1. Figure 2 Initiators of obesity-associated inflammation in adipocytes
Figure 2 | Initiators of obesity-associated inflammation in adipocytes. Gut-derived lipopolysaccharide might stimulate inflammatory pathways by binding to the pattern recognition receptor Toll-like receptor 4 (TLR4) at the plasma membrane. Similarly, free fatty acids (FFAs) can activate inflammatory signalling through either TLR4 or TLR2. Additionally, NLRP3 activation by damage-associated molecular proteins (DAMPs), which are released from dying adipocytes and recognized by NOD-like receptors (NLRs), might also be an important initiating step in inflammation. Hypoxic conditions are also associated with inflammation in adipocytes, but the exact mechanisms responsible for this association are unclear. Finally, mechanical stress caused by adipose tissue expansion through the extracellular matrix (ECM) is sensed by the RhoA–Rock pathway, which leads to downstream inflammatory signalling. NF‑κB is a signalling hub that has been suggested to be involved in inflammatory signalling downstream of all these diverse potential initiators of adipocyte inflammation in individuals with obesity. Expression of genes that encode downstream inflammatory proteins leads to expression of adipokines, including inflammatory cytokines that promote the recruitment and activation of pro-inflammatory immune cells. TNF, tumour necrosis factor.
Reilly, S. M. & Saltiel, A. R. (2017) Adapting to obesity with adipose tissue inflammation
Nat. Rev. Endocrinol. doi: /nrendo