Genetics: Is LADA just late onset type 1 diabetes?

Adult Age of Onset Cross-Sectional Studies Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Genetic Predisposition to Disease Humans Latent Autoimmune Diabetes in Adults Protein Tyrosine Phosphatase, Non-Receptor Type 22
HLA class II INS LADA (latent autoimmune diabetes in adults) PTPN22 Type 1 diabetes mellitus age of onset genetics

Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2022
Historique:
received: 09 04 2022
accepted: 04 07 2022
entrez: 29 8 2022
pubmed: 30 8 2022
medline: 31 8 2022
Statut: epublish

Résumé

There is a controversy regarding Latent Autoimmune Diabetes in Adults (LADA) classification and whether it should be considered a slowly progressing form of type 1 (T1) diabetes (DM) or a distinct type of DM altogether. This cross-sectional study assessed major genes associated with T1DM (class II  A total of 578 participants were included: 248 with T1DM (70 diagnosed after the age of 30), 256 with T2DM and 74 with LADA. High risk HLA alleles were significantly more frequent in LADA than in T2DM, whereas the opposite was true for protective alleles. We found a lower frequency of the high-risk DRB1*04-DQB1*03:02-DQA1*03:01 haplotype in LADA (21.1%) than in the overall T1DM (34.7%) (p<0.05), whereas no differences were found between these groups for DRB1*03-DQB1*02:01-DQA1*05:01 or for protective alleles. Only 12% the overall T1DM group had no risk alleles vs 30% of LADA (p<0.0005). However, HLA allele distribution was similar in LADA and T1DM diagnosed after the age of 30. A total of 506 individuals (195 with T1DM [21 diagnosed after age 30] 253 with T2DM and 58 with LADA) were genotyped for the  In this relatively small cross-sectional study, the genetic profile of subjects with LADA showed a similar T1DM-related risk allele distribution as in participants with T1DM diagnosed after the age of 30, but fewer risk alleles than those diagnosed before 30. Differences were present for HLA, as well as

Sections du résumé

Background
There is a controversy regarding Latent Autoimmune Diabetes in Adults (LADA) classification and whether it should be considered a slowly progressing form of type 1 (T1) diabetes (DM) or a distinct type of DM altogether.
Methods
This cross-sectional study assessed major genes associated with T1DM (class II 
Results
A total of 578 participants were included: 248 with T1DM (70 diagnosed after the age of 30), 256 with T2DM and 74 with LADA. High risk HLA alleles were significantly more frequent in LADA than in T2DM, whereas the opposite was true for protective alleles. We found a lower frequency of the high-risk DRB1*04-DQB1*03:02-DQA1*03:01 haplotype in LADA (21.1%) than in the overall T1DM (34.7%) (p<0.05), whereas no differences were found between these groups for DRB1*03-DQB1*02:01-DQA1*05:01 or for protective alleles. Only 12% the overall T1DM group had no risk alleles vs 30% of LADA (p<0.0005). However, HLA allele distribution was similar in LADA and T1DM diagnosed after the age of 30. A total of 506 individuals (195 with T1DM [21 diagnosed after age 30] 253 with T2DM and 58 with LADA) were genotyped for the 
Conclusion
In this relatively small cross-sectional study, the genetic profile of subjects with LADA showed a similar T1DM-related risk allele distribution as in participants with T1DM diagnosed after the age of 30, but fewer risk alleles than those diagnosed before 30. Differences were present for HLA, as well as

Identifiants

DOI: 10.3389/fendo.2022.916698 PMID: 36034444 PMC: PMC9404871
pubmed: 36034444
doi: 10.3389/fendo.2022.916698
pmc: PMC9404871
doi:

Substances chimiques

PTPN22 protein, human EC 3.1.3.48
Protein Tyrosine Phosphatase, Non-Receptor Type 22 EC 3.1.3.48

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

916698

Informations de copyright

Copyright © 2022 Hernández, Nóvoa-Medina, Faner, Palou, Esquerda, Castelblanco, Wägner and Mauricio.

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.

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Auteurs

M Hernández (M)

Department of Endocrinology and Nutrition, University Hospital Arnau de Vilanova, Lleida, Spain.
Lleida Biomedical Research Institute (IRB Lleida), University of Lleida (UdL), Lleida, Spain.

Y Nóvoa-Medina (Y)

Department of Pediatrics, Complejo Hospitalario Universitario Insular Materno-Infantil, Las Palmas de Gran Canaria, Spain.
Research Institute in Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria (ULPGC), Las Palmas de Gran Canaria, Spain.

R Faner (R)

Histocompatibility and Immunogenetics Laboratory, Blood and Tissue Bank, Barcelona, Spain.

E Palou (E)

Histocompatibility and Immunogenetics Laboratory, Blood and Tissue Bank, Barcelona, Spain.

A Esquerda (A)

Department of Laboratory Medicine, University Hospital Arnau de Vilanova, Lleida, Spain.

E Castelblanco (E)

Diabetis en Atenció Primària - Catalunya (DAP-Cat) Group, Unitat de Suport a la Recerca Barcelona, Fundació Institut Universitari per a la recerca a l'Atenció Primària de Salut Jordi Gol i Gurina, Barcelona, Spain.
Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine in St. Louis, St. Louis, MO, United States.

A M Wägner (AM)

Research Institute in Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria (ULPGC), Las Palmas de Gran Canaria, Spain.
Department of Endocrinology and Nutrition, Complejo Hospitalario Universitario Insular Materno-Infantil, Las Palmas de Gran Canaria, Spain.

D Mauricio (D)

Department of Endocrinology, Hospital de la Santa Creu i Sant Pau & Institut d'Investigació Biomèdica (IIB) Sant Pau, Barcelona, Spain.
Consorcio Centro de Investigación Biomédica en Red (CIBER) of Diabetes and Associated Metabolic Diseases, Instituto de Salud Carlos III, Barcelona, Spain.
Faculty of Medicine, University of Vic & Central University of Catalonia, Vic, Spain.

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Classifications MeSH

questionsmedicales.fr › Personnes › Tranches d'âge › Adulte › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Environnement et santé publique › Santé publique › Facteurs épidémiologiques › Facteurs âges › Âge de début › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Environnement et santé publique › Santé publique › Méthodes épidémiologiques › Caractéristiques des études épidémiologiques › Études épidémiologiques › Études transversales › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Maladies du système immunitaire › Maladies auto-immunes › Diabète de type 1 › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Maladies endocriniennes › Diabète › Diabète de type 2 › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Phénomènes génétiques › Génotype › Prédisposition génétique à une maladie › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Maladies du système immunitaire › Maladies auto-immunes › Diabète auto-immun latent de l'adulte › Genetics: Is LADA just late onset type 1 diabetes?
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › Protein Tyrosine Phosphatases › Protein Tyrosine Phosphatases, Non-Receptor › Protein Tyrosine Phosphatase, Non-Receptor Type 22 › Genetics: Is LADA just late onset type 1 diabetes?