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No role for mast cells in obesity-related metabolic dysregulation.
Front. Immunol. 7:524 (2016)
Obesity-related adipose tissue (AT) inflammation that promotes metabolic dysregulation is associated with increased AT mast cell numbers. Mast cells are potent inducers of inflammatory responses and could potentially contribute to obesity-induced AT inflammation and metabolic dysregulation. Conflicting findings were reported on obesity-related metabolic dysfunction in mast cell-deficient mice, thus creating a controversy that has not been resolved to date. Whereas traditional Kit hypomorphic mast cell-deficient strains featured reduced diet-induced obesity and diabetes, a Kit-independent model of mast cell deficiency, Cpa3(Cre/+) mice, displayed no alterations in obesity and insulin sensitivity. Herein, we analyzed diet-induced obesity in Mcpt5-Cre R-DTA mice, in which the lack of mast cells is caused by a principle different from mast cell deficiency in Cpa3(Cre/+) mice or Kit mutations. We observed no difference between mast cell-deficient and -proficient mice in diet-induced obesity with regards to weight gain, glucose tolerance, insulin resistance, metabolic parameters, hepatic steatosis, and AT or liver inflammation. We conclude that mast cells play no essential role in obesity and related pathologies.
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5.695
1.222
7
5
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Mast Cell Deficiency ; Diet-induced Obesity ; Metabolic Dysregulation ; Insulin Resistance ; Glucose Tolerance; Adipose-tissue Inflammation; Insulin-resistance; Protects Mice; Deficiency; Disease; Fat; Ige; Costimulation; Macrophages; Pathogens
Language
english
Publication Year
2016
HGF-reported in Year
2016
ISSN (print) / ISBN
1664-3224
e-ISSN
1664-3224
Journal
Frontiers in Immunology
Quellenangaben
Volume: 7,
Article Number: 524
Publisher
Frontiers
Publishing Place
Lausanne
Reviewing status
Peer reviewed
Institute(s)
Institute of Pancreatic Islet Research (IPI)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502600-001
WOS ID
WOS:000388337600001
Erfassungsdatum
2016-12-23