Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Four groups of type 2 diabetes contribute to the etiological and clinical heterogeneity in newly diagnosed individuals: An IMI DIRECT study
Univ Oxford, Wellcome Ctr Human Genet, Oxford, England..
KTH, Centra, Science for Life Laboratory, SciLifeLab. KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinitets-proteomik.ORCID-id: 0000-0001-8603-8293
KTH, Centra, Science for Life Laboratory, SciLifeLab. KTH, Skolan för kemi, bioteknologi och hälsa (CBH), Proteinvetenskap, Affinitets-proteomik.ORCID-id: 0000-0001-8141-8449
Univ Dundee, Dundee, Scotland..
Vise andre og tillknytning
2022 (engelsk)Inngår i: Cell Reports Medicine, E-ISSN 2666-3791 , Vol. 3, nr 1, artikkel-id 100477Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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 1 beta 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.

sted, utgiver, år, opplag, sider
Elsevier BV , 2022. Vol. 3, nr 1, artikkel-id 100477
HSV kategori
Identifikatorer
URN: urn:nbn:se:kth:diva-307778DOI: 10.1016/j.xcrm.2021.100477ISI: 000745037100001PubMedID: 35106505Scopus ID: 2-s2.0-85122950661OAI: oai:DiVA.org:kth-307778DiVA, id: diva2:1635561
Merknad

QC 20220207

Tilgjengelig fra: 2022-02-07 Laget: 2022-02-07 Sist oppdatert: 2023-08-25bibliografisk kontrollert

Open Access i DiVA

Fulltekst mangler i DiVA

Andre lenker

Forlagets fulltekstPubMedScopus

Person

Hong, Mun-GwanSchwenk, Jochen M.

Søk i DiVA

Av forfatter/redaktør
Hong, Mun-GwanSchwenk, Jochen M.
Av organisasjonen
I samme tidsskrift
Cell Reports Medicine

Søk utenfor DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric

doi
pubmed
urn-nbn
Totalt: 130 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf