Macrophage plays important role in cortisol and serotonin induced adipogenesis in vitro.

Psychological stress is an important cause to induce various metabolic disorders such as obesity, type II diabetes, and cardiovascular disorders by affecting the visceral adipose tissue. Pathophysiology of these diseases is often accompanied by the hyperactive immune system. The hyperactive immune system causes immune cells to infiltrate in the adipose tissue to increase the severity of metabolic disorders and to affect the levels of stress associated hormones, such as cortisol and serotonin. Cortisol and serotonin, alone or together, could regulate several aspects of the metabolic and immunological deregulations by manipulating the lipid accumulation or adipogenesis in cells. During adipogenesis, macrophages are recruited. Previous reports from the Aich laboratory established the roles of cortisol and serotonin to influence adipogenesis in pre-adipocytes 3T3-L1 in the presence and absence of macrophages. In the current study, we reported the role of macrophage RAW264.7, especially its polarized states, on differentiated murine adipocytes 3T3-L1 in the presence or absence of cortisol and serotonin. The current study also compares the differential role of macrophage recruitment on pre- and differentiated adipocytes.