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Frankó, A. ; Rodriguez Camargo, D.C. ; Böddrich, A.* ; Garg, D.* ; Rodriguez Camargo, A. ; Rathkolb, B. ; Janik, D. ; Aichler, M. ; Feuchtinger, A. ; Neff, F. ; Fuchs, H. ; Wanker, E.E.* ; Reif, B. ; Häring, H.-U. ; Peter, A. ; Hrabě de Angelis, M.

Epigallocatechin gallate (EGCG) reduces the intensity of pancreatic amyloid fibrils in human islet amyloid polypeptide (hIAPP) transgenic mice.

Sci. Rep. 8:1116 (2018)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The formation of amyloid fibrils by human islet amyloid polypeptide protein (hIAPP) has been implicated in pancreas dysfunction and diabetes. However, efficient treatment options to reduce amyloid fibrils in vivo are still lacking. Therefore, we tested the effect of epigallocatechin gallate (EGCG) on fibril formation in vitro and in vivo. To determine the binding of hIAPP and EGCG, in vitro interaction studies were performed. To inhibit amyloid plaque formation in vivo, homozygous (tg/tg), hemizygous (wt/tg), and control mice (wt/wt) were treated with EGCG. EGCG bound to hIAPP in vitro and induced formation of amorphous aggregates instead of amyloid fibrils. Amyloid fibrils were detected in the pancreatic islets of tg/tg mice, which was associated with disrupted islet structure and diabetes. Although pancreatic amyloid fibrils could be detected in wt/tg mice, these animals were non-diabetic. EGCG application decreased amyloid fibril intensity in wt/tg mice, however it was ineffective in tg/tg animals. Our data indicate that EGCG inhibits amyloid fibril formation in vitro and reduces fibril intensity in non-diabetic wt/tg mice. These results demonstrate a possible in vivo effectiveness of EGCG on amyloid formation and suggest an early therapeutical application.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Type-2 Diabetes-mellitus; Solid-state Nmr; Insulin Sensitivity; Metabolic Syndrome; Alpha-synuclein; Aggregation; Tea; Green; Iapp; Cells
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Zeitschrift Scientific Reports
Quellenangaben Band: 8, Heft: 1, Seiten: , Artikelnummer: 1116 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)
Institute of Diabetes Research and Metabolic Diseases (IDM)
Institute of Structural Biology (STB)
Research Unit Analytical Pathology (AAP)
CF Pathology & Tissue Analytics (CF-PTA)
POF Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
30203 - Molecular Targets and Therapies
30205 - Bioengineering and Digital Health
30505 - New Technologies for Biomedical Discoveries
Forschungsfeld(er) Genetics and Epidemiology
Helmholtz Diabetes Center
Enabling and Novel Technologies
PSP-Element(e) G-500600-001
G-502400-001
G-500692-001
G-503090-001
G-500390-001
A-630600-001
G-503000-001
G-501900-063
DOI 10.1038/s41598-017-18807-8
WOS ID WOS:000422739300079
Scopus ID 85040764862
PubMed ID 29348618
Erfassungsdatum 2018-03-02
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