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2017 ; 7
(1
): 2261
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The protective effect of human renal sinus fat on glomerular cells is reversed by
the hepatokine fetuin-A
#MMPMID28536464
Wagner R
; Machann J
; Guthoff M
; Nawroth PP
; Nadalin S
; Saleem MA
; Heyne N
; Königsrainer A
; Fend F
; Schick F
; Fritsche A
; Stefan N
; Häring HU
; Schleicher E
; Siegel-Axel DI
Sci Rep
2017[May]; 7
(1
): 2261
PMID28536464
show ga
Renal sinus fat (RSF) is a perivascular fat compartment located around renal
arteries. In this in vitro and in vivo study we hypothesized that the hepatokine
fetuin-A may impair renal function in non alcoholic fatty liver disease (NAFLD)
by altering inflammatory signalling in RSF. To study effects of the crosstalk
between fetuin-A, RSF and kidney, human renal sinus fat cells (RSFC) were
isolated and cocultured with human endothelial cells (EC) or podocytes (PO). RSFC
caused downregulation of proinflammatory and upregulation of regenerative factors
in cocultured EC and PO, indicating a protective influence of RFSC. However,
fetuin-A inverted these benign effects of RSFC from an anti- to a proinflammatory
status. RSF was quantified by magnetic resonance imaging and liver fat content by
(1)H-MR spectroscopy in 449 individuals at risk for type 2 diabetes. Impaired
renal function was determined via urinary albumin/creatinine-ratio (uACR). RSF
did not correlate with uACR in subjects without NAFLD (n?=?212, p?=?0.94), but
correlated positively in subjects with NAFLD (n?=?105, p?=?0.0005). Estimated
glomerular filtration rate ?(eGRF) was inversely correlated with RSF, suggesting
lower eGFR for subjects with higher RSF (r?=?0.24, p?0.0001). In conclusion,
our data suggest that in the presence of NAFLD elevated fetuin-A levels may
impair renal function by RSF-induced proinflammatory signalling in glomerular
cells.