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@ARTICLE{Rehn:1032435,
author = {Rehn, Fabian and Kraemer-Schulien, Victoria and Bujnicki,
Tuyen and Bannach, Oliver and Tschoepe, Diethelm and
Stratmann, Bernd and Willbold, Dieter},
title = {{IAPP} - oligomerisation levels in plasma of people with
type 2 diabetes},
journal = {Scientific reports},
volume = {14},
number = {1},
issn = {2045-2322},
address = {[London]},
publisher = {Macmillan Publishers Limited, part of Springer Nature},
reportid = {FZJ-2024-06241},
pages = {19556},
year = {2024},
abstract = {Islet amyloid polypeptide (IAPP) is co-secreted with
insulin from pancreatic ß-cells. Its oligomerisation is
regarded as disease driving force in type 2 diabetes (T2D)
pathology. Up to now, IAPP oligomers have been detected in
affected tissues. IAPP oligomer concentrations in blood have
not been analysed so far. Using the IAPP
single-oligomer-sensitive and monomer-insensitive
surface-based fluorescence intensity distribution analysis
(sFIDA) technology, levels of IAPP oligomers in blood plasma
from healthy controls and people with T2D in different
disease stages where determined. Subsequently, the level of
IAPP oligomerisation was introduced as the ratio between the
IAPP oligomers determined with sFIDA and the total IAPP
concentration determined with ELISA. Highest oligomerisation
levels were detected in plasma of people with T2D without
late complication and without insulin therapy. Their levels
stand out significantly from the control group. Healthy
controls presented with the lowest oligomerisation levels in
plasma. In people with T2D without complications, IAPP
oligomerisation levels correlated with disease duration. The
results clearly demonstrate that IAPP oligomerisation in
insulin-naïve patients correlates with duration of T2D.
Although a correlation per se does not identify, which is
cause and what is consequence, this result supports the
hypothesis that IAPP aggregation is the driving factor of
T2D development and progression. The alternative and
conventional hypothesis explains development of T2D with
increasing insulin resistance causing exhaustion of
pancreatic ß-cells due to over-secretion of insulin, and
thus IAPP, too, resulting in subsequent IAPP aggregation and
fibril deposition in the pancreas. Further experiments and
comparative analyses with primary tissues are warranted.},
cin = {IBI-7},
ddc = {600},
cid = {I:(DE-Juel1)IBI-7-20200312},
pnm = {5241 - Molecular Information Processing in Cellular Systems
(POF4-524)},
pid = {G:(DE-HGF)POF4-5241},
typ = {PUB:(DE-HGF)16},
pubmed = {39174611},
UT = {WOS:001304514000052},
doi = {10.1038/s41598-024-70255-3},
url = {https://juser.fz-juelich.de/record/1032435},
}