解的速度比人LDL更快，导致细胞胆固醇含量显著增加、ACAT活性增加以及HMG CoA还原酶活性显著下降。此外，大鼠成纤维细胞对该大鼠LDL组分的降解作为浓度的函数是双相的，即似乎存在一个高亲和力的降解组分。因此，看来大鼠成纤维细胞确实有同源脂蛋白的受体。然而，由于这些大鼠脂蛋白组分中同时存在载脂蛋白B和载脂蛋白E，观察到的效应可能与对这两种载脂蛋白中任何一种或两种的识别有关。大鼠或人成纤维细胞对大鼠传统定义的高密度脂蛋白（HDL）组分的代谢及代谢效应类似于人成纤维细胞中人LDL的情况。有人提出，大鼠HDL可能由于其载脂蛋白E含量以及相对于LDL在大鼠血浆中的浓度更高，在体内胆固醇稳态中发挥重要作用。
