Table 1.

Adipose Inflammatory Functions in Insulin Resistance and Cardiovascular Disease

Component	Function	Key References
Preadipocytes	Macrophage-like, pro-inflammatory, interfere     with adipocyte insulin signaling.	9
Innate immunity	Innate antigens and TLRs transduce adipocyte inflammation;     mediate diet-induced obesity and insulin resistance.	4, 10, 11
ATMs	Resident ATMs shift toward pro-inflammatory phenotype in     obesity, whereas high-fat diet recruits ATMs (CCR2+) via     chemokines; ATMs contribute to adipose inflammation     and insulin resistance.	15–18
Chemokines	CCL2 (MCP-1) and its receptor, CCR2, play a key role in     diet-induced recruitment and retention of ATMs, obesity, and     insulin resistance; RANTES promotes T-cell chemotaxis     and is elevated in obesity.	19, 20, 22
Adipokines	Adipose inflammation regulates adiponectin, resistin, leptin,     RBP-4, visfatin, and lipocalin-2 production; adipokines     modulate systemic insulin signaling, hepatic lipoprotein     production, innate immunity, and vascular inflammation.	5, 29
FFAs	Adipose inflammation induces higher adipocyte FFA     production; FFAs induce insulin resistance in skeletal     muscle and liver, modulate lipoprotein production, and     impair endothelial functions.	6
Cytokines	Adipose inflammation increases local and systemic cytokine     production, which induces adipocyte insulin resistance,     systemic insulin resistance, endothelial dysfunction, and     vascular inflammation.	45, 52, 53, 57

TLR, Toll-like receptor; ATM, adipose tissue macrophage; MCP, monocyte chemotactic protein; RANTES; regulated on activation, normal T cell expressed and secreted; RBP, retinol binding protein; FFA, free-fatty acid.