This article is a summary of the published study:Fasting induces a form of autonomic synaptic plasticity that prevents hypoglycemia
When we fast, our body activates a response called the counter-regulatory response (CRR) to prevent low blood sugar (hypoglycemia). One important part of this response is the autonomic nervous system, which controls the release of a hormone called epinephrine from certain cells in our adrenal glands. This hormone helps increase glucose production in our liver to maintain normal blood sugar levels. However, we don’t know if changes in how the autonomic nervous system works affect the strength of the CRR and our ability to withstand fasting without experiencing low blood sugar.
In this study, researchers found that fasting leads to changes in how signals are transmitted between nerve cells at a specific connection point called the synapse. These changes primarily involve an increase in the strength of communication between nerve cells before the release of epinephrine. Through genetic and drug-related experiments, the researchers discovered that a molecule called neuropeptide Y and its specific receptors in the adrenal glands play a crucial role in this process. When neuropeptide Y is absent, fasting no longer leads to an increase in epinephrine release, which can result in low blood sugar.
These findings show that changes in the autonomic nervous system during fasting can affect the CRR and our ability to maintain normal blood sugar levels. They highlight the importance of synaptic plasticity (changes in communication between nerve cells) in this process.
