IgG is elevated in obese white adipose tissue but does not induce glucose intolerance via Fcγ-receptor or complement

Background/Objectives: In obesity, B cells accumulate in white adipose tissue (WAT) and produce IgG, which may contribute to the development of glucose intolerance. IgG signals by binding to Fcγ receptors (FcγR) and by activating the complement system. The aim of our study was to investigate whether...

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Bibliographic Details
Published in:International Journal of Obesity 2018-02, Vol.42 (2), p.260-269
Main Authors: van Dam, A D, van Beek, L, Pronk, A C M, van den Berg, S M, Van den Bossche, J, de Winther, M P J, Koning, F, van Kooten, C, Rensen, P C N, Boon, M R, Verbeek, J S, van Dijk, K Willems, van Harmelen, V
Format: Article
Language:English
Subjects:
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Adipose Tissue, White - metabolism
Animals
Cells, Cultured
Complement C3 - metabolism
Diet, High-Fat
Disease Models, Animal
Epidemiology
Glucose Intolerance - metabolism
Health Promotion and Disease Prevention
Inflammation - metabolism
Inflammation - physiopathology
Internal Medicine
Male
Medicine
Medicine & Public Health
Metabolic Diseases
Mice
Mice, Knockout
Obesity - metabolism
Obesity - physiopathology
original-article
Public Health
Receptors, IgG - metabolism
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Summary:Background/Objectives: In obesity, B cells accumulate in white adipose tissue (WAT) and produce IgG, which may contribute to the development of glucose intolerance. IgG signals by binding to Fcγ receptors (FcγR) and by activating the complement system. The aim of our study was to investigate whether activation of FcγR and/or complement C3 mediates the development of high-fat diet-induced glucose intolerance. Methods: We studied mice lacking all four FcγRs (FcγRI/II/III/IV −/− ), only the inhibitory FcγRIIb (FcγRIIb −/− ), only the central component of the complement system C3 (C3 −/− ), and mice lacking both FcγRs and C3 (FcγRI/II/III/IV/C3 −/− ). All mouse models and wild-type controls were fed a high-fat diet (HFD) for 15 weeks to induce obesity. Glucose metabolism was assessed and adipose tissue was characterized for inflammation and adipocyte functionality. Results: In obese WAT of wild-type mice, B cells (+142%, P
ISSN:0307-0565
1476-5497
DOI:10.1038/ijo.2017.209