Apolipoprotein gene expression in analbuminemic rats and in rats with Heymann nephritis.
Apolipoprotein gene expression in analbuminemic rats and in rats with Heymann nephritis.
复制标题
无白蛋白血症大鼠和海曼肾炎大鼠中载脂蛋白基因的表达。
DOI：
10.1152/ajprenal.1992.262.5.f755
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Kaysen,GA
中科院分区：
文献类型：
--
作者：
Sun,X;JonesJr,H;Joles,JA;vanTol,A;Kaysen,GA
肾病综合征是由于肾小球选择透过性改变，导致尿蛋白丢失，白蛋白浓度降低，血压（pi）和高脂血症。肝脏脂质和载脂蛋白合成增加，脂蛋白催化剂减少。蛋白尿发作后脂蛋白催化剂减少，但如果无蛋白尿，则与遗传性无白蛋白血症无关[长濑无白蛋白血症大鼠（NAR）]。我们测定了Heymann肾炎（HN）或NAR大鼠血浆载脂蛋白（apo）AI、B和E水平，肝脏中它们的mRNA浓度，以及每种mRNA的转录率，以确定在无蛋白尿的NAR中发生了哪些改变。HN和NAR的血浆apo AI、B和E均升高。胆固醇和载脂蛋白AI与pi成反比，与尿蛋白丢失或血浆中存在白蛋白无关。相比之下，HN中的甘油三酯（TG）显著更高，并且与载脂蛋白B不成比例地增加。HN组和NAR组肝组织apo AI mRNA含量均增加，apo AI转录也增加。载脂蛋白E mRNA在HN和NAR中均未增加，而载脂蛋白B mRNA仅在HN中增加。载脂蛋白B和E的转录均未增加。血浆载脂蛋白AI水平可能在蛋白质合成水平上受到转录调控，而血浆载脂蛋白B和E水平在转录后、蛋白质催化剂水平或两个位点上受到调控。富含TG而缺乏载脂蛋白B的脂蛋白出现在蛋白尿发生后，但不是单纯的无白蛋白血症的结果。HN大鼠中富含TG的载脂蛋白B的蓄积可能是由于蛋白尿导致的脂解受损所致。
The nephrotic syndrome results from altered glomerular permselectivity, causing urinary protein loss, reduced albumin concentration, oncotic pressure (pi), and hyperlipidemia. Hepatic lipid and apolipoprotein synthesis increases and lipoprotein catabolism decreases. Decreased lipoprotein catabolism follows the onset of proteinuria but is not associated with hereditary analbuminemia [Nagase analbuminemic rat (NAR)] if proteinuria is absent. We measured plasma apolipoproteins (apo) AI, B, and E levels, their mRNA concentrations in liver, and the transcription rate of each mRNA in rats with Heymann nephritis (HN) or NAR to determine which alterations occurred in NAR alone without proteinuria. Plasma apo AI, B, and E were increased in both HN and NAR. Cholesterol and apo AI were inversely proportional to pi and independent of urinary protein loss or the presence of albumin in plasma. In contrast, triglycerides (TGs) were significantly greater in HN and were increased out of proportion to apo B. The concentration of apo AI mRNA increased in liver of both HN and NAR as did apo AI transcription. Apo E mRNA increased in neither HN nor NAR, whereas apo B mRNA increased only in HN. Transcription of neither apo B nor E increased. Plasma apo AI levels are likely to be regulated transcriptionally at the level of protein synthesis, whereas plasma apo B and E levels are regulated either posttranscriptionally, at the level of protein catabolism, or at both sites. Lipoproteins rich in TG and poor in apo B appear after the development of proteinuria but not as a consequence of analbuminemia alone. The accumulation of TG-rich apo B containing lipoproteins in rats with HN may result from impaired lipolysis occurring as a consequence of proteinuria.