A model of “phenotypic switching” of macrophages in AT of obesity was initially proposed, where there is a transformation in the polarized states of macrophages from an anti-inflammatory type M2 macrophages (induced by Th2 cytokines, such as IL-4, IL-10, and IL-13)—which primarily exist in lean adipose tissue and express high levels of arginase-1 (which inhibit nitric oxide synthase activity) and also secrete anti-inflammatory cytokines (such as IL-10 and IL-1 receptor antagonists) [73, 75]—to a more proinflammatory “classically activated” M1 type (both macrophages residing in AT). Here, IL10 is linked to obesity due to melanocortin 4 receptor deficiency.