Citation

BibTex format

@article{Woodcock:2015:10.1016/j.immuni.2014.12.023,
author = {Woodcock, KJ and Kierdorf, K and Pouchelon, CA and Vivancos, V and Dionne, MS and Geissmann, F},
doi = {10.1016/j.immuni.2014.12.023},
journal = {Immunity},
pages = {133--144},
title = {Macrophage-derived upd3 Cytokine causes impaired glucose homeostasis and reduced lifespan in drosophila fed a lipid-rich diet},
url = {http://dx.doi.org/10.1016/j.immuni.2014.12.023},
volume = {42},
year = {2015}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic activation of JAK-STAT signaling, reduced insulin sensitivity, hyperglycemia, and a shorter lifespan. Drosophila macrophages produced the JAK-STAT-activating cytokine upd3, in a scavenger-receptor (crq) and JNK-dependent manner. Genetic depletion of macrophages or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-κB signaling made no contribution to the phenotype observed. These results identify an evolutionarily conserved “scavenger receptor-JNK-type 1 cytokine” cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway.
AU - Woodcock,KJ
AU - Kierdorf,K
AU - Pouchelon,CA
AU - Vivancos,V
AU - Dionne,MS
AU - Geissmann,F
DO - 10.1016/j.immuni.2014.12.023
EP - 144
PY - 2015///
SN - 1097-4180
SP - 133
TI - Macrophage-derived upd3 Cytokine causes impaired glucose homeostasis and reduced lifespan in drosophila fed a lipid-rich diet
T2 - Immunity
UR - http://dx.doi.org/10.1016/j.immuni.2014.12.023
UR - https://www.sciencedirect.com/science/article/pii/S1074761314004907?via%3Dihub
UR - http://hdl.handle.net/10044/1/40221
VL - 42
ER -

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