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Publication : Lipoprotein Lipase Maintains Microglial Innate Immunity in Obesity.

First Author  Gao Y Year  2017
Journal  Cell Rep Volume  20
Issue  13 Pages  3034-3042
PubMed ID  28954222 Mgi Jnum  J:254843
Mgi Id  MGI:6104094 Doi  10.1016/j.celrep.2017.09.008
Citation  Gao Y, et al. (2017) Lipoprotein Lipase Maintains Microglial Innate Immunity in Obesity. Cell Rep 20(13):3034-3042
abstractText  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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