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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 Sci+Rep
2017 ; 7
(1
): 9680
Nephropedia Template TP
gab.com Text
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Lipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin
seen in plasma of type 2 diabetics with cardiovascular co-morbidities
#MMPMID28851981
Pretorius E
; Mbotwe S
; Kell DB
Sci Rep
2017[Aug]; 7
(1
): 9680
PMID28851981
show ga
Type 2 diabetes (T2D) has many cardiovascular complications, including a
thrombotic propensity. Many such chronic, inflammatory diseases are accompanied
(and may be exacerbated, and possibly even largely caused) by amyloid fibril
formation. Recognising that there are few strong genetic associations
underpinning T2D, but that amyloidogenesis of amylin is closely involved, we have
been seeking to understand what might trigger the disease. Serum levels of
bacterial lipopolysaccharide are raised in T2D, and we recently showed that
fibrin(ogen) polymerisation during blood clotting can be affected strongly by
LPS. The selectivity was indicated by the regularisation of clotting by
lipopolysaccharide-binding protein (LBP). Since coagulopathies are a hallmark of
T2D, we wondered whether they might too be caused by LPS (and reversed by LBP).
We show here, using SEM and confocal microscopy, that platelet-poor-plasma from
subjects with T2D had a much greater propensity for hypercoagulability and for
amyloidogenesis, and that these could both be reversed by LBP. These data imply
that coagulopathies are an important feature of T2D, and may be driven by
'hidden' LPS. Given the prevalence of amyloid formation in the sequelae of
diabetes, this opens up novel strategies for both the prevention and treatment of
T2D.
|Acute-Phase Proteins/*metabolism
[MESH]
|Adult
[MESH]
|Aged
[MESH]
|Aged, 80 and over
[MESH]
|Amyloid/*blood
[MESH]
|Blood Coagulation Disorders/*pathology
[MESH]
|Carrier Proteins/*metabolism
[MESH]
|Diabetes Mellitus, Type 2/*complications/*pathology
[MESH]