An obesogenic diet drives immune cell activation.
Although the role of dietary fat intake in obesity is a matter of considerable controversy, research has identified complex interrelationships between dietary components, inflammation, and immune function. For example, some evidence suggests that consumption of a diet high in fat drives inflammatory processes in the central nervous system and peripheral tissues, including the liver, adipose tissue, skeletal muscle, and gut, promoting metabolic dysfunction and weight gain. Findings from a recent study suggest that a high-fat diet promotes the activity of plasmacytoid dendritic cells, a type of immune cell.
Plasmacytoid dendritic cells, also known as natural interferon-producing cells, are critical components of both the innate and adaptive immune response. These specialized cells secrete copious amounts of type 1 interferons in response to a viral infection and then differentiate into professional antigen-presenting cells, which can stimulate T cell activity. Chronic stimulation of the plasmacytoid dendritic cells is linked with the development of autoimmune disorders and certain types of cancer. Although plasmacytoid dendritic cells are somewhat rare, they have been identified in visceral adipose tissue.
The investigators fed multiple groups of mice either a high-fat diet or standard chow for three weeks. They gave one group of mice on the high-fat diet a drug that blocks the migration of plasmacytoid dendritic cells into the visceral adipose tissue. Then they analyzed the animals’ blood, peripheral tissue, lymphatic organs, and visceral adipose tissue for the presence of plasmacytoid dendritic cells.
They found that after three weeks of a high-fat diet, plasmacytoid dendritic cells increased in the blood, liver, spleen, and visceral adipose tissue. The cells were especially abundant in fat-associated lymphoid clusters within the visceral adipose tissue. The animals on the high-fat diet gained weight and exhibited poor glucose tolerance, indicating metabolic dysfunction. Their visceral adipose tissue weight doubled during the three-week diet. Animals that received the drug that blocked plasmacytoid dendritic cell migration did not gain weight and demonstrated better glucose tolerance.
These findings suggest that an obesogenic diet drives visceral and peripheral weight gain, promotes glucose intolerance, and increases immune cell activation in the visceral adipose tissue of mice.
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