A pref-1-controlled non-inflammatory mechanism of insulin resistance.
Cell biology
Immunology
Molecular biology
Transcriptomics
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
16 Jun 2023
16 Jun 2023
Historique:
received:
24
01
2023
revised:
21
04
2023
accepted:
15
05
2023
medline:
7
6
2023
pubmed:
7
6
2023
entrez:
7
6
2023
Statut:
epublish
Résumé
While insulin resistance (IR) is associated with inflammation in white adipose tissue, we report a non-inflammatory adipose mechanism of high fat-induced IR mediated by loss of Pref-1. Pref-1, released from adipose Pref-1+ cells with characteristics of M2 macrophages, endothelial cells or progenitors, inhibits MIF release from both Pref-1+ cells and adipocytes by binding with integrin β1 and inhibiting the mobilization of p115. High palmitic acid induces PAR2 expression in Pref-1+ cells, downregulating Pref-1 expression and release in an AMPK-dependent manner. The loss of Pref-1 increases adipose MIF secretion contributing to non-inflammatory IR in obesity. Treatment with Pref-1 blunts the increase in circulating plasma MIF levels and subsequent IR induced by a high palmitic acid diet. Thus, high levels of fatty acids suppress Pref-1 expression and secretion, through increased activation of PAR2, resulting in an increase in MIF secretion and a non-inflammatory adipose mechanism of IR.
Identifiants
pubmed: 37283810
doi: 10.1016/j.isci.2023.106923
pii: S2589-0042(23)01000-3
pmc: PMC10239698
doi:
Types de publication
Journal Article
Langues
eng
Pagination
106923Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
R.B. is a co-inventor on issued Yale patents for MIF antagonists.
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