Metabolic factors in the regulation of hypothalamic innate immune responses in obesity.
Journal
Experimental & molecular medicine
ISSN: 2092-6413
Titre abrégé: Exp Mol Med
Pays: United States
ID NLM: 9607880
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
received:
03
05
2021
accepted:
13
05
2021
pubmed:
28
4
2022
medline:
11
5
2022
entrez:
27
4
2022
Statut:
ppublish
Résumé
The hypothalamus is a central regulator of body weight and energy homeostasis. There is increasing evidence that innate immune activation in the mediobasal hypothalamus (MBH) is a key element in the pathogenesis of diet-induced obesity. Microglia, the resident immune cells in the brain parenchyma, have been shown to play roles in diverse aspects of brain function, including circuit refinement and synaptic pruning. As such, microglia have also been implicated in the development and progression of neurological diseases. Microglia express receptors for and are responsive to a wide variety of nutritional, hormonal, and immunological signals that modulate their distinct functions across different brain regions. We showed that microglia within the MBH sense and respond to a high-fat diet and regulate the function of hypothalamic neurons to promote food intake and obesity. Neurons, glia, and immune cells within the MBH are positioned to sense and respond to circulating signals that regulate their capacity to coordinate aspects of systemic energy metabolism. Here, we review the current knowledge of how these peripheral signals modulate the innate immune response in the MBH and enable microglia to regulate metabolic control.
Identifiants
pubmed: 35474339
doi: 10.1038/s12276-021-00666-z
pii: 10.1038/s12276-021-00666-z
pmc: PMC9076660
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
393-402Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK063720
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK098722
Pays : United States
Informations de copyright
© 2022. The Author(s).
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