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Processes Underlying Glycemic Deterioration in Type 2 Diabetes: An IMI DIRECT Study
Author(s) -
Roberto Bizzotto,
Christopher Jennison,
Angus G. Jones,
Azra Kurbasic,
Andrea Tura,
Gwen Kennedy,
Jimmy D. Bell,
E. Louise Thomas,
Gary Frost,
Rebeca Eriksen,
Robert W. Koivula,
Søren Brage,
Jane Kaye,
Andrew T. Hattersley,
Alison Heggie,
Donna McEvoy,
Leen M. ‘t Hart,
Joline W. J. Beulens,
Petra Elders,
Petra Musholt,
Martin Ridderstråle,
Tue H. Hansen,
Kristine H. Allin,
Torben Hansen,
Henrik Vestergaard,
Agnete Troen Lundgaard,
Henrik S. Thomsen,
Federico De Masi,
Konstantinos D. Tsirigos,
Søren Brunak,
Ana Viñuela,
Anubha Mahajan,
Timothy J. McDonald,
Tarja Kokkola,
Ian M. Forgie,
Giuseppe N. Giordano,
Imre Pavo,
Hartmut Ruetten,
Emmanouil T. Dermitzakis,
Mark I. McCarthy,
Oluf Pedersen,
Jochen M. Schwenk,
Jerzy Adamski,
Paul W. Franks,
Mark Walker,
Ewan R. Pearson,
Andrea Mari,
Moustafa Abdalla,
Jonathan Adam,
Kofi Adragni,
Rosa Lundbye Allesøe,
Manimozhiyan Arumugam,
Naeimeh Atabaki Pasdar,
Tania Baltauss,
Karina Banasik,
Patrick Baum,
Margit Bergstrom,
Susanna Bianzano,
Amelie Bonneford,
Caroline Brorsson,
Andrew Brown,
Louise Cabrelli,
Robert Caïazzo,
Mickaël Canouil,
Matilda Dale,
David Davtian,
Adem Y. Dawed,
Nathalie de Préville,
Koen F. Dekkers,
Harshal Deshmukh,
Christiane Dings,
Louise A. Donnelly,
Avirup Dutta,
Beate Ehrhardt,
Line Engelbrechtsen,
Juan Fernandez,
Jorge Ferrer,
Hugo Fitipaldi,
Annemette Forman,
Francesca Frau,
Andreas Fritsche,
Philippe Froguel,
Johann Gassenhuber,
Nick N. Giordano,
Toni Giorgino,
Stephen Gough,
Ulrike GraefeMody,
Harald Grallert,
Rolf Grempler,
Lenka Groeneveld,
Leif Groop,
Valborg Guðmundsdóttir,
Mark Haid,
Ragna S. Häussler,
Anita M. Hennige,
Anita Hill,
Reinhard W. Holl,
MunGwan Hong,
Michelle Hudson,
Bernd Jablonka,
Yunlong Jiao,
Joachim Johansen,
Anna Jonsson,
Tugce Karaderi,
Maria Klintenberg,
Anitra D.M. Koopman,
Teemu Kuulasmaa,
Markku Laakso,
Thorsten Lehr,
Heather Loftus,
Gianluca Mazzoni,
Nicky McRobert,
Ian McVittie,
Miranda Mourby,
Pascal M. Mutie,
Rachel Nice,
Claudia Nicolay,
Agnes Martine Nielsen,
Birgitte Nilsson,
Nicholette D. Palmer,
François Pattou,
Helle K. Pedersen,
Mandy H. Perry,
Hugo PomaresMillan,
Simon Rasmussen,
Violeta Raverdy,
Neil Robertson,
Slieker Roderick,
Marianne Rodriquez,
Femke Rutters,
Peter Wad Sackett,
Nina Scherer,
Nisha Shah,
Sapna Sharma,
Iryna Sihinevich,
Nadja B. Søndertoft,
Hans-Henrik Staerfeldt,
Birgit Steckel-Hamann,
Leen M. t Hart,
Harriet Teare,
Cecilia Engel Thomas,
Melissa K. Thomas,
Barbara Thorand,
Claire E. Thorne,
J. Tillner,
Martina Troll,
Mathias Uhlén,
Nienke van Leeuwen,
Hélène Verkindt,
Josef Korbinian Vogt,
Dianne Wake,
Agata WesolowskaAndersen,
Brandon Whitcher,
Han Wu
Publication year - 2020
Publication title -
diabetes care
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.636
H-Index - 363
eISSN - 1935-5548
pISSN - 0149-5992
DOI - 10.2337/dc20-1567
Subject(s) - medicine , type 2 diabetes , glycemic , diabetes mellitus , lipid profile , insulin , logistic regression , odds ratio , insulin resistance , endocrinology
OBJECTIVE We investigated the processes underlying glycemic deterioration in type 2 diabetes (T2D). RESEARCH DESIGN AND METHODS A total of 732 recently diagnosed patients with T2D from the Innovative Medicines Initiative Diabetes Research on Patient Stratification (IMI DIRECT) study were extensively phenotyped over 3 years, including measures of insulin sensitivity (OGIS), β-cell glucose sensitivity (GS), and insulin clearance (CLIm) from mixed meal tests, liver enzymes, lipid profiles, and baseline regional fat from MRI. The associations between the longitudinal metabolic patterns and HbA1c deterioration, adjusted for changes in BMI and in diabetes medications, were assessed via stepwise multivariable linear and logistic regression. RESULTS Faster HbA1c progression was independently associated with faster deterioration of OGIS and GS and increasing CLIm; visceral or liver fat, HDL-cholesterol, and triglycerides had further independent, though weaker, roles (R2 = 0.38). A subgroup of patients with a markedly higher progression rate (fast progressors) was clearly distinguishable considering these variables only (discrimination capacity from area under the receiver operating characteristic = 0.94). The proportion of fast progressors was reduced from 56% to 8–10% in subgroups in which only one trait among OGIS, GS, and CLIm was relatively stable (odds ratios 0.07–0.09). T2D polygenic risk score and baseline pancreatic fat, glucagon-like peptide 1, glucagon, diet, and physical activity did not show an independent role. CONCLUSIONS Deteriorating insulin sensitivity and β-cell function, increasing insulin clearance, high visceral or liver fat, and worsening of the lipid profile are the crucial factors mediating glycemic deterioration of patients with T2D in the initial phase of the disease. Stabilization of a single trait among insulin sensitivity, β-cell function, and insulin clearance may be relevant to prevent progression.

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