Researchers from the University of Basel and University Hospital Basel have identified how the sensory perception of a meal generates a signal to the pancreas to ramp up insulin production: inflammatory factor interleukin 1 beta (IL1β), which is also involved in the immune response to pathogens or in tissue damage. The team reported their findings in Cell Metabolism.
The researchers, led by Marc Y. Donath, MD, write that they hypothesized that IL-1β exerts its secretagogue effect on insulin secretion via stimulation of the parasympathetic nervous system. “Using genetic and pharmacological models, we found IL1β to mediate its stimulatory effect on insulin secretion via central muscarinic signaling,” the authors write. “In order to substantiate the neuronal involvement of IL1β-mediated insulin release, we studied the cephalic phase insulin response as a prime example of centrally mediated insulin secretion. We identified IL1β as a crucial mediator of this cephalic phase reflex.”
The researchers found that the smell and sight of a meal stimulate microglia, which secrete IL1β, which the vagus nerve then relays to the pancreas, a process that is disrupted in mice and humans with obesity. “Our findings attribute a regulatory role to IL1β in the integration of nutrient-derived sensory information, subsequent neuronally mediated insulin secretion, and the dysregulation of autonomic cephalic phase responses in obesity,” the authors write. “This identifies a neuro-immunologic endocrine circuit in the regulation of insulin secretion.”
“Our results indicate that IL1β 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,” Donath says.
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