Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 18, Pages -Publisher
MDPI
DOI: 10.3390/ijms221810017
Keywords
chronic inflammation; obesity; M1; M2 macrophages; mesenchymal stem cells; CD4+T cells; natural killer cells; innate lymphoid cells; cytokine; non-obese metabolic disorder; 5-aminolevulinic acid
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Metabolic syndrome is caused by insulin resistance and multiple risk factors. Chronic inflammation due to obesity is primarily caused by pro-inflammatory M1 macrophages entering adipose tissue, which in turn recruit more pro-inflammatory immune cells to enhance the immune response.
Metabolic syndrome results from multiple risk factors that arise from insulin resistance induced by abnormal fat deposition. Chronic inflammation owing to obesity primarily results from the recruitment of pro-inflammatory M1 macrophages into the adipose tissue stroma, as the adipocytes within become hypertrophied. During obesity-induced inflammation in adipose tissue, pro-inflammatory cytokines are produced by macrophages and recruit further pro-inflammatory immune cells into the adipose tissue to boost the immune response. Here, we provide an overview of the biology of macrophages in adipose tissue and the relationship between other immune cells, such as CD4+ T cells, natural killer cells, and innate lymphoid cells, and obesity and type 2 diabetes. Finally, we discuss the link between the human pathology and immune response and metabolism and further highlight potential therapeutic targets for the treatment of metabolic disorders.
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