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

Autor: L. van Beek, J. Van den Bossche, M. de Winther, J S Verbeek, Frits Koning, K. Willems van Dijk, Patrick C.N. Rensen, Mariëtte R. Boon, S M van den Berg, A D van Dam, Amanda C. M. Pronk, Vanessa van Harmelen, C. van Kooten
Přispěvatelé: Amsterdam Gastroenterology Endocrinology Metabolism, AII - Inflammatory diseases, ACS - Atherosclerosis & ischemic syndromes, Amsterdam Cardiovascular Sciences, Amsterdam institute for Infection and Immunity, Medical Biochemistry
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Zdroj: International Journal of Obesity, 42(2), 260-269. Nature Publishing Group
International journal of obesity (2005), 42(2), 260-269. Nature Publishing Group
International Journal of Obesity, 42(2), 260-269
ISSN: 0307-0565
Popis: 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 Fc gamma receptors (Fc gamma R) and by activating the complement system. The aim of our study was to investigate whether activation of Fc gamma R and/or complement C3 mediates the development of high-fat diet-induced glucose intolerance. METHODS: We studied mice lacking all four Fc gamma Rs (Fc.RI/II/III/IV-/-), only the inhibitory Fc gamma RIIb (Fc gamma RIIb(-/-)), only the central component of the complement system C3 (C3(-/-)), and mice lacking both Fc gamma Rs and C3 (Fc gamma RI/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
Databáze: OpenAIRE