The sight of a mouthwatering dish can certainly be enough to send our senses into overdrive, and a new study has demonstrated how the mechanisms behind this may play an important role in type 2 diabetes. Scientists have shown for the first time how the sight or smell of a meal can trigger an inflammatory response that guides insulin production, and is also known to play a role in the onset of diabetes, creating some unique possibilities for intervention.
Whether it's patiently waiting for a pizza delivery or the arrival of a steak at a nice restaurant, the anticipation of food can cause a range of responses in the human body. While salivating is one most will be acquainted with, the body also begins producing insulin as a part of this process, a hormone that plays an important role in regulating blood sugar.
This phenomenon is known as the neurally mediated, or cephalic, phase of insulin secretion, but little is known about how exactly the anticipation of food prompts the pancreas to accelerate production of insulin. Researchers from the University of Basel explored this in mice, which were subjected to bouts of fasting and then introduced to food thereafter.
Sampling the blood of the mice immediately after their first bite enabled the scientists to monitor the increase in insulin secretion, and probe the underlying mechanics. Part of this involved a focus on an inflammatory factor called interleukin 1 beta (IL1B), which is part of the body's natural immune response to pathogens and tissue damage. The scientists uncovered another role it plays, by treating the mice with IL1B inhibitors that tempered neurally mediated insulin secretion as a result.
“Our results indicate 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,” said study leader Marc Donath.
In healthy individuals, the autonomic nervous system relays the IL1B signals to the pancreas to facilitate insulin secretion. But in mouse models and human studies of obesity, the scientists found that this type of signaling was impaired. The mouse models tied this to IL-1B and showed the dysfunction to be the result of an excessive inflammatory response that compromises insulin production.
Adding to the significance of the discovery is that IL1B is already known to play a role in type 2 diabetes, where it is produced and secreted in large amounts. In this context, it contributes to the chronic inflammation that damages the insulin-producing cells in the pancreas.
“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,” explains study leader Professor Marc Donath.
This raises the possibility that IL1B inhibitors could be deployed as treatments for diabetes, something the scientists are now looking to explore through clinical studies.
The research was published in the journal Cell Metabolism.
Source: University of Basel