Simply Looking at Food Triggers an Inflammatory Response in the Brain



The sight of food triggers an inflammatory reaction in the brain.

Even before carbohydrates enter the body, the sheer sight and smell of a meal trigger the release of insulin. Researchers from the University of Basel and University Hospital Basel have demonstrated for the first time that the insulin release in these circumstances is dependent on a transient inflammatory response. However, in obese individuals, this inflammatory response is so extreme that it can actually impair their capacity to secrete insulin.

The body reacts to food in many different ways, the most well-known of which is perhaps the wetting of the mouth. However, before we even take a mouthful of food, the hormone insulin, which controls blood sugar, enters the picture. The cephalic (or neurally mediated) phase of insulin secretion is this stage.

Meal boosts immunological response

Prior to this study, it was unclear how the sensory perception of a meal prompted the pancreas to produce more insulin. A vital component of the riddle has now been found by researchers from the University of Basel and University Hospital Basel. It is an inflammatory substance called interleukin 1 beta (IL1B), which is also involved in tissue damage or the immunological response to infections. The results of the team's research were released in the journal Cell Metabolism.

Since this inflammatory factor also contributes to the development of type 2 diabetes, it is surprising that it accounts for a sizable portion of normal insulin secretion in healthy individuals, says study leader Professor Marc Donath from the Department of Biomedicine and the Clinic of Endocrinology.

This type of diabetes, also referred to as "adult-onset diabetes," is brought on by a persistent inflammatory response that, among other things, harms the pancreatic cells responsible for making insulin. Another condition where IL1B is crucial is this one; in this instance, it is generated and secreted in extremely high levels. In light of this, clinical investigations are currently evaluating whether inhibitors of this inflammatory factor are appropriate for use as diabetic treatment drugs.

When it comes to neurally mediated insulin release, conditions are different. According to study author Dr. Sophia Wiedemann, a resident in internal medicine, "the smell and sight of a meal excite certain immune cells in the brain known as the microglia." These cells momentarily release IL1B, which then influences the vagus nerve and the autonomic nervous system. The signal is subsequently transmitted by this mechanism to the pancreas, which produces insulin.

However, this neurally mediated stage of insulin secretion gets messed up in cases of severe obesity. Particularly, by the initial exaggerated inflammatory reaction, as Kelly Trimigliozzi, a doctorate candidate who worked with Wiedemann to conduct the majority of the study, explained.

According to Marc Donath's findings, IL1B is critical in both regulating and connecting sensory input, such as the sight and smell of food, with subsequent neurally driven insulin release.

A study 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 entitled "The cephal Cell Metabolism, June 23, 2022.

By UNIVERSITY OF BASEL 

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