Researchers in Switzerland have found that just the sight and smell of food triggers a short-term inflammatory response in the brain—and that this response is excessive enough in overweight individuals to impair insulin secretion.
Just the anticipation of a meal triggers a series of responses in the body, perhaps the most familiar being the watering of the mouth. But the hormone insulin, which regulates blood sugar, is also produced even before the first bite of food. Experts refer to this as the neurally mediated, or cephalic, phase of insulin secretion.
However, it was previously unknown how the sensory perception of a meal generated a signal to the pancreas to ramp up insulin production. Now, researchers from the University of Basel and University Hospital Basel have 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,” says study leader Professor Marc Donath from the Department of Biomedicine and the Clinic of Endocrinology.
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.
Circumstances are different when it comes to neurally mediated insulin secretion. “The smell and sight of a meal stimulate specific immune cells in the brain known as the microglia,” says study author Dr. Sophia Wiedemann, resident physician for internal medicine. “These cells briefly secrete IL1B, which in turn affects the autonomic nervous system via the vagus nerve.”
This system then relays the signal to the pancreas, where insulin is secreted. In the case of morbid obesity, however, this neurally mediated phase of insulin secretion is disrupted. Specifically, by the initial excessive inflammatory response.
The study’s findings were published recently in the journal Cell Metabolism.