HOMA2-B enhances assessment of type 1 diabetes risk among TrialNet Pathway to Prevention participants.


Journal

Diabetologia
ISSN: 1432-0428
Titre abrégé: Diabetologia
Pays: Germany
ID NLM: 0006777

Informations de publication

Date de publication:
01 2022
Historique:
received: 09 02 2021
accepted: 07 07 2021
pubmed: 14 10 2021
medline: 1 4 2022
entrez: 13 10 2021
Statut: ppublish

Résumé

Methods to identify individuals at highest risk for type 1 diabetes are essential for the successful implementation of disease-modifying interventions. Simple metabolic measures are needed to help stratify autoantibody-positive (Aab+) individuals who are at risk of developing type 1 diabetes. HOMA2-B is a validated mathematical tool commonly used to estimate beta cell function in type 2 diabetes using fasting glucose and insulin. The utility of HOMA2-B in association with type 1 diabetes progression has not been tested. Baseline HOMA2-B values from single-Aab+ (n = 2652; mean age, 21.1 ± 14.0 years) and multiple-Aab+ (n = 3794; mean age, 14.5 ± 11.2 years) individuals enrolled in the TrialNet Pathway to Prevention study were compared. Cox proportional hazard models were used to determine associations between HOMA2-B tertiles and time to progression to type 1 diabetes, with adjustments for age, sex, HLA status and BMI z score. Receiver operating characteristic (ROC) analysis was used to test the association of HOMA2-B with type 1 diabetes development in 1, 2, 5 and 10 years. At study entry, HOMA2-B values were higher in single- compared with multiple-Aab+ Pathway to Prevention participants (91.1 ± 44.5 vs 83.9 ± 38.9; p < 0.001). Single- and multiple-Aab+ individuals in the lowest HOMA2-B tertile had a higher risk and faster rate of progression to type 1 diabetes. For progression to type 1 diabetes within 1 year, area under the ROC curve (AUC-ROC) was 0.685, 0.666 and 0.680 for all Aab+, single-Aab+ and multiple-Aab+ individuals, respectively. When correlation between HOMA2-B and type 1 diabetes risk was assessed in combination with additional factors known to influence type 1 diabetes progression (insulin sensitivity, age and HLA status), AUC-ROC was highest for the single-Aab+ group's risk of progression at 2 years (AUC-ROC 0.723 [95% CI 0.652, 0.794]). These data suggest that HOMA2-B may have utility as a single-time-point measurement to stratify risk of type 1 diabetes development in Aab+ individuals.

Identifiants

pubmed: 34642772
doi: 10.1007/s00125-021-05573-6
pii: 10.1007/s00125-021-05573-6
pmc: PMC8752172
mid: NIHMS1751299
doi:

Substances chimiques

Autoantibodies 0
Blood Glucose 0
Insulin 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

88-100

Subventions

Organisme : NIDDK NIH HHS
ID : U01 DK085476
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085453
Pays : United States
Organisme : BLRD VA
ID : I01 BX001733
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK106993
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103282
Pays : United States
Organisme : NIDDK NIH HHS
ID : UC4 DK106993
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061042
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085509
Pays : United States
Organisme : NIDDK NIH HHS
ID : UC4 DK117009
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK093954
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK127308
Pays : United States
Organisme : NIDDK NIH HHS
ID : UC4 DK104166
Pays : United States
Organisme : NIDDK NIH HHS
ID : R21 DK119800
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061010
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK127786
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085466
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103153
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061058
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK106984
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085499
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK107013
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103266
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK127236
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK127382
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK097512
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK107014
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK106994
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061034
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085461
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103180
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085465
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085504
Pays : United States

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Jamie L Felton (JL)

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

David Cuthbertson (D)

Health Informatics Institute, University of South Florida, Tampa, FL, USA.

Megan Warnock (M)

Health Informatics Institute, University of South Florida, Tampa, FL, USA.

Kuldeep Lohano (K)

Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

Farah Meah (F)

Hines VA Medical Center, Hines, IL, USA.

John M Wentworth (JM)

Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Department of Diabetes and Endocrinology, Royal Melbourne Hospital, Parkville, VIC, Australia.

Jay Sosenko (J)

Department of Medicine and the Diabetes Research Institute, Leonard Miller School of Medicine, University of Miami, Miami, FL, USA.

Carmella Evans-Molina (C)

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA. cevansmo@iu.edu.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA. cevansmo@iu.edu.
Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA. cevansmo@iu.edu.
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA. cevansmo@iu.edu.
Roudebush VA Medical Center, Indianapolis, IN, USA. cevansmo@iu.edu.

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