An inflammatory response in the brain is triggered by the sight of a meal.
The mere sight and smell of a meal triggers the release of insulin even before the carbohydrates enter the body. For the first time, scientists from the University of Basel and the University Hospital Basel have shown that the release of insulin under these conditions depends on a short-term inflammatory response. However, this inflammatory response is so exaggerated in obese people that it can actually reduce their ability to secrete insulin. Even just thinking about food causes the body to react in a number of ways, the most well-known of which is probably mouth watering. The sugar-regulating hormone insulin, however, also enters the picture before we ever take a bite of food. This phase of insulin secretion is known as the neuromediated (or cephalic) phase.
The meal stimulates the immune defense
However, it was not previously known how the sensory perception of a meal sent a signal to the pancreas to increase insulin production. Now, scientists from the University of Basel and the University Hospital Basel have discovered a crucial piece of the puzzle: an inflammatory factor called interleukin 1 beta (IL1B), which is also involved in the immune response to infection or tissue damage. The team’s findings were published 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 because it is also involved in the development of type 2 diabetes,” explains study leader Professor Marc Donath from the Department of Biomedicine and Clinical Endocrinology. Also known as “adult-onset diabetes,” this form of diabetes is caused by chronic inflammation that destroys insulin-producing cells in 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 amounts. With this in mind, clinical studies are now examining whether inhibitors against this inflammatory factor are suitable for use as therapeutic agents for diabetes.
Short-term inflammatory response
The circumstances are different when it comes to neuro-mediated insulin secretion: “The smell and sight of a meal stimulate specific immune cells in the brain known as microglia,” says study author Dr. Sophia Wiedemann, internal medicine physician. “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 site of insulin secretion – the pancreas. In the case of morbid obesity, however, this neuronally mediated phase of insulin secretion is disrupted. Specifically, from the initial exaggerated inflammatory response, explained PhD candidate Kelly Trimigliozzi, who conducted the main part of the study in collaboration with Wiedemann. “Our results show that IL1B plays an important role in linking sensory information such as the sight and smell of a meal to the subsequent neuronally mediated insulin secretion – and in regulating this link,” summarizes Marc Donath. Reference: “The cephalic phase of insulin release is modulated by IL-1β” by Sophia J. Wiedemann, Kelly Trimigliozzi, Erez Dror, Daniel T. Meier, Jose Alberto Molina-Tijeras, Leila Rachid, Christelle Le Foll, Christophe Magnan, Friederike Schulze, Marc Stawiski, Stéphanie P. Häuselmann, Hélène Méreau, Marianne Böni-Schnetzler and Marc Y. Donath, 23 June 2022, Cell Metabolism.DOI: 10.1016/j.cmet.2021.06.
