The macrophage switch in obesity development

The macrophage switch in obesity development

Author Castoldi, Angela Google Scholar
de Souza, Cristiane Naffah Google Scholar
Câmara, Niels Olsen Saraiva Autor UNIFESP Google Scholar
Moraes-Vieira, Pedro Manoel Google Scholar
Abstract Immune cell infiltration in (white) adipose tissue (AT) during obesity is associated with the development of insulin resistance. In AT, the main population of leukocytes are macrophages. Macrophages can be classified into two major populations: M1, classically activated macrophages, and M2, alternatively activated macrophages, although recent studies have identified a broad range of macrophage subsets. During obesity, AT M1 macrophage numbers increase and correlate with AT inflammation and insulin resistance. Upon activation, pro-inflammatory M1 macrophages induce aerobic glycolysis. By contrast, in lean humans and mice, the number of M2 macrophages predominates. M2 macrophages secrete anti-inflammatory cytokines and utilize oxidative metabolism to maintain AT homeostasis. Here, we review the immunologic and metabolic functions of AT macrophages and their different facets in obesity and the metabolic syndrome.
Keywords Obesity
Adipose Tissue
Insulin Resistance
Macrophage Polarization
Adipose Tissue InflammationAdipose-Tissue Inflammation
Induced Insulin-Resistance
Innate Lymphoid-Cells
Alternatively Activated Macrophages
Diet-Induced Obesity
Toll-Like Receptors
Regulatory T-Cells
Nlrp3 Inflammasome
Language English
Sponsor Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [11/15682-4, 12/02270-2, 14/10910-7, 15/18121-4]
Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq, Renal Immunopathogy Laboratory CNPq/Inserm and Complex Fluids INCT)
Grant number FAPESP: 11/15682-4
FAPESP: 12/02270-2
FAPESP: 14/10910-7
FAPESP: 15/18121-4
Date 2016
Published in Frontiers In Immunology. Lausanne, v. 6, p. UNSP 637, 2016.
ISSN 1664-3224 (Sherpa/Romeo, impact factor)
Publisher Pontificia Univ Catolica Sao Paulo
Extent UNSP 637
Access rights Open access Open Access
Type Revisão
Web of Science ID WOS:000367713900001

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