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Lipoprotein lipase maintains microglial innate immunity in obesity.
Cell Rep. 20, 3034-3042 (2017)
Consumption of a hypercaloric diet upregulates microglial innate immune reactivity along with a higher expression of lipoprotein lipase (Lpl) within the reactive microglia in the mouse brain. Here, we show that knockdown of the Lpl gene specifically in microglia resulted in deficient microglial uptake of lipid, mitochondrial fuel utilization shifting to glutamine, and significantly decreased immune reactivity. Mice with knockdown of the Lpl gene in microglia gained more body weight than control mice on a high-carbohydrate high-fat (HCHF) diet. In these mice, microglial reactivity was significantly decreased in the mediobasal hypothalamus, accompanied by downregulation of phagocytic capacity and increased mitochondrial dysmorphologies. Furthermore, HCHF-diet-induced POMC neuronal loss was accelerated. These results show that LPL-governed microglial immunometabolism is essential to maintain microglial function upon exposure to an HCHF diet. In a hypercaloric environment, lack of such an adaptive immunometabolic response has detrimental effects on CNS regulation of energy metabolism.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Nf-κb ; Tnf-α ; Autophagosomes ; Fuel Dependency ; Glutamine ; Hypothalamus ; Mitochondria ; Phagocytosis ; Phospholipid ; Very Low-density Lipoprotein; Alzheimers-disease; In-vivo; Macrophages; Activation; Glutamine; Dynamics; Neurons; Glucose; Alpha; Mouse
ISSN (print) / ISBN
2211-1247
e-ISSN
2211-1247
Journal
Cell Reports
Quellenangaben
Volume: 20,
Issue: 13,
Pages: 3034-3042
Publisher
Cell Press
Publishing Place
Cambridge
Non-patent literature
Publications
Reviewing status
Peer reviewed