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Gao, Y.* ; Vidal-Itriago, A.* ; Kalsbeek, M.J.* ; Layritz, C. ; García-Cáceres, C. ; Tom, R.Z. ; Eichmann, T.O.* ; Vaz, F.M.* ; Houtkooper, R.H.* ; van der Wel, N.* ; Verhoeven, A.J.* ; Yan, J.* ; Kalsbeek, A.* ; Eckel, R.H.* ; Hofmann, S.M. ; Yi, C.X.*

Lipoprotein lipase maintains microglial innate immunity in obesity.

Cell Rep. 20, 3034-3042 (2017)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
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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
Language english
Publication Year 2017
HGF-reported in Year 2017
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 20, Issue: 13, Pages: 3034-3042 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Regeneration Research (IDR)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s) 30201 - Metabolic Health
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502390-001
G-502200-001
PubMed ID 28954222
DOI 10.1016/j.celrep.2017.09.008
WOS ID WOS:000411684400004
Scopus ID 85029881981
Erfassungsdatum 2017-10-05
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