Overview: The simple sight and smell of a meal prior to consumption triggers the release of insulin. This insulin release is dependent on a short-term inflammatory response. In overweight people, this inflammatory response is so exaggerated that it can reduce insulin secretion.
Source: University of Basel
Even before carbohydrates reach the bloodstream, the sight and smell of a meal triggers the release of insulin.
For the first time, researchers from the University of Basel and the University Hospital Basel have shown that this insulin release is dependent on a short-term inflammatory response that occurs under these conditions.
In overweight individuals, however, this inflammatory response is so exaggerated that it can affect insulin secretion.
Even the anticipation of a meal to come triggers a series of reactions in the body, perhaps the most famous of which is mouth water. But the hormone insulin, which regulates blood sugar, also hits the spot before we eat the first bite. Experts call this the neurally mediated (or cephalic) phase of insulin secretion.
Meal stimulates the immune system
In the past, however, it was unclear how the sensory perception of a meal signaled the pancreas to increase 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 team reported their findings in the journal cell metabolism†
“The fact that this inflammatory factor is responsible for a significant proportion of normal insulin secretion in healthy individuals is surprising, as it is also involved in the development of type 2 diabetes,” explains study leader Professor Marc Donath of the Department of Biomedicine and the Clinic. of endocrinology.
This type of diabetes, also known as ‘adult diabetes’, is caused by chronic inflammation that damages the insulin-producing cells of the pancreas, among other things. This is another situation where IL1B plays a key role – in this case it is produced and secreted in excess.
With this in mind, clinical studies are now investigating whether inhibitors against this inflammatory factor are suitable for use as therapeutic agents for diabetes.
Short-lived inflammatory response
The 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, Physician Assistant for Internal Medicine.
“These cells transiently secrete IL1B, which in turn affects the autonomic nervous system through the vagus nerve.” This system then forwards the signal to the site of insulin secretion – that is, the pancreas.
However, in the case of morbid obesity, this neurally mediated phase of insulin secretion is disrupted. Particularly due to the initial excessive inflammatory response, as explained by PhD student Kelly Trimigliozzi, who conducted most of the research in collaboration with Wiedemann.
“Our results indicate that IL1B plays an important role in linking sensory information such as sight and smell of a meal with subsequent neurally mediated insulin secretion – and in regulating this connection,” summarizes Marc Donath.
About this inflammation research news
Original research: Open access.
†The cephalic phase of insulin release is modulated by IL-1bby Marc Donath et al. cell metabolism
The cephalic phase of insulin release is modulated by IL-1b
The initial cephalic phase of insulin secretion is mediated by the vagus nerve and is not due to glycemic stimulation of pancreatic cells. Recently, IL-1β was shown to stimulate postprandial insulin secretion.
Here we describe that this incretin-like effect of IL-1β involves neuronal transmission.
Furthermore, we found that the main phase insulin release was mediated by IL-1β derived from microglia. In addition, IL-1β activated the vagus nerve to induce insulin secretion and regulated the activity of the hypothalamus in response to cephalic stimulation.
Notably, cephalic phase insulin release was reduced in obesity in both mice and humans, and in mice this was due to dysregulated IL-1β signaling.
Our findings attribute a regulatory role to IL-1β in the integration of nutrient-derived sensory information, subsequent neuronally mediated insulin secretion, and the dysregulation of autonomic cephalic phase responses in obesity.