The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Robert Koivula

Robert Koivula

Assistant researcher

Robert Koivula

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

Author

  • Andrea Tura
  • Eleonora Grespan
  • Christian S. Göbl
  • Robert W. Koivula
  • Paul W. Franks
  • Ewan R. Pearson
  • Mark Walker
  • Ian M. Forgie
  • Giuseppe N. Giordano
  • Imre Pavo
  • Hartmut Ruetten
  • Emmanouil T. Dermitzakis
  • Mark I. McCarthy
  • Oluf Pedersen
  • Jochen M. Schwenk
  • Jerzy Adamski
  • Federico De Masi
  • Konstantinos D. Tsirigos
  • Søren Brunak
  • Ana Viñuela
  • Anubha Mahajan
  • Timothy J. McDonald
  • Tarja Kokkola
  • Jagadish Vangipurapu
  • Henna Cederberg
  • Markku Laakso
  • Femke Rutters
  • Petra J.M. Elders
  • Anitra D.M. Koopman
  • Joline W. Beulens
  • Martin Ridderstråle
  • Tue H. Hansen
  • Kristine H. Allin
  • Torben Hansen
  • Henrik Vestergaard
  • Andrea Mari

Summary, in English

Differences in glucose metabolism among categories of prediabetes have not been systematically investigated. In this longitudinal study, participants (N = 2,111) underwent a 2-h 75-g oral glucose tolerance test (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], or HbA1c indicative of prediabetes [IA1c]), two defects (IFG+IGT, IFG+IA1c, or IGT+IA1c), or all defects (IFG+IGT+IA1c). β-Cell function (BCF) and insulin sensitivity were assessed from OGTT. At baseline, in pooling of participants with isolated defects, they showed impairment in both BCF and insulin sensitivity compared with healthy control subjects. Pooled groups with two or three defects showed progressive further deterioration. Among groups with isolated defect, those with IGT showed lower insulin sensitivity, insulin secretion at reference glucose (ISRr), and insulin secretion potentiation (P < 0.002). Conversely, those with IA1c showed higher insulin sensitivity and ISRr (P < 0.0001). Among groups with two defects, we similarly found differences in both BCF and insulin sensitivity. 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 with the pooled group with isolated defects, those with double or triple defect showed progressive differences in diabetes incidence.

Department/s

  • Genetic and Molecular Epidemiology
  • EpiHealth: Epidemiology for Health
  • EXODIAB: Excellence of Diabetes Research in Sweden
  • eSSENCE: The e-Science Collaboration
  • Genomics, Diabetes and Endocrinology

Publishing year

2021-09-01

Language

English

Pages

2092-2106

Publication/Series

Diabetes

Volume

70

Issue

9

Document type

Journal article

Publisher

American Diabetes Association Inc.

Topic

  • Endocrinology and Diabetes

Status

Published

Research group

  • Genetic and Molecular Epidemiology
  • Genomics, Diabetes and Endocrinology

ISBN/ISSN/Other

  • ISSN: 1939-327X