mmpc-logo mmpc-logo
twitter-logo    bluesky-logo
| Create Account | login
Publication
JNK expression by macrophages promotes obesity-induced insulin resistance and
inflammation.
Authors Han MS, Jung DY, Morel C, Lakhani SA, Kim JK, Flavell RA, Davis RJ
Submitted By Roger Davis on 1/30/2013
Status Published
Journal Science (New York, N.Y.)
Year 2013
Date Published
Volume : Pages 339 : 218 - 222
PubMed Reference 23223452
Abstract The cJun NH(2)-terminal kinase (JNK) signaling pathway contributes to
inflammation and plays a key role in the metabolic response to obesity,
including insulin resistance. Macrophages are implicated in this process. To
test the role of JNK, we established mice with selective JNK deficiency in
macrophages. We report that feeding a high-fat diet to control and JNK-deficient
mice caused similar obesity, but only mice with JNK-deficient macrophages
remained insulin-sensitive. The protection of mice with macrophage-specific JNK
deficiency against insulin resistance was associated with reduced tissue
infiltration by macrophages. Immunophenotyping demonstrated that JNK was
required for pro-inflammatory macrophage polarization. These studies demonstrate
that JNK in macrophages is required for the establishment of obesity-induced
insulin resistance and inflammation.






Menu

Home
Contact
About MMPC
Animal Husbandry
Tests Data
Search Data
Analysis
Clients
MMPC Centers

Newsletter

Interested in receiving MMPC News?
twitter-logo Mouse Phenotyping
@NationalMMPC



2017 National MMPC. All Rights Reserved.