Researchers have discovered a new mechanism whereby certain brain networks can help control the release of insulin in mice.
Last week, we reported that the brain plays a crucial role for energy balance through compensatory changes in appetite that affect weight loss in obesity and type 2 diabetes.
This study suggests that a small group of neurons, called Proopiomelanocortin (POMC) neurons, may facilitate communication with the pancreas for blood glucose control.
According to researchers at the Institute for Research in Biomedicine, Barcelona, POMC neurons are involved in nutrient sensing and coordinate corresponding insulin release.
Those POMC neurons, located in the hypothalamus, have a protein expressed in their energy powerhouses, or mitochondria, that acts as a mediator in relaying information.
In an experiment, researchers tried removing this protein, called Mitofusin 1 (MFN1), from the POMC neurons of mice to see if it had any effect on their function.
Prior to this, the mice were kept in a fasting state, and researchers looked at what happened in the refeeding phase in the absence of MFN1.
The first observation was that the loss of MFN1 seemed to alter the capacity of those neurons to sense glucose between the fasting state and after being fed.
Second, they found that these defects in the mitochondria of POMC neurons had downstream effects on pancreatic beta cells, causing a lower secretion of insulin.
“It was surprising to discover that these neurons are involved not only in the control of the intake, which was already know, but also in the control of the amount of insulin secreted by beta cells,” one author of the study told Science Daily.
Looking more closely at the results, researchers found that the lack of MFN1 in POMC neurons led to increased oxidative stress, as evidenced by a rise in what’s known as reactive oxygen species (ROS).
High ROS production is thought to cause damage to mitochondria and can lead, in this case, to the death of POMC neurons.
Researchers tried decreasing oxidative stress by giving mice antioxidants, which resulted in preserving part of the function of POMC neurons, in response to which the pancreas started to secrete correct levels of insulin again.
Although we are still a long way from fully understanding the precise mechanisms underlying nutrient sensing in POMC neurons, these findings suggest that the brain plays a major role in regulating metabolism.