Novel Reclassification of Adult Diabetes Is Useful to Distinguish Stages of β-Cell Function Linked to the Risk of Vascular Complications: The DOLCE Study From Northern Ukraine.
adult diabetes
clustering
diabetes complications
genetics
β-cell function
Journal
Frontiers in genetics
ISSN: 1664-8021
Titre abrégé: Front Genet
Pays: Switzerland
ID NLM: 101560621
Informations de publication
Date de publication:
2021
2021
Historique:
received:
04
12
2020
accepted:
03
06
2021
entrez:
19
7
2021
pubmed:
20
7
2021
medline:
20
7
2021
Statut:
epublish
Résumé
Presently, persons with diabetes are classified as having type 1 (T1D) or type 2 diabetes (T2D) based on clinical diagnosis. However, adult patients exhibit diverse clinical representations and this makes treatment approaches challenging to personalize. A recent Scandinavian study proposed a novel classification of adult diabetes into five clusters based on disease pathophysiology and risk of vascular complications. The current study aimed to characterize new subgroups of adult diabetes using this strategy in a defined population from northern Ukraine. We analyzed 2,140 patients with established diabetes from the DOLCE study ( Severe autoimmune diabetes (SAID, 11 and 6%) and severe insulin-deficient diabetes (SIDD, 25 and 14%) clusters were twice as prevalent in patients with long-term as compared to those with new-onset diabetes. Patients with long duration in both SAID and SIDD clusters had highest risks of proliferative retinopathy, and elevated risks of CKD. Long-term insulin-resistant obese diabetes 1 (IROD1) subgroup had elevated risks of CKD, while insulin-resistant obese diabetes 2 (IROD2) cluster exhibited the highest HOMA2-B, lowest HbA The novel reclassification algorithm of patients with adult diabetes was reproducible in this population from northern Ukraine. It may be beneficial for the patients in the SIDD subgroup to initiate earlier insulin treatment or other anti-diabetic modalities to preserve β-cell function. Long-term diabetes cases with preserved β-cell function and lower risk for microvascular complications represent an interesting subgroup of patients for further investigations of protective mechanisms.
Sections du résumé
BACKGROUND
BACKGROUND
Presently, persons with diabetes are classified as having type 1 (T1D) or type 2 diabetes (T2D) based on clinical diagnosis. However, adult patients exhibit diverse clinical representations and this makes treatment approaches challenging to personalize. A recent Scandinavian study proposed a novel classification of adult diabetes into five clusters based on disease pathophysiology and risk of vascular complications. The current study aimed to characterize new subgroups of adult diabetes using this strategy in a defined population from northern Ukraine.
METHODS
METHODS
We analyzed 2,140 patients with established diabetes from the DOLCE study (
RESULTS
RESULTS
Severe autoimmune diabetes (SAID, 11 and 6%) and severe insulin-deficient diabetes (SIDD, 25 and 14%) clusters were twice as prevalent in patients with long-term as compared to those with new-onset diabetes. Patients with long duration in both SAID and SIDD clusters had highest risks of proliferative retinopathy, and elevated risks of CKD. Long-term insulin-resistant obese diabetes 1 (IROD1) subgroup had elevated risks of CKD, while insulin-resistant obese diabetes 2 (IROD2) cluster exhibited the highest HOMA2-B, lowest HbA
CONCLUSION
CONCLUSIONS
The novel reclassification algorithm of patients with adult diabetes was reproducible in this population from northern Ukraine. It may be beneficial for the patients in the SIDD subgroup to initiate earlier insulin treatment or other anti-diabetic modalities to preserve β-cell function. Long-term diabetes cases with preserved β-cell function and lower risk for microvascular complications represent an interesting subgroup of patients for further investigations of protective mechanisms.
Identifiants
pubmed: 34276762
doi: 10.3389/fgene.2021.637945
pmc: PMC8283002
doi:
Types de publication
Journal Article
Langues
eng
Pagination
637945Informations de copyright
Copyright © 2021 Fedotkina, Sulaieva, Ozgumus, Cherviakova, Khalimon, Svietleisha, Buldenko, Ahlqvist, Asplund, Groop, Nilsson and Lyssenko.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Diabetes Technol Ther. 2012 Nov;14(11):1033-42
pubmed: 22958196
Diabetes. 2009 Apr;58(4):894-905
pubmed: 19168596
Nat Genet. 2012 Sep;44(9):981-90
pubmed: 22885922
Science. 2007 Jun 1;316(5829):1341-5
pubmed: 17463248
J Clin Invest. 2007 Aug;117(8):2077-9
pubmed: 17671643
Front Pharmacol. 2016 Apr 06;7:83
pubmed: 27092078
Lancet Diabetes Endocrinol. 2019 Jun;7(6):442-451
pubmed: 31047901
Placenta. 2006 Jun-Jul;27(6-7):540-9
pubmed: 16125225
Sci Rep. 2020 Sep 3;10(1):14541
pubmed: 32883969
Atherosclerosis. 2019 Nov;290:87-93
pubmed: 31604171
Diabetes. 2014 Jun;63(6):2158-71
pubmed: 24296717
Diabetes. 2009 Oct;58(10):2409-13
pubmed: 19584308
Diabetes Care. 1998 Dec;21(12):2191-2
pubmed: 9839117
J Diabetes Sci Technol. 2020 Jul;14(4):754-755
pubmed: 32468843
Lancet. 2014 Mar 22;383(9922):1084-94
pubmed: 24315621
Diabetes. 2013 Aug;62(8):2978-83
pubmed: 23557703
Nat Genet. 2008 Sep;40(9):1092-7
pubmed: 18711367
Diabetes. 2018 Oct;67(10):1911-1922
pubmed: 30237159
Diabetes. 2013 Mar;62(3):987-92
pubmed: 23139357
Nat Genet. 2008 Sep;40(9):1098-102
pubmed: 18711366
Mol Metab. 2017 Jul 08;6(9):943-957
pubmed: 28951820
J Am Soc Nephrol. 2005 Jan;16(1):189-94
pubmed: 15548563
Nature. 2009 Dec 17;462(7275):868-74
pubmed: 20016592
Int J Methods Psychiatr Res. 2018 Jun;27(2):e1608
pubmed: 29484742
Diabetes. 2001 Dec;50(12):2763-9
pubmed: 11723059
Prim Care Diabetes. 2007 Dec;1(4):203-5
pubmed: 18632047
Lancet Diabetes Endocrinol. 2019 Sep;7(9):684-694
pubmed: 31345776
Nat Genet. 2006 Feb;38(2):209-13
pubmed: 16415888
Diabetologia. 2017 May;60(5):793-799
pubmed: 28175964
Lancet Diabetes Endocrinol. 2019 Jan;7(1):9-11
pubmed: 30577891
Oman Med J. 2012 Mar;27(2):108-13
pubmed: 22496934
Lancet Diabetes Endocrinol. 2018 May;6(5):361-369
pubmed: 29503172
J Nutr. 2001 Feb;131(2):354S-60S
pubmed: 11160560
Lancet Diabetes Endocrinol. 2015 Oct;3(10):787-94
pubmed: 26342852
Ther Adv Endocrinol Metab. 2017 Jun;8(6):97-108
pubmed: 28794851
BMJ Open Diabetes Res Care. 2020 Aug;8(1):
pubmed: 32816869
Nat Genet. 2010 Mar;42(3):255-9
pubmed: 20118932
J Clin Endocrinol Metab. 2005 Jan;90(1):501-6
pubmed: 15483097
Cell Death Dis. 2020 Aug 25;11(8):704
pubmed: 32843642