“…As many studies have demonstrated, increased C3 levels, such as those found in obese persons, automatically give rise to higher levels of C3a-desArg, which can affect adipocytes and macrophages in the adipose tissue (Mamane et al, 2009). It is conceivable that the turnover of C3 also results in an activation of C5 and that the anaphylatoxins C3a and C5a, acting via the C3aR, C5aR1, and C5aR2 receptors, cause low-grade inflammation (Phieler et al, 2013a(Phieler et al, , 2013b. This possibility is corroborated by the fact that in lean individuals, adipose tissue preferentially releases anti-inflammatory adipokines such as transforming growth factor beta (TGF-beta) (Ailhaud et al, 1992), interleukin (IL)-10, IL-4, IL-13, IL-1 receptor antagonist (IL-1Ra), and adiponectin (Maeda et al, 1996), whereas in obesity, adipose tissue secretes proinflammatory cytokines, among which are IL-6 (Mohamed-Ali et al, 1997), INF-␥, TNF, IL-, (Hotamisligil et al, 1993), angiotensin II, leptin (Caro et al, 1996), resistin, vistafin, and plasminogen activator inhibitor 1 (Ouchi et al, 2011).…”