PMID- 2384606
OWN - NLM
STAT- MEDLINE
DCOM- 19900914
LR  - 20181113
IS  - 0021-9738 (Print)
IS  - 0021-9738 (Linking)
VI  - 86
IP  - 2
DP  - 1990 Aug
TI  - Proteinuria, not altered albumin metabolism, affects hyperlipidemia in the 
      nephrotic rat.
PG  - 600-5
AB  - It has been established previously that nephrotic hyperlipidemia is characterized 
      by both an increase in lipid synthesis and a defect in removal of lipoproteins. 
      The relationship between these defects and altered albumin metabolism is 
      uncertain. One hypothesis is that hepatic lipogenesis increases in parallel with 
      albumin synthesis. To test this hypothesis, albumin synthesis was increased in 
      nephrotic rats fed an 8.5% protein diet (LPN) by increasing dietary protein to 
      40% (HPN). Proteinuria was modulated in half of the rats fed 40% protein by 
      enalapril (HPE). Albumin synthesis was the same in both HPN and HPE, but 
      proteinuria was reduced in HPE compared to HPN, and so were serum cholesterol and 
      triglycerides (TG). To examine the effect of serum albumin on lipid clearance in 
      the absence of proteinuria, plasma clearance of chylomicrons (CM) and VLDL was 
      measured in Nagase analbuminemic rats (NAR) and found to be no different than in 
      normal SD rats. When proteinuria was induced in NAR and in SD rats, a severe and 
      identical defect in both CM and VLDL clearance was acquired in both groups and 
      blood lipid levels were increased to a similar degree in both groups. Neither 
      hyperlipidemia nor defective removal of lipoproteins from the circulation are 
      linked to albumin synthesis or serum albumin concentration but result, at least 
      in part, from proteinuria. Postheparin lipoprotein lipase (LPL) activity was 
      reduced slightly in nephrotic animals compared to nonnephrotic controls, but the 
      most striking finding was a highly significant decrease in postheraprin LPL 
      activity in normal NAR compared to SD rats (P less than 0.001), suggesting that 
      reduced LPL activity is not responsible for reduced clearance of CM and VLDL in 
      nephrotic rats.
FAU - Davies, R W
AU  - Davies RW
AD  - Department of Medicine, Veteran's Administration Medical Center, Martinez, 
      California 94553.
FAU - Staprans, I
AU  - Staprans I
FAU - Hutchison, F N
AU  - Hutchison FN
FAU - Kaysen, G A
AU  - Kaysen GA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Clin Invest
JT  - The Journal of clinical investigation
JID - 7802877
RN  - 0 (Albumins)
RN  - 0 (Chylomicrons)
RN  - 0 (Dietary Proteins)
RN  - 0 (Lipoproteins, VLDL)
RN  - 69PN84IO1A (Enalapril)
SB  - IM
MH  - Albumins/*metabolism
MH  - Animals
MH  - Chylomicrons/metabolism
MH  - Dietary Proteins/metabolism
MH  - Enalapril/pharmacology
MH  - Hyperlipidemias/*physiopathology
MH  - Lipoproteins, VLDL/metabolism
MH  - Metabolic Clearance Rate
MH  - Nephrotic Syndrome/*physiopathology/urine
MH  - Proteinuria/*physiopathology
MH  - Rats
MH  - Rats, Inbred Strains
PMC - PMC296766
EDAT- 1990/08/01 00:00
MHDA- 1990/08/01 00:01
PMCR- 1990/08/01
CRDT- 1990/08/01 00:00
PHST- 1990/08/01 00:00 [pubmed]
PHST- 1990/08/01 00:01 [medline]
PHST- 1990/08/01 00:00 [entrez]
PHST- 1990/08/01 00:00 [pmc-release]
AID - 10.1172/JCI114750 [doi]
PST - ppublish
SO  - J Clin Invest. 1990 Aug;86(2):600-5. doi: 10.1172/JCI114750.