Much of the long-term harm caused by excess visceral fat tissue is due to raised levels of chronic inflammation, the inappropriate over-activation of the immune system characteristic of both obesity and aging. Chronic inflammation accelerates the progression of near all of the common age-related conditions. There are numerous mechanisms via which fat tissue rouses an immune response: cellular debris that triggers immune cells into action; generation of excessive numbers of senescent cells; inappropriate signaling from fat cells that mimics the response to infection; infiltration of inflammatory macrophages into fat tissue; and so forth. Researchers here investigate some of the details of the way in which the immune system interacts with visceral fat, focusing on a role for B cells in spurring the inflammation that results.
Previous work found that as people age, their body's ability to generate energy by burning belly fat is reduced. Consequently, fat that surrounds the internal organs increases in the elderly. Researchers had found that the immune cells necessary to the fat-burning process, called macrophages, were still active but their overall numbers declined as belly fat increased with aging. This latest study found that something else is happening as well. Adipose B cells in belly fat unexpectedly proliferated as animals aged, contributing to increased inflammation and metabolic decline. "These adipose B cells are a unique source of inflammation. Normally the B cells produce antibodies, and defend against infection. But with aging, the increased adipose B cells become dysfunctional, contributing to metabolic disease."
When they are working correctly, some B cells expand as needed to protect the body from infection, and then contract to baseline. But with aging, they don't contract in belly fat. This predisposes to diabetes and metabolic dysfunction like inability to burn fat. Researchers theorizes that this ongoing expansion may be due to increased human life expectancy - a pushing of the body's cells beyond their evolutionary limits. Researchers discovered that adipose B cells expand by receiving signals from nearby macrophages. Relatedly, they found that by reducing the macrophage signal and by removing adipose B cells, they could reverse the expansion process, and protect against age-induced decline in metabolic health.