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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Biol+Chem
2016 ; 291
(10
): 4913-27
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Alterations of Hepatic Metabolism in Chronic Kidney Disease via D-box-binding
Protein Aggravate the Renal Dysfunction
#MMPMID26728457
Hamamura K
; Matsunaga N
; Ikeda E
; Kondo H
; Ikeyama H
; Tokushige K
; Itcho K
; Furuichi Y
; Yoshida Y
; Matsuda M
; Yasuda K
; Doi A
; Yokota Y
; Amamoto T
; Aramaki H
; Irino Y
; Koyanagi S
; Ohdo S
J Biol Chem
2016[Mar]; 291
(10
): 4913-27
PMID26728457
show ga
Chronic kidney disease (CKD) is associated with an increase in serum retinol;
however, the underlying mechanisms of this disorder are poorly characterized.
Here, we found that the alteration of hepatic metabolism induced the accumulation
of serum retinol in 5/6 nephrectomy (5/6Nx) mice. The liver is the major organ
responsible for retinol metabolism; accordingly, microarray analysis revealed
that the hepatic expression of most CYP genes was changed in 5/6Nx mice. In
addition, D-box-binding protein (DBP), which controls the expression of several
CYP genes, was significantly decreased in these mice. Cyp3a11 and Cyp26a1,
encoding key proteins in retinol metabolism, showed the greatest decrease in
expression in 5/6Nx mice, a process mediated by the decreased expression of DBP.
Furthermore, an increase of plasma transforming growth factor-?1 (TGF-?1) in
5/6Nx mice led to the decreased expression of the Dbp gene. Consistent with these
findings, the alterations of retinol metabolism and renal dysfunction in 5/6Nx
mice were ameliorated by administration of an anti-TGF-?1 antibody. We also show
that the accumulation of serum retinol induced renal apoptosis in 5/6Nx mice fed
a normal diet, whereas renal dysfunction was reduced in mice fed a retinol-free
diet. These findings indicate that constitutive Dbp expression plays an important
role in mediating hepatic dysfunction under CKD. Thus, the aggravation of renal
dysfunction in patients with CKD might be prevented by a recovery of hepatic
function, potentially through therapies targeting DBP and retinol.
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