How gut bacteria negatively influences serotonin and blood sugar levels

Summary: A new study shows how the microbiome communicates with cells producing serotonin to influence blood sugar levels. The microbiome can worsen metabolism by signaling to cells in the gut that produce serotonin. This drives up serotonin levels. The rise in blood serotonin levels causes metabolic problems.

Source: Flinders University

Millions of people around the world experience serious blood sugar problems which can cause diabetes, but a world-first study is revealing how gut bacteria impact the normally feel-good hormone serotonin to negatively influence blood sugar levels.

Serotonin, a neurotransmitter in the brain, is nicknamed the ‘happy hormone’ and is normally linked with regulating sleep, well-being, and metabolism. But the gut actually produces 95 percent of it, and not in the happy form as we know about in the brain.

In a study published in the leading international journal Proceedings of the National Academy of Sciences (PNAS) today, researchers from Flinders, SAHMRI, and McMaster University in Canada show exactly how bacteria living in the guts of mice, the microbiome, communicate with cells producing serotonin to influence blood sugar levels in the host body.

Professor Damien Keating, Head of Molecular and Cellular Physiology at Flinders University and Deputy Director of the Flinders Health and Medical Research Institute, says this study sheds light on the unanswered question about exactly how bacteria in the microbiome communicate to control glucose levels in the metabolism.

“We found that the microbiome worsens our metabolism by signaling to cells in the gut that produce serotonin. They drive up serotonin levels, which we previously showed to be increased in obese humans, and this rise in blood serotonin causes significant metabolic problems.”

“The next step will be to understand exactly which bacteria do this, and how, in the hope that this could lead to new approaches to regulating blood sugar levels in humans,” says Professor Keating.

This study is the first to show how the microbiome, the bacteria that lives in the gut, effectively communicate with an organism to impact the hosts’ metabolism.

This is a drawing of a stomach

This study is the first to show how the microbiome, the bacteria that lives in the gut, effectively communicate with an organism to impact the hosts metabolism. The image is in the public domain.

If researchers can better understand which bacteria cause the signals to produce serotonin in the gut, treatments could one day be developed to reduce blood sugar levels, and this is a first step towards better understanding this process.

“This is an exciting revelation that can one day have direct implications for human health disorders such as diabetes, but much more research like this is required in the years to come.”

About this neuroscience research article

Source:
Flinders University
Media Contacts:
Damien Keating – Flinders University
Image Source:
The image is in the public domain.

Original Research: Open access
“The gut microbiome regulates host glucose homeostasis via peripheral serotonin”. Alyce M. Martin, Julian M. Yabut, Jocelyn M. Choo, Amanda J. Page, Emily W. Sun, Claire F. Jessup, Steve L. Wesselingh, Waliul I. Khan, Geraint B. Rogers, Gregory R. Steinberg, and Damien J. Keating.
Scientific Reports doi:10.1073/pnas.1909311116.

Abstract

The gut microbiome regulates host glucose homeostasis via peripheral serotonin

The gut microbiome is an established regulator of aspects of host metabolism, such as glucose handling. Despite the known impacts of the gut microbiota on host glucose homeostasis, the underlying mechanisms are unknown. The gut microbiome is also a potent mediator of gut-derived serotonin synthesis, and this peripheral source of serotonin is itself a regulator of glucose homeostasis. Here, we determined whether the gut microbiome influences glucose homeostasis through effects on gut-derived serotonin. Using both pharmacological inhibition and genetic deletion of gut-derived serotonin synthesis, we find that the improvements in host glucose handling caused by antibiotic-induced changes in microbiota composition are dependent on the synthesis of peripheral serotonin.

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