Crosstalk between Metabolic Disorders and Immune Cells.
Shinichi SaitohKoen Van WijkOsamu NakajimaPublished in: International journal of molecular sciences (2021)
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.
Keyphrases
- insulin resistance
- adipose tissue
- immune response
- high fat diet induced
- metabolic syndrome
- high fat diet
- type diabetes
- polycystic ovary syndrome
- natural killer cells
- risk factors
- oxidative stress
- glycemic control
- endothelial cells
- skeletal muscle
- cardiovascular disease
- diabetic rats
- dendritic cells
- signaling pathway
- risk assessment
- toll like receptor
- inflammatory response
- weight loss
- cell proliferation
- climate change
- physical activity
- drug induced
- weight gain
- combination therapy