Background. Although it is well known that adenovirus 36 (Ad36) is associated with obesity in humans as well as in animals, the detailed cellular mechanism is unclear.
Methods. Wild-type (WT) mice and monocyte chemoattractant protein-1 knockout (MCP-1−/−) mice were infected with Ad36, and their weights and inflammatory status were measured. Macrophage infiltration was examined in their reproductive fat pads and in a coculture system. The correlation between Ad36 antibody presence and MCP-1 levels was tested in human samples.
Results. We have shown that Ad36 infection stimulated an inflammatory state by increasing the level of MCP-1 through the activation of nuclear factor κB, which in turn induced the infiltration of macrophages into adipocytes. This induced inflammation resulted in viral obesity, which caused chronic inflammation and affected lipid metabolism. In contrast to WT mice, MCP-1−/− mice were protected from Ad36-induced inflammation and obesity. The MCP-1 levels in Ad36-antibody-positive human group were higher than those in the antibody-negative group.
Conclusions. These findings support the proposition that virus-induced inflammation is the cellular mechanism underlying Ad36-induced obesity. These results also suggest that MCP-1 plays a critical role in Ad36-induced obesity and that MCP-1 may be a therapeutic target in preventing virus-induced obesity.