PMID- 1590420
OWN - NLM
STAT- MEDLINE
DCOM- 19920624
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 262
IP  - 5 Pt 2
DP  - 1992 May
TI  - Apolipoprotein gene expression in analbuminemic rats and in rats with Heymann 
      nephritis.
PG  - F755-61
AB  - 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.
FAU - Sun, X
AU  - Sun X
AD  - Department of Medicine, Department of Veterans Affairs Medical Center, Martinez, 
      California 94553.
FAU - Jones, H Jr
AU  - Jones H Jr
FAU - Joles, J A
AU  - Joles JA
FAU - van Tol, A
AU  - van Tol A
FAU - Kaysen, G A
AU  - Kaysen GA
LA  - eng
GR  - 1-RO1 DK-42297-01/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Apolipoproteins B)
RN  - 0 (Apolipoproteins E)
RN  - 0 (RNA, Messenger)
RN  - 0 (Serum Albumin)
RN  - 0 (Triglycerides)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Animals
MH  - Apolipoprotein A-I/analysis/*genetics
MH  - Apolipoproteins B/blood/*genetics
MH  - Apolipoproteins E/blood/*genetics
MH  - Cholesterol/blood
MH  - *Gene Expression
MH  - Liver/metabolism
MH  - Nephritis/blood/*genetics
MH  - Nephrotic Syndrome/blood
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Serum Albumin/analysis/*deficiency
MH  - Triglycerides/blood
EDAT- 1992/05/11 19:15
MHDA- 1992/05/11 19:16
CRDT- 1992/05/11 19:15
PHST- 1992/05/11 19:15 [pubmed]
PHST- 1992/05/11 19:16 [medline]
PHST- 1992/05/11 19:15 [entrez]
AID - 10.1152/ajprenal.1992.262.5.F755 [doi]
PST - ppublish
SO  - Am J Physiol. 1992 May;262(5 Pt 2):F755-61. doi: 
      10.1152/ajprenal.1992.262.5.F755.