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Tura, A.* ; Grespan, E.* ; Göbl, C.S.* ; Koivula, R.W.* ; Franks, P.W.* ; Pearson, E.R.* ; Walker, M.* ; Forgie, I.M.* ; Giordano, G.N.* ; Pavo, I.* ; Ruetten, H.* ; Dermitzakis, E.T.* ; McCarthy, M.I.* ; Pedersen, O.* ; Schwenk, J.M.* ; Adamski, J. ; De Masi, F.* ; Tsirigos, K.D.* ; Brunak, S.* ; Viñuela, A.* ; Mahajan, A.* ; McDonald, T.J.* ; Kokkola, T.* ; Vangipurapu, J.* ; Cederberg, H.* ; Laakso, M.* ; Rutters, F.* ; Elders, P.J.M.* ; Koopman, A.D.M.* ; Beulens, J.W.* ; Ridderstråle, M.* ; Hansen, T.H.* ; Allin, K.H.* ; Hansen, T.* ; Vestergaard, H.* ; Mari, A.* ; IMI DIRECT Consortium (Grallert, H. ; Sharma, S. ; Thorand, B.)

Profiles of glucose metabolism in different prediabetes phenotypes, classified by fasting glycemia, 2-hour OGTT, glycated hemoglobin, and 1-hour OGTT: An IMI DIRECT study.

Diabetes 70, 2092-2106 (2021)
Publ. Version/Full Text Postprint DOI PMC
Open Access Green
Differences in glucose metabolism among categories of prediabetes have not been systematically investigated. In this longitudinal study, participants (N=2111) underwent 2h-75g OGTT at baseline and 48 months. HbA1c was also measured. We classified participants as having isolated prediabetes defect (impaired fasting glucose, IFG; impaired glucose tolerance, IGT; HbA1c-prediabetes, IA1c), two defects (IFG+IGT, IFG+IA1c, IGT+IA1c), or all defects (IFG+IGT+IA1c). Beta-cell function (BCF) and insulin sensitivity (IS) were assessed from OGTT. At baseline, when pooling participants with isolated defects, they showed impairment in both BCF and IS compared to healthy controls. Pooled groups with two or three defects showed progressive further deterioration. Among groups with isolated defect, IGT showed lower IS, insulin secretion at reference glucose (ISRr), and insulin secretion potentiation (p<0.002). Conversely, IA1c showed higher IS and ISRr (p<0.0001). Among groups with two defects, we similarly found differences in both BCF and IS. At 48 months, we found higher type 2 diabetes incidence for progressively increasing number of prediabetes defects (odds ratio >2, p<0.008). In conclusion, the prediabetes groups showed differences in type/degree of glucometabolic impairment. Compared to the pooled group with isolated defects, those with double or triple defect showed progressive differences in diabetes incidence.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Beta-cell Dysfunction; Cardiovascular Risk Profile; Insulin-resistance; Plasma-glucose; Identify Subjects; Tolerance; Individuals; Hyperglycemia; Sensitivity; Regression
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Journal Diabetes
Quellenangaben Volume: 70, Issue: 9, Pages: 2092-2106 Article Number: , Supplement: ,
Publisher American Diabetes Association
Publishing Place Alexandria, VA.
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Experimental Genetics (IEG)
Institute of Epidemiology II (EPI2)
Grants Pfizer
Servier
Sanofi
Novo Nordisk A/S
Eli Lilly
Boehringer Ingelheim
Novo Nordisk Foundation postdoctoral fellowship
STAR Award Novo Nordisk
European Federation of Pharmaceutical Industries and Associations (EFPIA)
European Union's Seventh Framework Programme
Merck
Janssen
Takeda
Roche
AstraZeneca
AbbVie
National Institute for Health Research (NIHR)
Wellcome Investigator
Innovative Medicines Initiative Joint Undertaking