Just Looking At Food Triggers An Inflammatory Response In The Brain, And It’s Important

The findings for the first time show how insulin release depends on a short-term inflammatory response in the brain after the sensory perception of food.
In anticipation of a meal, our bodies set off an array of responses that stimulate digestion and help control our blood sugar levels. One important physiological change is the secretion of insulin – even before the first bite is taken. Until now, it has been unclear how the sensory perception of a meal stimulates the pancreas to secrete insulin, but scientists now have identified an important part that may explain it.

Reporting in the journal Cell Metabolism, the researchers found that the inflammatory factor interleukin 1 beta (IL1B), typically involved in the immune response against pathogens and tissue damage, plays an important role in the stimulation of insulin secretion from the pancreas by sensory perception.

“The fact that this inflammatory factor is responsible for a considerable proportion of normal insulin secretion in healthy individuals is surprising, because it’s also involved in the development of type 2 diabetes,” explains study leader Professor Marc Donath in a statement.

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This process is known as neurally mediated insulin secretion, and relies on IL1B to trigger a cascade of signaling that stimulates the pancreas.

“The smell and sight of a meal stimulate specific immune cells in the brain known as the microglia,” says study author Dr Sophia Wiedemann. “These cells briefly secrete IL1B, which in turn affects the autonomic nervous system via the vagus nerve.” This process then signals down to the pancreas to release insulin.

The short-lived inflammatory response by sensory perception of food is important to secrete insulin – however, in people with type 2 diabetes, this system becomes overactive.

Chronic inflammation that damages pancreatic cells that secrete insulin can lead to adult-onset diabetes. In this case, the same inflammatory response by the sensory perception of food stimulates too much production and secretion of IL1B, which can cause overactivation of the system.

In obesity, however, the neurally mediated phase of insulin secretion becomes disrupted by the initial overstimulation of the inflammatory response. Hence, the new findings open up the potential to target IL1B therapeutically in adult-onset diabetes and obesity.

“Our results indicate that IL1B plays an important role in linking up sensory information such as the sight and smell of a meal with subsequent neurally mediated insulin secretion – and in regulating this connection,” concludes Professor Donath.

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