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Wesolowska-Andersen, A.* ; Brorsson, C.A.* ; Bizzotto, R.* ; Mari, A.* ; Tura, A.* ; Koivula, R.W.* ; Mahajan, A.* ; Viñuela, A.* ; Tajes, J.F.* ; Sharma, S. ; Haid, M. ; Prehn, C. ; Artati, A. ; Hong, M.G.* ; Musholt, P.B.* ; Kurbasic, A.* ; De Masi, F.* ; Tsirigos, K.D.* ; Pedersen, H.K.* ; Gudmundsdottir, V.* ; Thomas, C.E.* ; Banasik, K.* ; Jennison, C.* ; Jones, A.* ; Kennedy, G.* ; Bell, J.* ; Thomas, L.* ; Frost, G.* ; Thomsen, H.* ; Allin, K.* ; Hansen, T.H.* ; Vestergaard, H.* ; Hansen, T.* ; Rutters, F.* ; Elders, P.* ; t'Hart, L.* ; Bonnefond, A.* ; Canouil, M.* ; Brage, S.* ; Kokkola, T.* ; Heggie, A.* ; McEvoy, D.* ; Hattersley, A.* ; McDonald, T.A.* ; Teare, H.* ; Ridderstråle, M.* ; Walker, M.* ; Forgie, I.* ; Giordano, G.N.* ; Froguel, P.* ; Pavo, I.* ; Ruetten, H.* ; Pedersen, O.* ; Dermitzakis, E.* ; Franks, P.W.* ; Schwenk, J.M.* ; Adamski, J. ; Pearson, E.* ; McCarthy, M.I.* ; Brunak, S.*

Four groups of type 2 diabetes contribute to the etiological and clinical heterogeneity in newly diagnosed individuals: An IMI DIRECT study.

Cell Rep. Med. 3:100477 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The presentation and underlying pathophysiology of type 2 diabetes (T2D) is complex and heterogeneous. Recent studies attempted to stratify T2D into distinct subgroups using data-driven approaches, but their clinical utility may be limited if categorical representations of complex phenotypes are suboptimal. We apply a soft-clustering (archetype) method to characterize newly diagnosed T2D based on 32 clinical variables. We assign quantitative clustering scores for individuals and investigate the associations with glycemic deterioration, genetic risk scores, circulating omics biomarkers, and phenotypic stability over 36 months. Four archetype profiles represent dysfunction patterns across combinations of T2D etiological processes and correlate with multiple circulating biomarkers. One archetype associated with obesity, insulin resistance, dyslipidemia, and impaired β cell glucose sensitivity corresponds with the fastest disease progression and highest demand for anti-diabetic treatment. We demonstrate that clinical heterogeneity in T2D can be mapped to heterogeneity in individual etiological processes, providing a potential route to personalized treatments.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Archetypes ; Disease Progression ; Glycaemic Deterioration ; Multi-omics ; Patient Clustering ; Patient Stratification ; Precision Medicine ; Soft-clustering ; Type 2 Diabetes; Genome-wide Association; Insulin-resistance; Cell Dysfunction; Fat-content; Onset; Normalization; Mechanisms; Generation; Subgroups; Atlas
ISSN (print) / ISBN 2666-3791
e-ISSN 2666-3791
Zeitschrift Cell Reports Medicine
Quellenangaben Band: 3, Heft: 1, Seiten: , Artikelnummer: 100477 Supplement: ,
Verlag Cell Press
Verlagsort Radarweg 29, 1043 Nx Amsterdam, Netherlands
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Molekulare Endokrinologie und Metabolismus (MEM)
CF Metabolomics & Proteomics (CF-MPC)
Institute of Experimental Genetics (IEG)
Förderungen Innovative Medicines Initiative 2 Joint Undertaking
European Union
Novo Nordisk Foundation
Wellcome Trust New Investigator Award
NIDDK
Wellcome Trust
Innovative Medicines Initiative Joint Undertaking