It has been known for some time that insulin production increases upon sensory perception of a meal. How exactly this happens, however, has remained a mystery until now.
In the present study, researchers at the University of Basel and University Hospital Basel have identified an inflammatory factor important in the immune response to pathogens and tissue damage known as interleukin 1 beta (1L1B) that plays a key role in insulin release from sensory perception.
"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," explained study leader Professor Marc Donath from the Department of Biomedicine and the Clinic of Endocrinology. In type 2 diabetes, 1L1B is produced and secreted in large quantities.
Through genetic and pharmacological mouse models, the researchers discovered that the smell and sight of a meal stimulate immune cells known as microglia in the brain. These cells then briefly secrete 1L1B, which affects the autonomous nervous system via the vagus nerve, which then relays signals to the pancreas to increase insulin production.
The researchers further noted that in obesity, this neurally-mediated phase of insulin secretion is disrupted due to an excessive inflammatory response, leading to less insulin release.
The researchers concluded that IL1B has a regulatory role in the neuronal stimulation of insulin secretion and in the dysregulation of autonomic responses in obesity.
As for limitations, they wrote that while they found that IL1B induces insulin secretion via stimulation of parasympathetic nerves, they note that the precise mechanisms that link IL1B to rapid neuronal activation require further study.
Sources: Science Daily, Cell Metabolism
