PMID- 7783403
OWN - NLM
STAT- MEDLINE
DCOM- 19950717
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 47
IP  - 4
DP  - 1995 Apr
TI  - Non-iron mediated alteration in hepatic transferrin gene expression in the 
      nephrotic rat.
PG  - 1068-77
AB  - Both transferrin and the iron it carries are lost in the urine in the nephrotic 
      syndrome. Patients may develop hypochromic microcytic anemia and synthesis of 
      transferrin, a protein regulated in large part by iron availability, is 
      increased. Transferrin synthesis has also been reported to be increased in liver 
      slices from rats with hereditary analbuminemia, and their plasma transferrin 
      levels are increased, suggesting that transferrin synthesis may be stimulated by 
      processes other than iron depletion in this hypoalbuminemic condition. 
      Transferrin metabolism was studied in rats with Heymann nephritis (HN), in a 
      strain of Sprague-Dawley (SD) rats with hereditary analbuminemia [Nagase 
      analbuminemic rats (NAR)], and in normal SD rats. Plasma transferrin 
      concentration and mass was decreased significantly in HN, but increased in NAR. 
      Transferrin synthesis was increased both in NAR (measured either as the 
      disappearance of [125I] labeled transferrin or as the incorporation of [3H] 
      phenylalanine) and in HN (incorporation of [3H] phenylalanine). The fractional 
      rate of transferrin catabolism was unchanged in NAR. Thus transferrin mass was 
      increased in NAR entirely as a consequence of increased synthesis. Transferrin 
      and albumin synthesis correlated with one another in both HN and SD (P < 0.001). 
      Transferrin mRNA was increased in both HN and NAR and was unaffected by 
      administration of iron to HN. Hepatic transferrin and albumin mRNA levels were 
      also correlated positively in HN and SD, suggesting that increased hepatic 
      synthesis of both proteins might be responding to the same stimuli. Transferrin 
      gene transcription was increased in both HN and NAR and was unaffected by 
      administration of iron to HN. Transferrin mRNA was not increased in the testis in 
      either HN or NAR, suggesting that augmentation in transferrin gene expression is 
      driven by a non-iron dependent process and is confined to the liver.
FAU - Kaysen, G A
AU  - Kaysen GA
AD  - Department of Medicine, University of California Davis School of Medicine, USA.
FAU - Sun, X
AU  - Sun X
FAU - Jones, H Jr
AU  - Jones H Jr
FAU - Martin, V I
AU  - Martin VI
FAU - Joles, J A
AU  - Joles JA
FAU - Tsukamoto, H
AU  - Tsukamoto H
FAU - Couser, W G
AU  - Couser WG
FAU - al-Bander, H
AU  - al-Bander H
LA  - eng
GR  - R01 DK 42297/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Albumins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transferrin)
RN  - E1UOL152H7 (Iron)
SB  - IM
MH  - Albumins/*biosynthesis/deficiency/genetics
MH  - Animals
MH  - Autoradiography
MH  - Female
MH  - Gene Expression
MH  - Iron/blood/*pharmacology
MH  - Liver/metabolism/pathology
MH  - Male
MH  - Nephrotic Syndrome/*metabolism
MH  - RNA, Messenger/genetics/*metabolism
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Rats, Sprague-Dawley
MH  - *Transcription, Genetic
MH  - Transferrin/*biosynthesis/genetics
EDAT- 1995/04/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1995/04/01 00:00
PHST- 1995/04/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1995/04/01 00:00 [entrez]
AID - S0085-2538(15)58917-5 [pii]
AID - 10.1038/ki.1995.153 [doi]
PST - ppublish
SO  - Kidney Int. 1995 Apr;47(4):1068-77. doi: 10.1038/ki.1995.153.