The cephalic phase of insulin release is modulated by IL-1b . 2022

pattismith

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https://doi.org/10.1016/j.cmet.2022.06.001

SUMMARY

The initial cephalic phase of insulin secretion is mediated through the vagus nerve and is not due to glycemic stimulation of pancreatic b cells.
Recently, IL-1b was shown to stimulate postprandial insulin secretion.

Here, we describe that this incretin-like effect of IL-1b involves neuronal transmission.

Furthermore, we found that cephalic phase insulin release was mediated by IL-1b originating from microglia

. Moreover, IL-1b activated the vagus nerve to induce insulin secretion and regulated the activity of the hypothalamus in response to cephalic stimulation.

Notably, cephalic phase insulin release was impaired in obesity, in both mice and humans, and in mice, this was due to dysregulated IL-1b signaling.

Our 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
 

pattismith

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Indeed, the chronic activation of IL-1b in patients with metabolic syndrome promotes b cell toxicity and ultimately failure—characteristic features of type 2 diabetes (Bo ̈ ni-Schnet- zler et al., 2008; Maedler et al., 2002).
In contrast to these dele- terious long-term effects, acute food intake primes myeloid cells to produce IL-1b, which then contributes to the physiological postprandial stimulation of insulin secretion (Dror et al., 2017).
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This indicates that a chronic excess of endogenous IL-1b activity due to obesity dysregulates the cephalic phase of insulin release in humans and mice, and this can be prevented by IL-1b antagonism.
this is an interesting study, showing that chronic inflammation reduces the insulin rise induced by the sugar taste.
Impaired muscarinic function of the vagus nerve should have the same effect.