Table 2 Biomarkers related to obesity and their relevance in the inflammatory response
Biomarkers | Relevance | References |
|---|---|---|
MMP-2 | Ability to break down ECM. Potential role as activator or inhibitor in tissue remodeling, atherosclerosis, cardiovascular diseases, and obesity. Levels are increased in obesity | |
MMP-9 | Ability to break down ECM. Potential role as activator or inhibitor in tissue remodeling, cardiovascular diseases, and obesity. Levels are diminished in obesity | [36] |
CXCR2 | Expressed on circulating neutrophils; critical for directing their migration to inflammatory sites | [39] |
IL-12 | Associated with insulin resistance. Divergently regulated in relation to inflammatory stress, excessive energy intake, and genetic obesity | [40] |
CCL3 (MIP-1α) | High transcript and protein levels in the white adipose tissue of the obese. Correlated with fasting plasma insulin concentrations in humans. Required for macrophage infiltration in adipose tissue with CCL2 | |
CCL2 (MCP1) | Required for macrophage infiltration of adipose tissue Adipose-tissue and serum CCL2 expression is increased through insulin stimuli, more in insulin-resistant than in insulin-sensitive lean mice | [44] |
IL-1β | Produced by macrophages. Implicated in the development of obesity-associated insulin resistance through inhibition of insulin signal transduction | [45] |
TNF-α | Expressed and secreted by adipose tissue. Levels associated with degree of adiposity and insulin resistance. Targeting TNF-α and/or its receptors has been suggested as a promising treatment for insulin resistance and type 2 diabetes mellitus | [46] |
Nrf2 | Involved in resistance to oxidative stress. Functions as a xenobiotic-activated receptor (XAR) to regulate the adaptive response to oxidants | |
IL-6 | Pleiotropic cytokine. A central player in the regulation of inflammation, hematopoiesis, immune responses, and host defense mechanisms. Influences secretion of adipokines from adipocytes. Involved in the etiology of obesity-related comorbidities, including insulin resistance and accelerated atherosclerosis, in humans | |
iNOS | Synthesizes large quantities of nitric oxide (NO), which acts with reactive oxidative species to producing nitrosative stress, thus playing a key role in adipocyte function and glucose tolerance | |
CD 40 | Ameliorates inflammation in visceral adipose tissue. Attenuates obesity-induced insulin resistance | [49] |
CD 80 | Plays a homeostatic role in preventing adipose inflammation | [50] |
ICAM-1 | Levels increased in obesity. Positively correlated with central adiposity and insulin resistance | |
CD 163 | Marker of macrophages with anti-inflammatory properties. Increased basal CD163 levels are related to obesity and its metabolic complications | |
CD 206 | Marker of M2-like macrophages in adipose tissues. Inhibits growth and differentiation of adipocyte progenitors, thus controlling adiposity and systemic insulin sensitivity | [62] |
Arginase | Marker of M2 macrophages. Also expressed in endothelial cells. Involved in obesity-induced vascular dysfunction | |
IL-10 | Anti-inflammatory cytokine. High levels found in obese women. Low levels are associated with the metabolic syndrome | [65] |
IL-1RA | Indirectly elicits an anti-inflammatory response. Competitively binds to the IL-1 receptor on the cell surface, thereby inhibiting the inflammatory effects of IL-1 | |
TGF-β1 | Anti-inflammatory cytokine. Counteracts the effects of the pro-inflammatory cytokines such as IL-8. Inhibits differentiation of pre-adipocytes | |
Bax, Bcl-2 | Part of the Bcl-2 family of proteins, which constitute a cell-death pathway. Bcl-2 is a death antagonist, and Bax, a death agonist. The setpoint that determines cell susceptibility to apoptosis is determined by the ratio of these molecules. Related to brown adipose tissue atrophy (BAT) in obesity, in part due to apoptosis of adipocytes | |
Caspase 3 and Caspase 9 | Mediate the inflammatory response and apoptotic cell death to maintain homeostasis. Caspase-dependent apoptosis is involved in the pathogenesis of obesity and progression of severe nonalcoholic steatohepatitis (NASH). Caspase 9 is an initiator and caspase 3 is an executioner of cell death |