Food Consumption Elicits Protective Inflammation

Findings from a recent study suggest that every meal consumed promotes inflammation due to the introduction of new bacterium into the body.

Since the body is tasked with ingesting food and glucose, and fighting off bacteria, an inflammatory response is triggered. Counterintuitively, this inflammatory response is actually beneficial, and produces a protective effect.

However, in individuals who are overweight, this protective response fails, and can lead to diabetes, according to a study published by Nature Immunology.

Patients with type 2 diabetes are known to have chronic inflammation that leads to numerous adverse health effects. Therefore, many studies have attempted to treat patients with diabetes by inhibiting high production of interleukin-1beta (IL-1beta), which is involved with inflammatory processes.

In healthy patients, short-term inflammatory responses are important in glucose uptake, and immune system activation, according to the study.

In the study, the researchers discovered that the prevalence of macrophages increases during meals. These immune cells then create IL-1beta in accordance with the concentration of glucose in the blood. For example, more IL-1beta would be created after the consumption of food with a high amount of sugar.

IL-1beta production leads to increased insulin production in pancreatic beta cells, which then causes macrophages to ramp up insulin production, according to the study. Insulin and IL-1beta work in unison to regulate blood sugar, and IL-1beta transports glucose to the immune system to keep it active.

The study authors said that metabolism and the immune system working together is dependent on the bacteria and nutrients that are consumed each meal. Ideal amounts of nutrients allow the immune system to fight off foreign bacteria that may have resulted from consuming raw or undercooked food.

If inadequate nutrients are consumed, calories that would be used to stimulate the immune system are allocated to more important life functions, which may explain why certain infectious diseases have spread during times of famine, according to the study.

Additional studies are needed to confirm these effects, but if proven, this may present a new treatment target for patients with diabetes whose inflammatory response is inadequate.