Scientists from the University of Basel found that even before carbohydrates reach the bloodstream, the very sight and smell of a meal trigger the release of insulin.
They found that this insulin release depends on a short-term inflammatory response that takes place in these circumstances.
In overweight people, however, this inflammatory response is so excessive that it can impair insulin secretion.
The research is published in the journal Cell Metabolism and was conducted by Professor Marc Donath et al.
Even the anticipation of a forthcoming meal triggers a series of responses in the body, perhaps the most familiar of which is the watering of the mouth.
But the hormone insulin, which regulates blood sugar, also arrives on the scene even before we tuck into the first mouthful of food. Experts refer to this as the neurally mediated (or cephalic) phase of insulin secretion.
In the study, the team identified an important piece of the puzzle: an inflammatory factor known as interleukin 1 beta (IL1B), which is also involved in the immune response to pathogens or in tissue damage.
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.
Also known as “adult-onset diabetes,” this form of diabetes is caused by chronic inflammation that damages the insulin-producing cells of the pancreas, among other things.
This is another situation in which IL1B plays a key role—in this case, it is produced and secreted in excessively large quantities.
With this in mind, clinical studies are now examining whether inhibitors against this inflammatory factor are suitable for use as therapeutic agents for diabetes.
The current results showed 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.
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