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The serum levels of IL-6 positively correlate with obesity in humans and predict the risk of development of insulin resistance and diabetes mellitus type 2. 4 IL-6 is produced by a variety of metabolic tissues that include WAT, hepatocytes, ß-cells, and skeletal muscle. Thus, circulating IL-6 could mediate a crosstalk between these organs that results in a downward spiral toward systemic insulin resistance and decreased insulin secretion. 5 Furthermore, obesity was found to be associated with macrophage accumulation in murine and human WAT. 6 Chemokines such as CCL2/monocyte chemoattractant protein-1 (MCP-1) and CCL3/macrophage inflammatory protein.
Plasma concentration of cytokines/chemokines, IFN-?, IL-6, IL-12p40, TNF, sCD40L, IL-1 ß, IL-4, IL-10, IL-13, IL-RA, MCP-1, fractakine, eotaxin, IL-15, IL-17A, TGF-a, macrophage inflammatory proteins-1a, (MIP-1a or CCL3), Macrophage inflammatory proteins.
The major growth factors, cytokines and chemokines identified at the fracture site are noted in Table 1, along with references to their potential to induce migration of MSCs and endothelial-type cells. Studies that either decrease or increase the concentration of these factors during bone healing show that they have a significant impact on the fracture healing process. However, their potential role as chemotactic agents during healing is largely unknown, as it is difficult to clearly separate effects on cell recruitment from significant effects on cell proliferation, differentiation and angiogenesis. Surprisingly, there is sparse information regarding the expression of specific chemokines (CXC, CC, (X)C and CX3C families) during fracture healing, with the exception of CXCL12. Increased expression of CCL2 (monocyte chemotactic protein-1) and CCL3 (macrophage inflammatory protein.