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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)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Zeitschrift Cell Reports
Quellenangaben Band: 20, Heft: 13, Seiten: 3034-3042 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge
Begutachtungsstatus Peer reviewed