An intriguing new animal study, led by researchers from the University of Southern California, is suggesting a hunger-regulating hormone secreted from the stomach may also influence memory and cognitive function. The study builds on a growing body of research into gut-brain communication via the vagus nerve.
In 2018 a team of USC researchers published a compelling study investigating the cognitive repercussions gut-brain communication disruptions. The research focused on the vagus nerve, a long nerve that mediates communication between the digestive system and the brain.
Disrupting the vagus nerve unsurprisingly impaired an animal’s ability to regulate its eating behaviors but the study also discovered unexpected cognitive impairments. The earlier study found animals with this gut-brain communication pathway severed displayed spatial working memory impairments. This suggested gut-brain communication via the vagus nerve played some kind of unforeseen role in memory function.
Following up on that study, the USC team’s latest project focused on a key hormone called ghrelin. Secreted by cells in the gastrointestinal tract, ghrelin is known as the “hunger hormone” due to its function regulating eating behaviors. The hypothesis underpinning this new research is that ghrelin may be influencing broader cognitive functions beyond feeding behaviors.
In rats, the researchers blocked the activity of ghrelin receptors on gut neurons. These are the receptors that communicate with the brain, via the vagus nerve, in response to ghrelin secretions in the gut. So unlike the prior UCS study, which broadly impaired vagus nerve communication, this study focused specifically on ghrelin’s communication with the brain via the vagus nerve.
Scott Kanoski, lead author on the new study, says the experiments first saw the animals, unsurprisingly, eating more frequently. The rats both gained weight, and displayed disruptions to glucose regulation. However, this ghrelin gut-brain block strangely did not lead to the animals eating more food in totality.
“… it didn't seem to be affecting how much food they ate," says Kanoski. “[Instead] they increased their frequency of eating, so that they consumed more meals and they compensated for that by reducing the size of their meals. We think that the increased eating frequency is related to their memory impairment. Memory from when you last ate will influence how soon you eat again. It led the rats in our study to eat sooner.”
This memory impairment induced by blocking ghrelin signaling did not alter the animals’ ability to remember where their food was, but it did seem to result in the animals rapidly forgetting they had eaten a given meal.
"The animals were impaired in a certain type of memory, called episodic memory," explains Elizabeth Davis, co-author on the new study. "This is the type of memory that helps you remember your first day of school, or what you ate for breakfast yesterday.”
Davis stresses the need for much more research before this particular gut-brain pathway could be leveraged as a human clinical treatment. However, the new study does add to the evidence suggesting a potential future gut-brain role in treatments for dementia and cognitive decline.
The new study was published in the journal Current Biology.
Source: USC
