Researchers are attempting to understand how the inflammatory response in the brain can increase the risk of diabetes. Building upon the recognition that predictable physiologic responses occur when food is presented, such as salivation, the scientists explored whether similar triggers also generate insulin production.
On July 5, 2022, the researchers published their findings in Cell Metabolism. They discovered that at the sight of food, interleukin 1 beta (IL-1B)—an inflammatory factor also involved in the immune response to attack pathogens—plays a significant role in mealtime insulin production and may open new doors for the treatment of diabetes.
It is well established that the sight and smell of food signals the pancreas to produce and release insulin, but researchers from the University of Basel and University Hospital Basel have discovered that IL-1B, an inflammatory factor responsible for attacking pathogens or in responding to tissue damage, also "regulated the activity of the hypothalamus in response to cephalic stimulation" and neurally mediated insulin secretion.
This IL-1B factor regulates the physiologic response to tissue damage and pathogens; however, it has also been associated with its additional role of glucose metabolism. The authors referenced the chronic activation of IL-1B in patients with metabolic syndrome as a catalyst to beta-cell toxicity and subsequent hallmark failure of these cells in type 2 diabetes. With this in mind, the researchers examined whether inhibitors against this inflammatory factor could be options for developing novel pharmacologic agents for the treatment of diabetes.
According to lead author, Professor Marc Donath from the Department of Biomedicine and the Clinic of Endocrinology, and other colleagues involved in the study, "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."
The researchers highlighted that the key findings of their study included that the initial phase of insulin secretion is regulated by the vagus nerve and not because of the stimulation of pancreatic beta cells. Additionally, IL-1B was recently shown to stimulate postprandial insulin secretion via an incretin-like effect that does involve neuronal transmission.
The researchers reported that the initial insulin release—the cephalic phase—is mediated by IL-1B, which originates from microglia, and subsequently regulates both the activity of the hypothalamus as well as inducing insulin secretion. The researchers emphasized that they observed impaired insulin release during the cephalic phase in both obese humans and obese mice, which they attributed to dysregulation in IL-1B signaling.
The authors wrote that their "findings attribute a regulatory role to IL-1B in the integration of nutrient-derived sensory information, subsequent neuronally mediated insulin secretion, and the dysregulation of autonomic cephalic phase responses in obesity."
Dr. Donath concluded, "Our results indicate that IL-1B 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."
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