Hyperglycemia Is Associated with Psoriatic Inflammation in Both Humans and Mice.
Animals
Blood Glucose
/ analysis
Cross-Sectional Studies
Disease Models, Animal
Female
Glycated Hemoglobin
/ analysis
Humans
Hyperglycemia
/ blood
Imiquimod
/ immunology
Insulin
/ metabolism
Interleukin-17
/ antagonists & inhibitors
Male
Mice
Middle Aged
Phototherapy
Psoriasis
/ complications
Retrospective Studies
Severity of Illness Index
Skin
Treatment Outcome
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
03
08
2018
revised:
16
01
2019
accepted:
25
01
2019
pubmed:
19
2
2019
medline:
10
5
2020
entrez:
19
2
2019
Statut:
ppublish
Résumé
Chronic low-grade inflammation can cause several metabolic syndromes. Patients with psoriasis, a chronic immunological skin inflammation, often develop diabetes. However, it is not clear to date how psoriasis leads to, or is correlated with, glucose intolerance. Here, we investigate whether psoriasis itself is correlated with hyperglycemia in humans and mice. In patients, the severity of psoriasis was correlated with high blood glucose levels, and treatment of psoriasis by phototherapy improved insulin secretion. Imiquimod-induced systemic and cutaneous inflammation in mice, with features of human psoriasis, also resulted in hyperglycemia. Although it should be determined if psoriasis-like cutaneous inflammation alone can induce hyperglycemia, imiquimod-treated mice showed impairment of insulin secretion without significant islet inflammation. Administration of anti-IL-17A monoclonal antibody improved hyperglycemia in patients with psoriasis and imiquimod-treated mice with psoriasiform features. These results suggest that hyperglycemia is highly associated with psoriasis, mainly through IL-17.
Identifiants
pubmed: 30776434
pii: S0022-202X(19)30117-4
doi: 10.1016/j.jid.2019.01.029
pii:
doi:
Substances chimiques
Blood Glucose
0
Glycated Hemoglobin A
0
IL17A protein, human
0
Il17a protein, mouse
0
Insulin
0
Interleukin-17
0
hemoglobin A1c protein, human
0
Imiquimod
P1QW714R7M
Types de publication
Journal Article
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1329-1338.e7Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.